Protective immunity against Cryptocaryon irritans

[ThRoewer]

This seems to be the standard reply around here:

A small number of fish develop temporary immunity to the strain of cryptocaryon irritans they encounter. However, they are carriers of that strain and can infect other newly introduced fish.

But if you read the actual works on this and not just the overly simplified and rather careful worded abstracts, the picture is quite a bit different:

Most (if not all) otherwise healthy and fit fish will develop immunity to Cryptocaryon irritans after surviving a non lethal infection and then enough rest to recover.
They will maintain this immunity as long as Cryptocaryon is present and their immune system is not compromised through stress or other external factors.

The level of immunity seems to relate to the level of the immunizing infection. While not being tested in those studies I assume the level of immunity may also increase with duration of exposure, at least that is what my personal observations indicate.

Not fully immune fish may of course be carriers of the infection.

Burgees' tests (1992 Dissertation) showed that all exposed fish acquired immunity and that this immunity will last at least 6 months without the presence of Cryptocaryon.
Fish challenged wit a lethal dose after 3 months were 100% immune (no infection could be found).
After 6 months 2 previously unchallenged fish were challenged with a lethal dose of Cryptocaryon but only contracted a minor infection.
None of the immunized fish died due to challenge with a lethal dose in any of the studies.

Other studies had different timelines but otherwise corresponding findings.

There have been plenty of tests on this under laboratory settings but they usually only had a single non lethal immunization exposure and a single challenge.
I have not yet found any repots on long term exposure studies. Though my own observations and those of others here indicate that most fish may actually gain full immunity in the prolonged present of Cryptocaryon and that the parasite eventually will die out due to lack of suitable hosts in the system unless reintroduced with new acquisitions.
From my observations I would also assume that this immunity is not strain specific.

Fish that are under constant stress may only gain partial or no immunity. This includes being constantly sick with Cryptocaryonosis.


Here are some more recent works on this I could find in full text versions:

Protective immunity in grouper (Epinephelus coioides) following exposure to or injection with Cryptocaryon irritans
X.-C. Luo et al. / Fish & Shellfish Immunology 22 (2007) 427e432
http://scsagr.scsfri.ac.cn/upimg/200853010029.pdf

Misumi, I. 2009
THE CILIATED PROTOZOAN PARASITE, Cryptocaryon irritans, AND PROTECTIVE IMMUNITY IN MARINE FISH
http://nsgl.gso.uri.edu/hawau/hawauy09002.pdf


Now, that nobody get's me wrong: this is not a call to skip QT or not do TTM or other preventive measures.
Even if Cryptocaryon is not of concern there are plenty of other diseases that can kill your fish.
Also, most do not keep their fish in a stress free environment. For example any tang in a too small tank will be too stressed out to ever gain full immunity, and most tanks are way too small for the tangs kept in them.

 

[snorvich]

i would comment, but my current medical situation has sapped my energy.

 

[alprazo]

THRoewer, excellent reply. :thumbsup:

 

[laga77]

Nice work! Thanks.

 

[ThRoewer]

It seems the same immunity responses exist for Amyloodinium and likely all other protozoan parasites.

Acquired immunity to amyloodiniosis is associated with an antibody response.

Abstract

The dinoflagellate Amyloodinium ocellatum, which causes amyloodiniosis or 'marine velvet disease', is one of the most serious ectoparasitic diseases plaguing warmwater marine fish culture worldwide. We report that tomato clownfish Amphiprion frenatus develop strong immunity to Amyloodinium ocellatum infection following repeated nonlethal challenges and that specific antibodies are associated with this response. Reaction of immune fish antisera against dinospore and trophont-derived antigens in Western blots indicated both shared and stage-specific antibody-antigen reactions. A mannan-binding-protein affinity column was used to isolate IgM-like antibody from A. frenatus serum. The reduced Ig consisted of one 70 kD heavy chain and one 32 kD light chain with an estimated molecular weight of 816 kD for the native molecule. Immunoglobulin (Ig) isolated from immune but not non-immune fish serum significantly inhibited parasite infectivity in vitro. An enzyme-linked immunosorbent assay (ELISA) was developed using polyclonal rabbit antibody produced against affinity-purified A. frenatus Ig. Anti-Amyloodinium serum antibody was not always detectable in immune fish, although serum antibody titers in immune fish increased after repeated exposure to the parasite. These results suggest that there may be a localized antibody response in skin/gill epithelial tissue, although antibody was rarely detected in skin mucus.

It seems also that acquired immunity may in some cases even be transferred to naïve fish in the same system or passed on to offspring:

Immunization against parasitic diseases of fish.

Abstract

Parasitologists have not, in the past, exploited the immune system to protect fish against parasitic diseases. In the past few years, however, there has been an increased interest in adopting this strategy, and we have made steady and promising progress against a few parasites which are of economic importance. Amyloodinium ocellatum is an ectoparasitic dinoflagellate on brackish and marine fishes, which may also cause problems to aquarium fishes. Antiserum from fish inoculated intraperitoneally (i.p.) with living dinospores of the parasite immobilizes and agglutinates living dinospores; it also reduces parasite infectivity in cell culture. Cryptobia salmositica is a pathogenic haemoflagellate of salmonids on the Pacific coast of North America, causing mortality in semi-natural and intensive salmon culture facilities. A live attenuated vaccine inoculated i.p. protects susceptible juvenile and adult fish for at least 24 months. The protection involves production of complement fixing antibodies, phagocytosis, and antibody-dependent and antibody-independent T-cell cytotoxicity. A monoclonal antibody against a surface membrane glycoprotein (199-200 kDa is therapeutic in that it significantly reduces parasitaemias when inoculated into fish with acute disease. Ichthyophthirius multifiliis is an ectoparasitic ciliate of freshwater fishes with world wide distribution, usually causing disease when fish are stressed and/or when environmental conditions are favourable for parasite multiplication. Live theronts injected into the body cavity protect fish, and monoclonal antibodies with immobilizing activity upon parasites have been developed. There is some evidence of passive transfer of protective immunity from immune to naive fish, and to eggs. Diplostomum spathaceum is an intestinal parasite of gulls; the metacercaria stage of the parasite encyst and causes disease and mortality in numerous species of freshwater fish in Europe and in North America. Fish injected i.p. with sonicated/killed cercariae or metacercariae have fewer metacercariae in the eyes and survives longer. Lepeophtheirus salmonis and Caligus elongatus are parasitic copepods (sea lice), and they are important parasites of Atlantic salmon in cage cultures. A vaccine against fish lice is plausible, and the efficacy of about 20 candidate antigens in protecting fish is being tested.

Protective immunity in fish against protozoan diseases.

Abstract

The demand for and costs of producing land-based animal protein continues to escalate as the world population increases. Fish is an excellent protein, but the catch-fishery is stagnant or in decline. Intensive cage culture of fish is a viable option especially in countries with lakes/rivers and/or a long coastline; however, disease outbreaks will likely occur more frequently with cage culture. Hence protective strategies are needed, and one approach is to exploit the piscine immune system. This discussion highlights immunity (innate/natural and adaptive/acquired) in fish against three pathogenic protozoa (Amyloodinium ocellatum, Ichthyophthirius multifiliis and Cryptobia salmositica). Histone-like proteins in the mucus and skin of naturally resistant fish kill trophonts of A. ocellatum, and also may cause abnormal development of tomonts. Breeding of Cryptobia-resistant brook charrs is possible as resistance is controlled by a dominant Mendelian locus, and the parasite is lysed via the Alternative Pathway of Complement Activation. Production of transgenic Cryptobia-tolerant salmon is an option. Recovered fish are protected from the three diseases (acquired immunity). Live I. multifiliis theronts injected intraperitoneally into fish elicit protection. Also, a recombinant immoblizing-antigen vaccine against ichthyophthirosis has been developed but further evaluations are necessary. The live Cryptobia vaccine protects salmonids from infections while the DNA-vaccine stimulates production of antibodies to neutralize the disease causing factor (metalloprotease) in cryptobiosis; hence infected fish recover more rapidly.

 

[ThRoewer]

This might also be of interest:

Studies on Amyloodinium ocellatum (Dinoflagellata) in Mississippi Sound: natural and experimental hosts (Full PDF here)

Abstract

Four species of parasitic dinoflagellates have been found to occur naturally on the gills and fins of Mississippi Sound fishes: Amyloodinium ocellatum (Brown 1931) Brown and Hovasse 1946, Oodinium cyprinodontum Lawler 1967, and two undescribed species. Sixteen of 43 species of fishes examined had natural gill infections of A. ocellatum. Seventy-one of 79 species of fishes exposed to A. ocellatum dinospores were susceptible, and succumbed, to the dinoflagellate. Eight did not die even though exposed to numerous dinospores. The most common signs in an infested fish were spasmodic gasping and uncoordinated movements. Trophonts of A. ocellatum were found on the gills, skin, fins, eyes, pseudobranchs, membranes of the branchial cavity and around the teeth; and in the lateral line pits, nasal passages, esophagus, and intestine of experimentally infected fishes. The dinoflagellate causes extensive mortalities of fishes held under closed-system mariculture conditions

 

[Deinonych]

Good stuff. Thanks for posting.

 

[ThRoewer]

Anybody feel free to add whatever you find

 

[snorvich]

Fish that are newly acquired are not often healthy and fit. Furthermore, many are placed in environments that are stressful (aggressive neighbors, over crowding, insufficient feeding, etc). Depending on immunity, IMO, will result in some unhappy aquarists. Studies rarely provide all variables and often do not match aquarist environments. A great intellectual treatise . . .

 

[HumbleFish]

Very interesting information!

 

[ThRoewer]

For those interested, here is Peter Burgess complete dissertation on protective immunity against Cryptocaryon:

CRYPTOCARYON IRRITANS BROWN, 1951 (CILIOPHORA):
TRANSMISSION AND IMMUNE RESPONSE
IN THE MULLET CHELON LABROSUS (RISSO, 1826)
by
PETER JOHN BURGESS
B.Sc. (Hons.), M.Sc., M.Phil.​

Direct link to PDF: https://pearl.plymouth.ac.uk/bitstr...PETER JOHN BURGESS.PDF?sequence=1&isAllowed=y

 

[snorvich]

Fish that are newly acquired are not often healthy and fit. Furthermore, many are placed in environments that are stressful (aggressive neighbors, over crowding, insufficient feeding, etc). Depending on immunity, IMO, will result in some unhappy aquarists. Studies rarely provide all variables and often do not match aquarist environments. A great intellectual treatise . . .

This. Aquarium conditions and lab conditions are not congruent. So we will just have to disagree.,

 

[Dmorty217]

Though the studies are intriguing, the risk/reward involved is hardly worth hoping that your fish will develop immunity. Ich is really the least of the problems disease wise. Flukes, velvet, and brook will kill fish much more quickly and there is no immunity for flukes I'm aware of, short term or otherwise.

 

[ThRoewer]

This. Aquarium conditions and lab conditions are not congruent. So we will just have to disagree.,

Yes, lab tanks are usually less accommodating for fish. Lab conditions are geared for control and repeatability, not for comfort of the fish.

Of course immunity (to Cryptocaryon) is not to be expected with severely stressed or freshly imported fish, yet even there I have observed it.
Even in quarantine tanks under less than stellar conditions I have seen ich come and go and never return.

It is not that I say this is a safe or even recommended path, yet it is a possibility that should not be outright dismissed.
It is for sure more common in the hobby than generally acknowledged as most fish that make it here have had at some point contact with ich and developed immunity.

In the end everyone needs to make an informed decision on which path is the best and most suitable for the situation on hand. That's what this thread is about: knowledge.

Though the studies are intriguing, the risk/reward involved is hardly worth hoping that your fish will develop immunity. Ich is really the least of the problems disease wise. Flukes, velvet, and brook will kill fish much more quickly and there is no immunity for flukes I'm aware of, short term or otherwise.

Correct. Ich is the only parasite I don't worry too much about.

I would never take a chance with velvet or brook, even though some level of immunity to those is possible as well. But these are just too fast in killing fish.

So far I haven't found anything about immunity against flukes (or rather monogeneans), though given the direct and on the fish lifecycle I wouldn't be surprised if there is something along those lines. Or how would fish survive them in the wild?

 

[Deinonych]

Or how would fish survive them in the wild?

Cleaner shrimp.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4338302/

 

[ThRoewer]

Cleaner shrimp.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4338302/

Great article! Thanks for sharing.

I have cleaner shrimp in two of my tanks, but those seem to be pretty lazy. My regals literally need to chase and push them to get "cleaned". Of course that reluctancy may also be due to the fact that there is not much nutritious to find for the shrimp besides some minor ich which they don't care much for.

 

[ThRoewer]

Histone-like proteins from fish are lethal to the parasitic dinoflagellate Amyloodinium ocellatum (Full PDF)
E. J. NOGA, Z. FAN and U. SILPHADUANG

Abstract

Antimicrobial proteins were purified from acid extracts of rainbow trout (Oncorhynchus mykiss) and sunshine bass (Morone saxatilis male×M. chrysops female) skin, gill and spleen by reverse-phase HPLC. Mass spectrometry and amino acid sequence data suggest that these proteins are closely related to histone H2B and histone H1 and thus they were designated histone-like proteins (HLPs). These proteins were lethal to Amyloodinium ocellatum, which is one of the most important parasitic agents affecting fish. Antibiotic concentrations as low as 12·5 μg/ml were inhibitory. Activity was directed against the trophont (feeding) stage of the parasite, while the disseminative (dinospore) stage was unaffected. Thus, HLPs act unlike typical drugs used to treat amyloodiniosis, which usually target the dinospore. Both the ability of the parasite to infect host cells, as well as the ability to grow and differentiate after infection were severely inhibited. This is in contrast to magainin 2, which was similarly toxic to both the dinospore and trophont stages. These findings provide further evidence that histone-like proteins may be important defensive molecules in fish.

Host site of activity and cytological effects of histone-like proteins on the parasitic dinoflagellate Amyloodinium ocellatum (Full PDF)
Edward J. Noga, Zhiqin Fan, Umaporn Silphaduang

Abstract

Histone-like proteins (HLPs) are broad-spectrum, endogenously produced antibiotics which we have isolated from tissues of rainbow trout Oncorhynchus mykiss and hybrid striped bass (Morone saxatilis male × M. chrysops female). Here, we show that HLP-1, which has high sequence homology to histone H2B, equally inhibited both young and mature trophonts of the important ectoparasite Amyloodinium ocellatum. In addition to direct killing of Amyloodinium trophonts, there was evidence that HLP-1 from both rainbow trout and hybrid striped bass caused severe developmental abnormalities, including delayed development, in both the parasitic trophont stage as well as the reproductive tomont stage. The deleterious effects of HLP-1 also were manifested in what appeared to be ‘delayed mortality’, where parasites of normal appearance would die later in development.
Similar serious damage was also seen with calf histone H2B and the unrelated peptide antibiotic magainin 2. A comparison of the antibiotic activity in mucus versus epidermis compartments of the skin of hybrid striped bass suggested that the majority of antibiotic (including HLP-1) activity resided in the epidermis, although some activity was present in the mucus. These data suggest that normal, nonimmune fish skin contains potent defenses against protozoan ectoparasites and that the effects of these defenses may extend beyond their transient interactions with the parasites, which has important implications for this host-parasite relationship.

KEY WORDS: Histone-like proteins · Innate immunity · Fish

Detection of antibody response against Amyloodinium ocellatum (Brown, 1931) in serum of naturally infected European sea bass by an enzyme-linked immunosorbent assay (ELISA) (Full PDF)
S. Cecchini, M. Saroglia, G. Terova, F. Albanesi

Abstract

Blood samples of nineteen sea bass from a naturally infected cultured population were analysed in order to evaluate specific antibody response against the parasitic dinoflagellate Amyloodinium ocellatum. The specific antibody response was evaluated by an indirect enzyme-linked immunosorbent assay (ELISA), using whole parasite crude antigen and rabbit IgG anti sea bass-IgM. Experimental data showed that some of sampled specimens developed an adaptive immunological response against the parasite, detectable by indirect ELISA. Results let to conjecture that sea bass, showing an acquired immunity against A. ocellatum, could develop a partial resistance against new infections of the dinoflagellate.

While these articles show that immunity against A. ocellatum is a reality I would still not trust on it as this parasite is too virulent once unleashed.
But it should be a good incentive to keep your fish at optimum conditions - just in case.

 

[ThRoewer]

Here the paper that shows that Cryptocaryon irritans (marine ich) and Ichthyophthirius multifiliis (freshwater ich) are not as closely related as previously thought:

Taxonomic affinities of Cryptocaryon irritans and Ichthyophthirius multifiliis inferred from ribosomal RNA sequence data (Full PDF)

Abstract
Comparison of partial sequences of the 18s rRNA gene of the parasitic ciliates Cryptocaryon irritans and Ichthyophthirius multifiliis confirmed that these taxa are not as closely related as was first thought. Phylogenetic trees generated from sequence data grouped I. multifiliis with 3 species of Tetrahyrnena, supporting the existing taxonomic classification of these 2 genera together in the Order Hymenostomatida, Class Oligohymenophora. In contrast, C. irritans was grouped with Colpoda inflata (Class Colpodea) supporting the theory that the lifecycle and morphological similarities evident between I. multifiliis and C. irritans are an example of convergent evolution.

KEY WORDS: Cryptocaryon irritans - Ichthyophthirius multifiliis - 18s rRNA gene - Molecular taxonomy

 

[Deinonych]

Here the paper that shows that Cryptocaryon irritans (marine ich) and Ichthyophthirius multifiliis (freshwater ich) are not as closely related as previously thought:

Nice find. Provides even more supporting evidence that treatments for one should not be applied to the other (e.g. raising temperature etc.)

 

[ThRoewer]

Looks like fish can develop immunity against pretty much all ectoparasites, even Monoganeans (here usually incorrectly referred to as "Flukes"):

Interactions between monogenean parasites and their fish hosts

Abstract
Parasite factors associated with recognition and selection of the host and the mechanisms in the host responsible for acceptance or rejection of the invading organism were evaluated. Sensory structures in parasites are able to detect differences between different fish species and this ability to discern between fishes may be based on both chemical and mechanical stimuli on the host surface. Complex glycoproteins, proteins, carbohydrates and simple molecules attract parasites or modify their behaviour. Furthermore, attachment of the monogenean parasite to a host is dependent on both mechanical structures and chemical factors in the parasite. These systems comprise anterior pads, posterior haptors, gland secretions, and muscular elements. The parasite needs access to appropriate nutrients which can be absorbed and used for reproduction and in this context signals from the host are needed for an optimal physiological response of the parasite. The innate and adaptive immune systems of the host are important elements in this question. Investigations have indicated that innate host factors (complement, lectins, acute phase reactants, macrophages) can bind to monogeneans and elicit severe damage to the parasites. The targets for these hostile products are not only the monogenean tegument, but may involve the gastrodermis and glands. However, the parasite's ability to avoid and even exploit the wide array of immunological elements of the host may be an important player in the dynamic interactions between host and monogenean determining host specificity. Even fish hosts susceptible to a certain parasite show an ability to mount a protective response at post-infection periods. Elevation of the host's production of adaptive and non-adaptive factors following monogenean infections of a certain duration may explain the acquired response.

Keywords
Monogenea; Fish; Interaction; Host response; Humoral immunity; Cellular immunity; Host recognition; Specificity; Vaccination

Immune mechanisms in fish skin against monogeneans - a model (Full PDF Article)

Abstract.
Host responses against skin inhabiting monogeneans are commonly observed but the responsible immune mechanisms in the fish skin are insufficiently described. Based on recent knowledge of fish immunity and skin response mechanisms in mammals a model for the skin immunity in fish to monogenean infections is proposed. Important cellular components of the model are the epithelial cells, the mucous cells and leucocytes. The release of cytokines, e.g. IL-1, following mechanical or chemical injury of the epithelial cells, initiates a series of events leading to decrease of the ectoparasite population. Cytokines (e.g. IL-1, TNF, INF) are suggested to affect secretions from mucous cell and attract neutrophils and macrophages. Leukotrienes are probably involved in the inflammatory reactions. The subsequent production of humoral substances (among others complement factors and peptides) could be responsible for the antiparasitic response in the later stages of infection. Although non-specific factors dominate the response, the involvement of specific antibodies and lymphocytes cannot be excluded.

Key words:
Monogenea, fish immunity, skin immune system, cytokines, complement, humoral factors, cellular responses

This should not be seen as a reason to skip quarantine, but rather as a warning that even fish that seem healthy may be partially immune carriers and may infect fish naïve to these parasites. These parasite have a way too fast live cycle for infected fish to develop the defenses in time.