Impacts of Anthropogenic Pollution on V. Cholera

As atmospheric CO2 levels continue increasing, the chemical composition of the ocean, which acts as a major carbon sink, is heavily altered. [7] The addition of excess carbon dioxide into the seawater reacts with H20 forming carbonic acid. Due to the weak and unstable nature of this acid it then dissociates into bicarbonate and hydrogen ions. The acidic nature of these hydrogen ions triggers a decrease in the overall pH of seawater. Even slight changes in ocean acidity hold the potential to shape the behavior and survival of both marine organisms and people. [10] For example, decreasing pH affects aqueous bacteria and related communities of microorganisms, ultimately leading to potential negative impacts on human health.  

Vc is a gram-negative bacteria which lives primarily in aqueous habitats and is susceptible to the impacts of ocean acidification. Vc is represented by over 200 serotypes, among which are the Classical 0139 and El Tor 01 strains responsible for previous and currently ongoing global cholera pandemics[11].  Previous estimates predict that there are up to 4 million cases of cholera yearly, with outbursts located primarily in countries with limited access to potable water[11]. 

Vc is among many bacterial species which utilize the production of biofilm in order to enhance resistance against stressful environmental factors. Vc biofilm is a formed by a community of microorganisms which interact and attach with VPS in its self-produced biofilm matrix.  Vc biofilm develops primarily on chitin surfaces in its natural aquatic habitat. Through the use of flagellar propulsion coded for by the flaA gene loci, Vc approaches and attatches to suitable surfaces[9]. Ultimately, c-di-GMP regulates the transition from motile to sessile attachment through modulation of mannose sensitive hemagglutinin(mshA)[6]. mshA pili acts as a break, tethering to chitin surfaces and triggering irreversible attachment and secretion of VPS(vibrio polysaccharides)[15].   

Following secretion, Vibrio Polysaccharides bind to matrix proteins, playing an essential role in the structure of biofilm in Vc.  Monosaccharide analysis reveals that VPS structure is characterized primarily of the polysaccharides glucose and galactose[17]. The biosynthesis of VPS is controlled by gene clusters VPS-I and VPS-II, the presence of which is necessary for biofilm formation. [17] Following VPS biosynthesis, RbmA, an essential matrix protein which facilitates cell to cell interactions, is then expressed. [13] This matrix protein crosslinks with VPS, binding sister cells as they divide and grow. [13] Other matrix proteins RbmC and Bap1 ensure surface adhesion in Vc biofilms through cell to substrate interactions facilitated by crosslinks with VPS. [13] 

Among the many pH sensitive chemical structures essential to V. Cholera  biofilm formation, carboxyl groups(a combination of carbonyl and hydroxyl groups attached to a single carbon atom), are highly reactive to changing acidities[12].  Imaging by Patel et al. shows the relationship between oxidation time(0-48 hours) and content (mmol kg^-1) of carbonyl or carboxyl groups[12].  Testing acidity levels varying between 5 and 7 they graphed the resulting fluctuations in carbonyl/carboxyl content. [12] Analysis of depolymerized VPS structure  reveals the presence of carboxyl groups in VPS structure[8]. Monosaccharide analysis  of depolymerized VPS reveals glucose, galactose, LD-heptose, glucosamine, and perosamine as the major building blocks of VPS [18].  However further studies reveal the presence of a free carboxyl group linked to a guluronic acid bound with a glycine adduct [8].  Thus, fluctuations in carboxyl group content will directly impact VPS structure and its ability to crosslink with matrix proteins Bap1, RmbA, and RbmC[18].

Vc  which lacks proper biofilm structure and integrity will face increasing difficulty in resisting environmental stressors. Subsequently, anthropogenic pollution directly limits the favorability of vc survival in marine habitats.