At this time of the year, fish keepers and aquaculturists may be a bit apprehensive about Aeromonas infection. Does it really cause disease? When does it cause disease? Can we tell the difference between normal strains and bad strains of the bacteria?
So, I’ve taken the liberty to write a summary about the bug. Sorry it’s a bit techy.
The passages below have been paraphrased from Austin B, Austin DA: Bacterial Fish Pathogens: Disease in Farmed and Wild Fish. 4th edition. Springer-Praxis, Goldalming, 2007.
INTRODUCTION
Aeromonas hydrophila (previously A. formicans and A. liquefaciens) can cause haemorrhagic septicaemia, red sore disease and fin rot. It has a worldwide distribution, is rife in freshwater environments (including on aquatic plants, fish and fish eggs) and can affect many freshwater fish species and occasionally, marine fish. There is some contention over whether this is a primary pathogen or merely a secondary invader of already compromised hosts.
Disease signs include eroded fins, haemorrhages on the skin, sloughing of scales, skin ulcers and haemorrhaging in the intestine wall. Exopthalmia (pop-eye) and ascites with subcutaneous oedema (dropsy) can also be observed. Mortality rate can be high.
HOW IS THE BACTERIA IDENTIFIED?
Generally speaking, A. hydrophila is a Gram-negative, straight bacterial rod, and they are motile by a single polar flagellum, plus or minus lateral flagella. It is speculative whether or not the fish isolates belong as A. hydrophila or in any of the other Aeromonas Hybridisation Groups. It is apparent that the bacteria has considerable exo-enzyme potential including haemolysins, serine and metallo-protease and some of which have relevance in fish pathology. There is definitely marked phenotypic, biochemical, serological and genotypic differences (e.g. presence or absence of the 21kb plasmid detected in pathogenic isolates associated with ulcerative disease syndrome) and improvements in aeromonad taxonomy may eventuate with the emergence of other taxa as fish pathogens.
CAN WE TELL WHICH ISOLATES ARE BAD?
Are we able to identify which A. hydrophila are pathogenic, and which ones aren’t? This could be a million dollar question that a lot of work has not found an easy answer. There is no direct correlation between virulence and haemagglutination. The surface array matrix (S-layer that influences bacterial interaction with its environment) that has been shown to be a prerequisite for virulence in A. salmonicida does not apply to A. hydrophila. Bacterial surface-binding expression to I-labelled collagen, fibronectin and laminin (common to isolates from diseased fishes) cannot be used because its properties were influenced by in vitro culture conditions. One study reported that precipitation of the bacteria after boiling was an important measure of virulence, but this is debatable.
What has shown promise in identifying virulence include the action of their adhesins (these situated on bacteria’s outer membrane protein [OMP], to attach to selected host cells/tissue proteins [e.g. collagen, fibronectin, serum proteins and glycoproteins], of which AHA1 [a 43 kDa protein] has shown to be present in virulent strains), the presence of a 40 kDa protein in their OMP, the presence of haemolytic (heamolysins) and proteolytic (proteases such as caseinase, elastase, and metallo- and serine proteases) extracellular products (ECP). A further study identified acetylcholinestrase (a 15.5 kDa polypeptide) in the ECP and regarded this to be a major lethal factor with possible neurotoxic activity. Some strains show enterotoxigenicity and those that possess the O-antigen (somatic antigen) and K-antigen were present in most virulent isolates. Comparison of virulent and avirulent isolates using molecular techniques (suppression subtractive hybridisation) identified 69 genemic regions absent from the latter. Genes considered to represent known virulence attributes include haemolysin, histone-like protein, oligoprotease A, OMP and multi-drug resistance protein. Other genes encoded synthesis of O-antigen.
WHAT ARE THE RISK FACTORS TO YOUR POND?
One of the biochemical characteristics of A. hydrophila is that it reduces nitrates. Given this, and the fact that high levels of nitrates (dirty pond with insufficient water changes) are immunosuppressive, could we then infer that ponds with high levels of nitrates could be a predisposing factor? Having said this, could being too clean be harmful? The other school of thought is to maintain a good balance of a diversity of bacterial flora.
The bacteria exhibit a chemotactic response to the mucus of freshwater fish. The evidence points to a stress-mediated disease condition which is influenced by elevated water temperatures (temperatures above 9.4 degrees Celsius). The presence of pollutants increases susceptibility to infection.
One in vitro study showed that calcium in the growth medium enhanced the expression of the bacterial extracellular matrix protein surface receptors. These surface receptors are important for the bacteria to latch on to the fish. Extrapolating this, could it mean that water with a higher calcium content may be a risk factor?
Many bacterial pathogens utilise iron and the haemolysins in A. hydrophila are iron-regulated. Could an elevated iron content in the water be a risk factor?
SUMMARY
Aeromonas hydrophila is ubiquitous, it is present in every freshwater fish pond. It has the potential to cause disease, usually in association with other factors. Current methods are unable to identify virulent versus avirulent strains. Risk factors include host health, environmental factors and bacterial virulence.
