**6. High hydrostatic pressure**

osmolytes from the external environment to restore osmotic balance within cells. The solute-mediated osmoprotection stimulates the growth of cells subjected to high salt concentrations. Deletions of these osmolyte transporters reduce the growth of *Listeria* under conditions of hyperosmolarity [14, 30, 35]. In addition to previously mentioned compatible solutes (glycine, betaine, and carnitine), proline is important for the survival under hyperosmolarity conditions [36]. σB factor, as an important part of the overall stress response of *L. monocytogenes,* mediates the expression of *ctc* gene and the use of betaine and carnitine as

In response to osmotic stress, two genes involved in cell envelope modification have been identified: *lmo2085*, a putative peptidoglycan-linked protein, and *lmo1078*, a putative UDPglucose phosphorylase that catalyzes the formation of UDP-glucose, a precursor of mem-

A further mechanism of osmotic adaptation is the modification of genetic expression leading to an increased or a decreased synthesis of several proteins. Salt-shock proteins are rapidly induced and overexpressed for a short time period, being similar to those induced in coldshock response (CSPs and CAPs). Among CSPs induced in *L. monocytogenes,* there are two general stress response proteins, DnaK that acts as a heat-shock protein stabilizing cellular proteins and Ctc that is involved in high osmolarity resistance in the lack of osmoprotectants, such as glycine, betaine, and carnitine, in the medium [38]. Additional stress response proteins, including ClpC (an ATPase), ClpP (a protease), and HtrA (a protease), are essential for osmotic and acid stress adaptation in *L. monocytogenes* [39]. HtrA may play a role in degrading misfolded proteins and is beneath LisRK control, a two-component regulatory system impor-

Desiccation tolerance defines the bacteria's aptitude to survive for extended periods on a surface, deficient of nutrients and water. As so, *L. monocytogenes* desiccation tolerance is most likely associated with the ability to persist in food production surfaces and consequently cross-contaminate food products [40]. The low aw resulting from high osmolarity decreases turgor pressure in a bacterial cell inhibiting bacterial growth [41]. Drying and addition of salt or sugar are traditional methods to lower food aw and therefore enhance its prolonged shelf life. *L. monocytogenes* grows optimally at aw ≥ 0.97, although it may survive in foods with low aw [42]. When compared to other common infectious foodborne pathogens, *L. monocytogenes* does not appear to grow at aw < 0.90 but it can survive in these conditions, particularly under refrigeration, for long periods. To date, existing information regarding *L. monocytogenes* desiccation survival is limited and primarily focuses on factors influencing the survival to osmotic stress [40, 43–46]. Strains of serotypes 1/2c and 1/2b were the most tolerant to desiccation, followed by 4b and 1/2a [47]. Hansen and Vogel [46] showed the protective effect of osmoadaptation and also the formation of biofilms on

osmoprotectors.

94 Listeria Monocytogenes

brane glycolipids and of the cell wall [37].

tant for osmoregulation [36].

the desiccation survival.

**5. Desiccation stress response**

A high hydrostatic pressure (HHP) represents the application of pressure in the range of 50–1000 MPa, though the inactivation of vegetative cells of bacterial species is typically reached from 300 to 700 MPa, and bacterial spores inactivation demands higher pressure levels up to 1000 MPa [48]. However, depending on the pressure level, HHP treatments can fully inactivate bacteria or impose sublethal injuries. For pressures up to 400 MPa, the integrity of Gram-positive bacterial cells and metabolic activity are maintained, with very limited cell destruction [49]. Over the last years, it has been stated that *L. monocytogenes* is potentially capable of recovering culturability following HHP exposure [49–52]. Physiological studies have also demonstrated that increasing pressure levels results in an accelerated decline of metabolic indicators, such as the activity of the LmrP membrane transport system [53]. These findings suggest that bacteria exposed to HHP are unable to grow due to cell injury, but yet can mount a nonspecific response to high pressure. A proportion of the cell population is able to maintain cellular activity of some kind after HHP, demonstrating the capacity to cellular repair and regrow, when adequate conditions are available [49].

To date, little research has been conducted regarding the mechanisms of bacterial adaptation and resistance to high pressure. Wemekamp-Kamphuis et al. [54] demonstrated that one of the responses that enable *Listeria* survival upon HHP treatment results from induction of the general stress response mediated by σB. *L. monocytogenes sigB* deletion mutant was more susceptible to HHP exposure than the wild type, while induction of σB resulted in an increased HHP protection relative to the untreated control strain.

Several pressure-induced proteins have been increasingly synthesized when compared to the synthesis of other control proteins at atmospheric pressure [55]. *L. monocytogenes* has shown to actively express many genes as a response to high pressure, but some functional categories appear more affected than others. Genes that tend to be expressed at higher levels under high pressure are genes encoding for transport and binding, signal transduction and chemotaxis, cellular processes, transcriptional regulators, metabolism, and protein fate [56]. The stabilization and maintenance of the bacteria cell is at high focus, showed by the significant regulation of ribosomes and proteins, together with components involved in the cell envelope and the septal ring. It is assumed that the activation of genes involved in the lipid and peptidoglycan biosynthetic pathways is connected to this function. Upregulation of genes associated with generalized repair and maintenance has been proved, where the activation of cold- and heatshock genes is an example for this [57, 58]. When high pressure demands more energy to be used on repair, energy production and conversion is suppressed. The repression of several energy production/conversion, carbohydrate, and other carbon compound catabolic genes may represent a diminishment of catabolism in cells imposed by HPP treatments. This can be seen by the pressure-induced switch from active growth to a cell repair state, the stationary phase, resulting in a decreased growth rate [59].

Several genes associated with cell formation and shape, as well as synthesis or reassembly of cell-wall constituents, in particular peptidoglycan and fatty acids, were observed to have an increased expression. Because of this, genes involved in such functions can be considered as very central in the response to high pressure. It is presumed that *L. monocytogenes* increases both cell division and cell-envelope-associated gene expression aiming to replace damaged components and thus compensate membrane and wall damages [59].

**Involvement Proteins/function Ref.**

*Class III stress-response regulator, a transcription repressor.*

*transcription.*

**SigmaB (σB)**

**CtsR**

**HrcA**

**InlB**

*membrane.*

**PC-PLC**

**Mpl**

**HtrA**

**Bsh**

**ClpC**

**ClpP**

*condition.*

*macrophages and thus virulence.*

*transcription repressor.*

*the E-cadherin.*

*General stress transcription factor.*

*Positive regulatory factor A, central virulence regulator of virulence gene*

The Impact of Environmental Stresses in the Virulence Traits of *Listeria monocytogenes* Relevant…

*Heat regulation at controlling inverted repeat of chaperone expression elements. A*

*Internalin A, surface protein that mediates entry into cells expressing its receptor,*

*Internalin B, surface protein that mediates entry into cells expressing one of the receptors gC1qR, HGF-SF, Met, and the glycosaminoglycanes (GAGs).*

*Listeriolysin O, hemolysin required for vacuole escape by lysis of the phagosome*

*Phospholipase activated by proteolytic cleavage involving Mpl or by cellular*

*proteases. Required for the lysis of the double-membrane vacuole.*

*Hexose phosphate transporter required for intracytosolic proliferation.*

*Bile salt hydrolase involved in the intestinal and hepatic phases of listeriosis.*

*Serine protease involved in proteolysis and required for growth under stress*

*ATPase protein promoting early bacterial escape from the phagosome of*

*Actin assembly-inducing protein, involved in cell-to-cell spread*.

*Serine protease involved in acid and osmotic stress response.*

*Metalloprotease required for the maturation of PC-PLC.*

[68]

97

http://dx.doi.org/10.5772/intechopen.76287

[69]

[70]

[71]

[65]

[72]

[73]

[74]

[75]

[76]

[77]

[78]

[79]

[80]

[81]

Regulation **PrfA**

Attachment and invasion **InlA**

Lysis of vacuoles **LLO**

Intracellular multiplication **Hpt**

Cell-to-cell spread **ActA**

Environmental stress response

and virulence

Cell membranes damage by HPP may possibly be a main cause of inactivation or death in Gram-negative bacteria, but it is fallacious to admit that in Gram-positive bacteria. Cell membrane and wall stabilization in the stationary growth phase do provide a protective effect against HPP, being a major factor for the survival of HPP-induced damage [60]. Beyond cell envelope damage, HPP interferes within the nascent septal ring formation along with other associated cell-wall formation and chromosome segregation processes [59].

#### **7. Stress impact on** *L. monocytogenes* **virulence**

*L. monocytogenes* has a profound ability to adapt to unfavorable stressful environments, switching from a saprophyte to an intracellular pathogen capable of causing serious infection to the host [61]. In this transformation, σB dominates both in the external environment and during gastrointestinal transit, while positive regulatory factor A (PrfA) plays a central role on the intracellular infection. In concert with PrfA, σB activates the transcription of several *L. monocytogenes* virulence genes: (1) *bsh*, encoding bile salt hydrolase, essential in gastrointestinal colonization prior to invasion; (2) *inlA*, encoding internalin A, mediates entry into human intestinal epithelial cells; and (3) *gadA*, encoding part of the glutamate decarboxylase system, crucial for acid survival [62]. σB also contributes to the transcriptional activation of *prfA*, encoding PrfA, a central virulence regulator of virulence gene expression in *L. monocytogenes* [63].

PrfA-dependent virulence gene cluster or LIPI-1 (*Listeria* pathogenicity island 1) encodes most virulence factors involved in the pathogenic infectious cycle. This chromosomal locus comprises the following genes: (1) *hly*, encoding listeriolysin O (LLO), a pore-forming toxin crucial in the escape from phagocytic vacuoles; (2) *plcA* and *plcB*, encoding two phospholipases C which cooperate with LLO in the escape from bacterial phagosomes; (3) *mpl*, encoding a metalloprotease implicated in the maturation of proenzyme pro-PlcB; (4) *actA*, encoding ActA protein involved in the intra- and intercellular motility of the bacteria; and (5) *prfA*, encoding PrfA, a transcriptional activator of LIPI-1 genes [64]. The expression of additional genes dispersed on the chromosome may be PrfA-regulated, as the internalin locus *inlAB* [65], the genes encoding internalins InlA and InlB cell-wall-anchored proteins which induce *Listeria* phagocytosis [66].

Following the complete genome sequencing of several *L. monocytogenes* strains, an increasing number of virulence-related proteins are being identified and their specific involvement during infectious stages deciphered (**Table 1**).

In addition to other factors, the infectious potential of *L. monocytogenes* is conditioned by the environmental conditions prior to host invasion. A correlation between stress response and virulence seems to exist and associates strains having more effective stress response mechanisms to being also more virulent [84]. Early studies by Durst [84] and Wood and Woodbine [85] demonstrated that cold storage may enhance virulence of some strains because the

increased expression. Because of this, genes involved in such functions can be considered as very central in the response to high pressure. It is presumed that *L. monocytogenes* increases both cell division and cell-envelope-associated gene expression aiming to replace damaged

Cell membranes damage by HPP may possibly be a main cause of inactivation or death in Gram-negative bacteria, but it is fallacious to admit that in Gram-positive bacteria. Cell membrane and wall stabilization in the stationary growth phase do provide a protective effect against HPP, being a major factor for the survival of HPP-induced damage [60]. Beyond cell envelope damage, HPP interferes within the nascent septal ring formation along with other

*L. monocytogenes* has a profound ability to adapt to unfavorable stressful environments, switching from a saprophyte to an intracellular pathogen capable of causing serious infection to the host [61]. In this transformation, σB dominates both in the external environment and during gastrointestinal transit, while positive regulatory factor A (PrfA) plays a central role on the intracellular infection. In concert with PrfA, σB activates the transcription of several *L. monocytogenes* virulence genes: (1) *bsh*, encoding bile salt hydrolase, essential in gastrointestinal colonization prior to invasion; (2) *inlA*, encoding internalin A, mediates entry into human intestinal epithelial cells; and (3) *gadA*, encoding part of the glutamate decarboxylase system, crucial for acid survival [62]. σB also contributes to the transcriptional activation of *prfA*, encoding PrfA, a central virulence regulator of virulence gene expression in *L. monocytogenes* [63].

PrfA-dependent virulence gene cluster or LIPI-1 (*Listeria* pathogenicity island 1) encodes most virulence factors involved in the pathogenic infectious cycle. This chromosomal locus comprises the following genes: (1) *hly*, encoding listeriolysin O (LLO), a pore-forming toxin crucial in the escape from phagocytic vacuoles; (2) *plcA* and *plcB*, encoding two phospholipases C which cooperate with LLO in the escape from bacterial phagosomes; (3) *mpl*, encoding a metalloprotease implicated in the maturation of proenzyme pro-PlcB; (4) *actA*, encoding ActA protein involved in the intra- and intercellular motility of the bacteria; and (5) *prfA*, encoding PrfA, a transcriptional activator of LIPI-1 genes [64]. The expression of additional genes dispersed on the chromosome may be PrfA-regulated, as the internalin locus *inlAB* [65], the genes encoding internalins InlA and InlB cell-wall-anchored proteins which induce *Listeria* phagocytosis [66]. Following the complete genome sequencing of several *L. monocytogenes* strains, an increasing number of virulence-related proteins are being identified and their specific involvement dur-

In addition to other factors, the infectious potential of *L. monocytogenes* is conditioned by the environmental conditions prior to host invasion. A correlation between stress response and virulence seems to exist and associates strains having more effective stress response mechanisms to being also more virulent [84]. Early studies by Durst [84] and Wood and Woodbine [85] demonstrated that cold storage may enhance virulence of some strains because the

components and thus compensate membrane and wall damages [59].

96 Listeria Monocytogenes

associated cell-wall formation and chromosome segregation processes [59].

**7. Stress impact on** *L. monocytogenes* **virulence**

ing infectious stages deciphered (**Table 1**).

Garner et al. [93] reported an intensified invasiveness of *L. monocytogenes* for Caco-2 cells when grown at 7°C rather than at 37°C, and, for both temperatures, the invasion ability was greater in cells grown at pH 7.4 compared to growth at pH 5.5. A growth temperature of 37°C, pH 7.4, in the presence of NaCl or sodium lactate, enhanced *L. monocytogenes* invasiveness; however, the pre-exposure to gastric fluid (pH 4.5), even for as short as 10 s, substantially reduced its invasion. These findings intimate that listerial virulence-associated characteristics seem to be affected by specific food properties (e.g., the presence of organic acids or salt). The authors further showed that *L. monocytogenes* growth phase affects its ability to invade Caco-2 cells. The invasion by logphase cells was 9.5-fold lower than invasion by stationary-phase cells, corroborating other studies which demonstrate that exposure of *L. monocytogenes* to different environmental conditions can change invasiveness and virulence [93]. Accordingly, the increased stationary-phase invasiveness also coincides with stationary-phase induction of σB activity [90]. In stationary-phase cells, *inlA* expression is regulated in a σB-dependent manner, and growth phase-dependent effects on invasion appear independent of PrfA [94, 95], contributing to *inlA* transcription [96].

The Impact of Environmental Stresses in the Virulence Traits of *Listeria monocytogenes* Relevant…

http://dx.doi.org/10.5772/intechopen.76287

99

Complementary studies demonstrate that *L. monocytogenes* pathogenicity requires an adaptive acid tolerance response, so the ability to survive gastric acid fluid and to invade host cells is related to ATR activation [30, 89, 97]. This finding is supported by the fact that the glutamate decarboxylase (GAD) system, as the ATR most important component, is required for listerial survival in the gastric environment, and also LisRK deletion, a two-component system involved in acid resistance regulation, caused a dramatic reduction in virulence [29, 98].

A further prerequisite for *L. monocytogenes* infection depends on the ability to counteract conditions of elevated osmolarity in the gastrointestinal tract. As mentioned in Section 2.1, the carnitine uptake system (OpuC) is directly linked to osmotic stress resistance of *L. monocytogenes* and to its ability to reach and proliferate in the liver and spleen [17]. Carnitine (produced from the desquamation of the gastrointestinal epithelial layer) was formerly proved to act as a crucial osmoprotectant, facilitating growth in this gastrointestinal environment, once changing the carnitine transported OpuC resulted in a significant reduction in *Listeria* ability to colonize the upper small intestine and cause subsequent systemic infection [99, 100]. A supporting study by Wemekamp-Kamphuis et al. [17] demonstrated that a triple mutant, defective in all three compatible uptake systems (BetL, Gbu, and OpuC), showed a similar phenotype to that of a single opuC mutant, mutually revealing a decreased ability to cause systemic infection relative to the parent. Those were clear evidences that *betL* and *gbu* do not play a significant role in *L. monocytogenes* pathogenesis and that it is the carnitine uptake system that most induces listerial virulence. In addition, Joseph et al. [101] also identified OpuCA and OpuCB as being induced intracellularly. Since the contribution of each transporter is dependent on the external environment, there are occurrences

when each system is tailored for optimal effects within a certain environmental niche.

Over the last years, novel trends in food production tend to preserve the natural flavor and texture of products using minimal processing. Non-thermal food preservation usually allows a significant microbial reduction, and mounting evidence also demonstrates that the conditions applied by alternative technologies may influence bacterial virulence [102]. The application of HHP has been shown not to induce mutations in the internal genes, *inlA* and *inlB*, implicated in the adhesion and internalization of *L. monocytogenes* in human cells. However, when the effect of HPP on the *ctsR* gene is observed, a reduction in virulence potential of

**Table 1.** Stress response and virulence-associated proteins in *Listeria monocytogenes* (adapted from reference [67]).

pathogen virulence rather increases when grown under refrigeration than at optimal growth temperature. By contrast, virulence gene expression was reported to be downregulated at temperatures below 30°C, besides PrfA is only formed at 37°C [85]. According to Loh et al. [86], the expression of *prfA* is nearly 16-times higher at 37°C compared to that at 30°C, and imperceptible in cells cultivated at 20°C. The specific pathogenicity of LLO can be fully recovered in less than 24 h by incubating refrigerated cells at 37°C [87]. This virulence recovery after heat shock reinforces the importance of eliminating *L. monocytogenes* from minimally processed ready-to-eat foods held at refrigeration temperatures for long periods.

Low pH and high salt content are common factors often found in foods contaminated with *L. monocytogenes* [89]. Even though at these conditions, the growth of most foodborne and spoilage bacteria is restricted, *L. monocytogenes* is capable of surviving and even grow in such environments; long-term adaptation to these sublethal stress conditions results in altered virulence [88].

Conte et al. [31, 89] demonstrated that short-term exposure (1 h) of *L. monocytogenes* to a sublethal acidic environment (pH 5.1) not only increased its invasiveness to the human colon adenocarcinoma cell line Caco-2 but also increased the ability of *L. monocytogenes* to survive and proliferate in macrophage-like cells, suggesting that exposure to a low pH (e.g., in the human stomach) may enhance listerial overall virulence. In addition, LLO excreted by virulent *L. monocytogenes* showed a maximal activity at pH 4.0–5.0. In another study, the exposure of *L. monocytogenes* to acidic shock has induced the transcription of two important virulence genes (*inlA* and *bsh*) [90]. Conversely, a study by Rieu et al. [91] reported a decrease in virulence gene transcription after 5 h at pH 4.0 achieved with acetic acid. This conflicting finding may be sustained by the use of organic acids since they might be more harmful to the bacteria. Some weak organic acids enhance pathogenicity of the bacterium, while others reduce it, as the secretion of LLO is increased by citrate, acetate, and lactate, whereas sorbate inhibited this hemolysin [92]. This knowledge would be important for the selection of acidulants to be used in different foods.

Garner et al. [93] reported an intensified invasiveness of *L. monocytogenes* for Caco-2 cells when grown at 7°C rather than at 37°C, and, for both temperatures, the invasion ability was greater in cells grown at pH 7.4 compared to growth at pH 5.5. A growth temperature of 37°C, pH 7.4, in the presence of NaCl or sodium lactate, enhanced *L. monocytogenes* invasiveness; however, the pre-exposure to gastric fluid (pH 4.5), even for as short as 10 s, substantially reduced its invasion. These findings intimate that listerial virulence-associated characteristics seem to be affected by specific food properties (e.g., the presence of organic acids or salt). The authors further showed that *L. monocytogenes* growth phase affects its ability to invade Caco-2 cells. The invasion by logphase cells was 9.5-fold lower than invasion by stationary-phase cells, corroborating other studies which demonstrate that exposure of *L. monocytogenes* to different environmental conditions can change invasiveness and virulence [93]. Accordingly, the increased stationary-phase invasiveness also coincides with stationary-phase induction of σB activity [90]. In stationary-phase cells, *inlA* expression is regulated in a σB-dependent manner, and growth phase-dependent effects on invasion appear independent of PrfA [94, 95], contributing to *inlA* transcription [96].

Complementary studies demonstrate that *L. monocytogenes* pathogenicity requires an adaptive acid tolerance response, so the ability to survive gastric acid fluid and to invade host cells is related to ATR activation [30, 89, 97]. This finding is supported by the fact that the glutamate decarboxylase (GAD) system, as the ATR most important component, is required for listerial survival in the gastric environment, and also LisRK deletion, a two-component system involved in acid resistance regulation, caused a dramatic reduction in virulence [29, 98].

pathogen virulence rather increases when grown under refrigeration than at optimal growth temperature. By contrast, virulence gene expression was reported to be downregulated at temperatures below 30°C, besides PrfA is only formed at 37°C [85]. According to Loh et al. [86], the expression of *prfA* is nearly 16-times higher at 37°C compared to that at 30°C, and imperceptible in cells cultivated at 20°C. The specific pathogenicity of LLO can be fully recovered in less than 24 h by incubating refrigerated cells at 37°C [87]. This virulence recovery after heat shock reinforces the importance of eliminating *L. monocytogenes* from minimally

**Table 1.** Stress response and virulence-associated proteins in *Listeria monocytogenes* (adapted from reference [67]).

**Involvement Proteins/function Ref.**

*Chaperone heat-shock proteins encoded by the dnaK operon and required for*

*Chaperone proteins which regulate HrcA posttranscriptionally.*

*The glutamate decarboxylase system, involved in acid stress response.*

*Glycine betaine transport system I, involved in osmotic stress response.*

*Glycine betaine transport system II, involved in osmotic stress response.*

*Carnitine transport system, involved in cold and osmotic stress response.*

[22]

[23]

[29]

[82]

[15]

[83]

**DnaKJ**

98 Listeria Monocytogenes

**GAD**

**BetL**

**Gbu**

**OpuC**

*phagocytosis.*

**GroES, GroEL**

Low pH and high salt content are common factors often found in foods contaminated with *L. monocytogenes* [89]. Even though at these conditions, the growth of most foodborne and spoilage bacteria is restricted, *L. monocytogenes* is capable of surviving and even grow in such environments; long-term adaptation to these sublethal stress conditions results in altered virulence [88]. Conte et al. [31, 89] demonstrated that short-term exposure (1 h) of *L. monocytogenes* to a sublethal acidic environment (pH 5.1) not only increased its invasiveness to the human colon adenocarcinoma cell line Caco-2 but also increased the ability of *L. monocytogenes* to survive and proliferate in macrophage-like cells, suggesting that exposure to a low pH (e.g., in the human stomach) may enhance listerial overall virulence. In addition, LLO excreted by virulent *L. monocytogenes* showed a maximal activity at pH 4.0–5.0. In another study, the exposure of *L. monocytogenes* to acidic shock has induced the transcription of two important virulence genes (*inlA* and *bsh*) [90]. Conversely, a study by Rieu et al. [91] reported a decrease in virulence gene transcription after 5 h at pH 4.0 achieved with acetic acid. This conflicting finding may be sustained by the use of organic acids since they might be more harmful to the bacteria. Some weak organic acids enhance pathogenicity of the bacterium, while others reduce it, as the secretion of LLO is increased by citrate, acetate, and lactate, whereas sorbate inhibited this hemolysin [92]. This knowledge would be important for the selection of acidulants to be used in different foods.

processed ready-to-eat foods held at refrigeration temperatures for long periods.

A further prerequisite for *L. monocytogenes* infection depends on the ability to counteract conditions of elevated osmolarity in the gastrointestinal tract. As mentioned in Section 2.1, the carnitine uptake system (OpuC) is directly linked to osmotic stress resistance of *L. monocytogenes* and to its ability to reach and proliferate in the liver and spleen [17]. Carnitine (produced from the desquamation of the gastrointestinal epithelial layer) was formerly proved to act as a crucial osmoprotectant, facilitating growth in this gastrointestinal environment, once changing the carnitine transported OpuC resulted in a significant reduction in *Listeria* ability to colonize the upper small intestine and cause subsequent systemic infection [99, 100]. A supporting study by Wemekamp-Kamphuis et al. [17] demonstrated that a triple mutant, defective in all three compatible uptake systems (BetL, Gbu, and OpuC), showed a similar phenotype to that of a single opuC mutant, mutually revealing a decreased ability to cause systemic infection relative to the parent. Those were clear evidences that *betL* and *gbu* do not play a significant role in *L. monocytogenes* pathogenesis and that it is the carnitine uptake system that most induces listerial virulence. In addition, Joseph et al. [101] also identified OpuCA and OpuCB as being induced intracellularly. Since the contribution of each transporter is dependent on the external environment, there are occurrences when each system is tailored for optimal effects within a certain environmental niche.

Over the last years, novel trends in food production tend to preserve the natural flavor and texture of products using minimal processing. Non-thermal food preservation usually allows a significant microbial reduction, and mounting evidence also demonstrates that the conditions applied by alternative technologies may influence bacterial virulence [102]. The application of HHP has been shown not to induce mutations in the internal genes, *inlA* and *inlB*, implicated in the adhesion and internalization of *L. monocytogenes* in human cells. However, when the effect of HPP on the *ctsR* gene is observed, a reduction in virulence potential of surviving cells was noted. Likewise, virulence and reduced motility may be the result of a mutation in this gene corresponding to the loss of a single amino acid. This suppression could be related to a high-pressure tolerance [70, 103].

**References**

1997;**63**(4):1252-1255

1986. pp. 1235-1245

Microbiology. 2002;**68**(4):1697-1705

[1] Saavedra L, Bellomio A, Hebert EM, Minahk C, Suarez N, Sesma F. Listeria: Epidemiology, pathogenesis and novel potential treatments. In: Romano A, Giordano CF, editors. Listeria Infections: Epidemiology, Pathogenesis and Treatment. New York: Nova

The Impact of Environmental Stresses in the Virulence Traits of *Listeria monocytogenes* Relevant…

http://dx.doi.org/10.5772/intechopen.76287

101

[2] EFSA. The European Union summary report on trends and sources of zoonoses, zoonotic agents and food-borne outbreaks in 2016.  Reported foodborne outbreaks due to fresh produce in the United States and European Union: Trends and causes. Foodborne Pathogens and Disease. 2015 Jan;**12**(1):32-38

[5] Lou Y, Yousef AE. Adaptation to sublethal environmental stresses protects *Listeria monocytogenes* against lethal preservation factors. Applied and Environmental Microbiology.

[6] Junttila JR, Niemelä SI, Hirn J. Minimum growth temperatures of *Listeria monocytogenes* and non-haemolytic Listeria. The Journal of Applied Bacteriology. 1988 Oct;**65**(4):321-327

[7] Walker SJ, Archer P, Banks JG. Growth of *Listeria monocytogenes* at refrigeration tempera-

[8] Seeliger HPR, Jones D. Listeria. In: Sneath PHA, Mair NS, Sharpe NE, Holt JG, editors. Bergey's Manual of Systematic Bacteriology. Vol 2. Baltimore: Williams and Wilkins;

[9] Bayles DO, Annous BA, Wilkinson BJ. Cold stress proteins induced in *Listeria monocytogenes* in response to temperature downshock and growth at low temperatures. Applied

[10] Schmid B, Klumpp J, Raimann E, Loessner MJ, Stephan R, Tasara T. Role of cold shock proteins in growth of *Listeria monocytogenes* under cold and osmotic stress conditions.

[11] Liu S, Graham JE, Bigelow L, Ii PDM, Wilkinson BJ.Identification of *Listeria monocytogenes* genes expressed in response to growth at low temperature. Applied and Environmental

[12] Mansilla MC, Cybulski LE, Albanesi D, de Mendoza D. Control of membrane lipid fluidity by molecular thermosensors. Journal of Bacteriology. 2004 Oct;**186**(20):6681-6688

[13] Annous BA, Becker LA, Bayles DO, Labeda DP, Wilkinson BJ. Critical role of anteiso-C15:0 fatty acid in the growth of *Listeria monocytogenes* at low temperatures. Applied and

tures. The Journal of Applied Bacteriology. 1990 Feb;**68**(2):157-162

Applied and Environmental Microbiology. 2009 Mar;**75**(6):1621-1627

and Environmental Microbiology. 1996 Mar;**62**(3):1116-9

Environmental Microbiology. 1997 Oct;**63**(10):3887-3894

Portugal, March 2009 to February 2012. Euro Surveillaince. 2015;**20**(17):pii=21104

Science Publishers, Incorporated; 2012. pp. 67-98

#### **8. Conclusions**

Exposure of *L. monocytogenes* to sublethal environmental stresses can enhance its survival to subsequent lethal conditions and additionally induce the expression of the organism's virulence genes. Therefore, exposure of *L. monocytogenes* to food-associated stresses such as high salt concentrations or low temperatures during refrigerated storage may result in increased virulence and thus a higher risk for listeriosis. Any strain of *L. monocytogenes* present in food is actually considered equally pathogenic. However, results from several studies support the idea that the heterogeneity among strains regarding the response to stress and virulence potential should be considered, once responses to food matrix and storage conditions are often strain specific.

Although significant advances in our understanding on stress response and virulence potential have been achieved in the last years, there is still a need to fulfill knowledge gaps on molecular mechanisms behind *L. monocytogenes* response to stress and virulence. Further studies on the influence of food matrix on stress tolerance and virulence potential of different strains, recovered from foods and from patients, are needed. This information can be further used by regulators to refine previous risk assessments and also in the definition of control measures by the food industry.

#### **Acknowledgements**

This work was supported by National Funds from FCT—Fundação para a Ciência e a Tecnologia through project UID/Multi/50016/2013. Publication in open access was co-financed by the project NORTE-01-0246-FEDER-000011, supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF). Financial support for author Sofia Pereira was provided by ESF—European Social Fund, under the PORTUGAL 2020 Partnership Agreement, through doctoral fellowship NORTE-08-5369-FSE-000007\_BD\_1.

#### **Author details**

Sofia Araújo Pereira, Ângela Alves, Vânia Ferreira and Paula Cristina Maia Teixeira\*

\*Address all correspondence to<EMAIL_ADDRESS>
Universidade Católica Portuguesa, CBQF - Centro de Biotecnologia e Química Fina – Laboratório Associado, Escola Superior de Biotecnologia, Porto, Portugal


**5. Characteristic HRV profiles in depression**

**Figure 6** presents the characteristic HRV profiles at the baseline rest condition (Rest), during the task load (Task) and during the rest condition after the task (After) in the control healthy subjects, in the patients with major depressive disorder (MDD) and in the patients with a general anxiety disorder (GAD). The HRV profiles of MDD and GAD were used in the present chapter to represent that in depression and anxiety. The schematic diagrams are made based on our published data [13]. The data in each measurement condition are connected by lines to clarify the characteristic profiles. LF data are connected by dashed lines to indicate that the inter-subject differences are large not only in the healthy subjects but in the patients with MDD and GAD.

The healthy HF pattern takes the form of a V shape and the healthy LF/HF and HR patterns have inverted V shapes. HF decreases, and LF/HF and HR increase during Task, and they return to the original level at After. This indicates that the breathingrelated control of heart rate reflecting parasympathetic activity decreases during Tasks in healthy subjects. It is interesting that inhibition of parasympathetic activity during task load is observed in this paradigm. The parasympathetic inhibition during task load should be a healthy response of the autonomic system to stressful events. LF responses are not consistent. HF and LF react to stressful events differently. HR behaves similar to LF/HF.

#### **Figure 6.**

*Schematic diagrams of heart rate variability profiles in major depressive disorder (MDD) and generalized anxiety disorder (GAD). Detailed descriptions are found in the text.*

#### *Characteristic Profiles of Heart Rate Variability in Depression and Anxiety DOI: http://dx.doi.org/10.5772/intechopen.104205*

In depression, HF at the resting state is low, indicating the underactivity of parasympathetic system. Parasympathetic underactivity is found not only in depression but in cardiovascular, neurological, and other psychiatric disturbances. In ischemic heart disorder and diabetic neuropathy, the peripheral autonomic nerve function is disturbed. In dementia and epilepsy, organic changes of the brain lead to autonomic alteration. In depression, functional changes of the responsible brain areas should involve the central autonomic system to generate HRV changes.

In addition to baseline change of the parasympathetic activity reflected in low HF, response of HF to the task load is disturbed in depression, making Task/ Rest ratio high. Parasympathetic activity cannot be switched off during the task indicating the difficulty in modifying the autonomic activity in response to alteration of arousal level or attention. Unresponsiveness of HF is found not only in MDD [11] but in normal subjects with high depressiveness and anxiety [12]. Subjective scores for depressiveness and anxiety were correlated with Task/Rest ratio of HF in normal controls. Depressiveness and anxiety may be related to parasympathetic unresponsiveness to stress.

Depression is also accompanied by an increase of HF during the rest period after the task load. The rebound-like increase starts after the end of the task and lasts for several tens of seconds. The functional significance of this transient change of HF may be related to excessive excitation of the parasympathetic system after suppression during the task load. Overall, depression is accompanied by continuous suppression together with the uncontrollability of the parasympathetic system.

As for LF, a reduction in the baseline level is observed in depression. But the rebound-like increase is present at the resting state after the task load possibly because LF reflects both sympathetic and parasympathetic activity. LF/HF and HR are higher in depression than in control. Parasympathetic underactivity is also responsible for these changes. It is interesting to observe that LF/HF and HR increase in response to task load although HF and LF are unchanged during the task load. Individual differences during the task load may account for this discrepancy.

### **6. Characteristic HRV profiles in anxiety**

On the other hand, the patients with GAD show an elevation of both HF and LF when they are free of a panic attack or severe phobic symptoms. In contrast to the HRV profile in depression, the parasympathetic system is activated, and breathingrelated and blood pressure-dependent modulation of heart rate is enhanced. The elevation of HF and LF at the resting state may be considered as a regulation of autonomic activity to cope with anxiety-related changes. When the regulation does not work, panic attack may occur. During panic attacks and exacerbation of anxiety symptoms, HF decreases and LF/HF increases, reflecting parasympathetic inhibition [6]. But when the anxious state is ameliorated, HRV indices return to the original level [13].

The elevated HF in GAD reacts to the task load by decreasing as in the normal control. Reactivity of parasympathetic activity is maintained in anxiety patients. The elevated LF can contribute to the stabilization of blood flow when the fluctuation of blood flow is large. Such fluctuation would be present during the time of stress. LF elevation may be the sign of an increased control of stress-induced circulatory changes. HRV profiles in GAD can be the result of autonomic accommodation to the anxious state.


**Abstract**

Vascular access (VA) for hemodialysis (HD) is the lifeline of a patient. Arteriovenous fistula (AVF) is the gold standard of VA, but there are challenging situations when providing long-term VA becomes challenging, in the presence of central vein stenosis (CVS), which is common in patients on hemodialysis, but its exact prevalence is not known. It would be ideal to have proper venous mapping with imaging modality to be able to plan central venous access. This prior venous mapping will help to plan the target vein and delineate venous path to be able to place HD catheter in the best position or resolve the VA-related problems. However, digital subtraction angiography remains the gold standard of the procedure, during which the target vein is accessed via ultrasound guidance, and subsequent passage of wire is done under fluoroscopic guidance. Venous angiography and, if indicated, angioplasty are performed. For complete chronically occluded thrombotic veins, recanalization needs to be attempted. Stenting is reserved for a select group of patients. There are advances in endovascular techniques to deal with CVS, and it needs a multidisciplinary team approach to tackle the complex issues of VA-related central venous disease (CVD).

**Keywords:** hemodialysis vascular access, central venous disease, central venous stenosis, central vein angioplasty, central vein stenting, complete thrombotic occlusion of central veins


In order to ensure that the inflow water is uniformly distributed across the entire wetland area, multiple entry openings or gates should be considered rather than single to deliver the range of design flow regimes required. Flow control structures should be used to control inflow rate and maintain water levels. Control valves or weirs or a combination can be used depending on the type of inlet structured selected. Since the wetland system is for water quality improvement, high incoming water velocities should be discouraged. Therefore, energy dissipation system may be required for the incoming water to provide protection for the wetland inlet. The inlet openings should be designed large enough to avoid obstruction. Inlet zones should provide access for sampling and flow monitoring.

Wetland outlet design is essential in avoiding possible dead zones and controlling water level and for monitoring flow and water quality. Depending on the size of the wetland, a combination of outlets (primary and secondary) or multiple outlets consisting of hydraulic control structures can be considered to collect and discharge treated water for the range of design flow regimes and maintain required water storage level. The purpose of the primary outlets is for water quality control, while

*Designing River Diversion Constructed Wetland for Water Quality Improvement DOI: http://dx.doi.org/10.5772/intechopen.92119*

the secondary is to act as a spillway and control flows in excess of the maximum design flow regime. Different types of control structures are available that can be used to control water level within the wetland. These may include number of individual pipes that fit together in a combination to obtain the desired water level, drop structures, or weirs. The design requirements of drop control structures and weirs can be found in hydraulic books. The outlet or water level control structure should be able to completely dewater the wetland when needed and allow for changes to be made easily.

#### **7. Conclusion**

Wetland cell size depends primarily on water quality treatment needs and cost

The actual area of the wetland is then computed using Eq. (16). Based on the computed values, the actual area of the wetland is thus selected as the maximum of areas obtained for each of the target pollutants (BOD, nitrogen, phosphorus, and

Wetland system configuration is an important element in the design of river diversion constructed wetland technology. After determining an appropriate wetland size, it is necessary to define the system configuration or layout by choosing an appropriate aspect ratio. Aspect ratio represents length (L) to width (W) ratio (L/W) of the wetland. It was suggested that choosing a good aspect ratio can assist to minimize short-circuiting and maximize flow distribution within the wetland system for biological activities [54]. Aspect ratio of as low as 1:1 was recommended for SSF [55], while length to width ratio of between 3:1 and 5:1 was recommended for FWS from an optimal point of view by [23]. However, based on findings by [56], 10:1 was recommended for FWS for good hydraulic efficiency. For water quality improvement, a river diversion wetland should be designed to operate with

Wetland bed slopes are also critical to maintain a uniform water depth through-

circuiting, a uniform bed slope from inlet to outlet is recommended. Thus, the bed slope for SSF should be 2% or less, while that for FWS should be 0.5% or less [14]. A river diversion wetland can also be designed to operate with similar bed slope as

**6. Water conveying system: inlet and outlet structures of the wetland**

This aspect of the wetland design focused on selecting or designing a water conveying system, inlet and outlet control structures that can facilitate flow and distribute inflow and drain outflow water from the wetland effectively. Depending on the type of river diversion wetland, flow diversion structure may be designed to consist of either a pipe or channel system and should function to provide a controlled flow of water to the wetland. However, it is necessary to be explicit about flow capacity at the time of design so that appropriate sizing of flow diversion structure can be made. Generally, the design flow conveyance structure is based on hydraulic;

therefore the reader is referred to hydraulic books for detailed information.

should provide access for sampling and flow monitoring.

**66**

In order to ensure that the inflow water is uniformly distributed across the entire wetland area, multiple entry openings or gates should be considered rather than single to deliver the range of design flow regimes required. Flow control structures should be used to control inflow rate and maintain water levels. Control valves or weirs or a combination can be used depending on the type of inlet structured selected. Since the wetland system is for water quality improvement, high incoming water velocities should be discouraged. Therefore, energy dissipation system may be required for the incoming water to provide protection for the wetland inlet. The inlet openings should be designed large enough to avoid obstruction. Inlet zones

Wetland outlet design is essential in avoiding possible dead zones and controlling water level and for monitoring flow and water quality. Depending on the size of the wetland, a combination of outlets (primary and secondary) or multiple outlets consisting of hydraulic control structures can be considered to collect and discharge treated water for the range of design flow regimes and maintain required water storage level. The purpose of the primary outlets is for water quality control, while

out the wetland system and facilitate drainage. In order to minimize short-

recommended for FWS since they are related in mode of operation.

considerations.

*Inland Waters - Dynamics and Ecology*

coliform bacteria).

the most efficient aspect ratio.

The management and restoration of water bodies like rivers should go beyond protection through the use of regulations. It should also make the most of opportunities that arise from using ecosystem properties to enhance self-purification capacity of rivers for water quality improvement. A key consideration is the use of constructed river diversion wetlands.

This chapter provided guidance on the design of a river diversion constructed wetland aimed at improving quality of river water. The use of a combination of empirical equations was presented to guide in the estimation of the actual wetland area rather than relying on an assumed rate. The design approach using these equations may present a promising method for the design of river diversion wetlands. Furthermore, this novel approach may be useful to wetland experts as some of the procedures adopted are not popular in wetland studies. This may provide opportunity for wetland designers to document approaches that have been found promising and come up with suitable design criteria for constructed river diversion wetlands.

#### **Acknowledgements**

The authors wish to express appreciation for the funding support provided by the Regional Water and Environmental Sanitation Centre, Kumasi (RWESCK), at the Kwame Nkrumah University of Science and Technology (KNUST), Kumasi, which is funded by the Government of Ghana and the World Bank under the Africa Centres of Excellence Project. Also, the authors wish to thank the National Water Resources Institute (NWRI), Nigeria, for providing opportunity and support for the study that led to the generation of knowledge and information presented in this chapter. We declare that the views expressed in this chapter are those of the authors and do not necessarily reflect those of the World Bank, Ghana Government, KNUST, and NWRI.

#### **Conflict of interest**

None declared.

*Inland Waters - Dynamics and Ecology*

### **Author details**

Sani Dauda Ahmed1,2\*, Sampson Kwaku Agodzo1 and Kwaku Amaning Adjei1

**References**

[1] Carr GM, Neary JP. Water Quality for Ecosystem and Human Health. 2nd ed. Ontario, Canada: United Nations Environment Programme (UNEP)- Global Environment Monitoring Systems (GEMS)/Water Programme; 2008

*DOI: http://dx.doi.org/10.5772/intechopen.92119*

*Designing River Diversion Constructed Wetland for Water Quality Improvement*

constructed serial wetland cells and its implication on nonpoint-source

pollution control. Hydrological Sciences Journal. 2016;**61**(16):2946-2956. DOI: 10.1080/02626667.2016.1171323

[9] Zalewski M. Ecohydrology—The use of ecological and hydrological processes for sustainable management of water resources. Hydrological Sciences

[10] Bodin H. Wastewater treatment in constructed wetlands: Effects of vegetation, hydraulics and data analysis methods [PhD thesis]. Sweden: Linkoping UniversityAccession No. 1509; 2013

[11] Konnerup D, Koottatep T, Brix H. Treatment of domestic wastewater in tropical subsurface flow constructed wetlands planted with *Canna and Heliconia*. Ecological Engineering. 2009;

[12] Mangangka IR. Role of hydraulic factors in constructed wetland and bioretention basin treatment

performance [PhD thesis]. Australia: Queensland University of Technology;

[13] Rousseau DPL, Vanrolleghemb PA, De Pauwa N. Model-based design of horizontal subsurface flow constructed treatment wetlands: A review. Water

Research. 2004;**38**:1484-1493

[14] Ellis JB, Shutes RBE, Revitt DM. Guidance Manual for Constructed Wetlands. Research Development Technical Report No. P2-159/TR2. Bristol, UK: Environment Agency; 2003

[15] Vymazal J. Constructed wetlands for wastewater treatment. Water. 2010;**2**: 530-549. DOI: 10.3390/w2030530

[16] Kadlec RH, Wallace SD. Treatment Wetlands. 2nd ed. Boca Raton, New York, USA: CRC Press; 2009

Journal. 2002;**47**:825-834

**35**(2):248-257

2013

[2] Wang HT, Omosa IB, Keller AA, Li FT. Ecosystem protection, integrated management and infrastructure are vital for improving water quality in Africa. Environmental Science and Technology.

[3] Meybeck M. Global analysis of river systems: From earth system controls to anthropocene syndromes. Philosophical Transactions of the Royal Society of London B: Biological Science. 2003;

[4] ITRC (Interstate Technology and Regulatory Council). Technical and Regulatory Guidance Document for Constructed Treatment Wetlands. USA: Interstate Technology and Regulatory Council (ITRC); 2003. Available from:

[5] Mao X, Yuan D, He L, Wei X, Chen Q,

[6] Borges AKP, Tauk-Tornisielo SM, Domingos RN, Angelis DF. Performance of the constructed wetland system for the treatment of water from the

Corumbatai River. Brazilian Archives of Biology and Technology. 2008;**51**(6):

[7] Fink DF, Mitsch WJ. Hydrology and nutrient biogeochemistry in a created river diversion oxbow wetland.

Ecological Engineering. 2007;**30**:93-102

[8] Jia Z, Tang S, Luo W, Hai Y. Water quality improvement through five

Bian L, et al. How long, narrowly constructed wetlands purify irrigation return water: A case study of Ulansuhai Lake, China. Advances in Meteorology. 2015;**2015**:1-6. DOI: 10.1155/2015/142036

2012;**46**(9):4699-4700

**358**(1440):1935-1955

www.itrcweb.org

1279-1286

**69**

1 Regional Water and Environmental Sanitation Centre Kumasi (RWESCK), Kwame Nkrumah University of Science and Technology, Kumasi, Ghana

2 National Water Resources Institute, Kaduna, Nigeria

\*Address all correspondence to<EMAIL_ADDRESS>
© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

*Designing River Diversion Constructed Wetland for Water Quality Improvement DOI: http://dx.doi.org/10.5772/intechopen.92119*

#### **References**

[1] Carr GM, Neary JP. Water Quality for Ecosystem and Human Health. 2nd ed. Ontario, Canada: United Nations Environment Programme (UNEP)- Global Environment Monitoring Systems (GEMS)/Water Programme; 2008

[2] Wang HT, Omosa IB, Keller AA, Li FT. Ecosystem protection, integrated management and infrastructure are vital for improving water quality in Africa. Environmental Science and Technology. 2012;**46**(9):4699-4700

[3] Meybeck M. Global analysis of river systems: From earth system controls to anthropocene syndromes. Philosophical Transactions of the Royal Society of London B: Biological Science. 2003; **358**(1440):1935-1955

[4] ITRC (Interstate Technology and Regulatory Council). Technical and Regulatory Guidance Document for Constructed Treatment Wetlands. USA: Interstate Technology and Regulatory Council (ITRC); 2003. Available from: www.itrcweb.org

[5] Mao X, Yuan D, He L, Wei X, Chen Q, Bian L, et al. How long, narrowly constructed wetlands purify irrigation return water: A case study of Ulansuhai Lake, China. Advances in Meteorology. 2015;**2015**:1-6. DOI: 10.1155/2015/142036

[6] Borges AKP, Tauk-Tornisielo SM, Domingos RN, Angelis DF. Performance of the constructed wetland system for the treatment of water from the Corumbatai River. Brazilian Archives of Biology and Technology. 2008;**51**(6): 1279-1286

[7] Fink DF, Mitsch WJ. Hydrology and nutrient biogeochemistry in a created river diversion oxbow wetland. Ecological Engineering. 2007;**30**:93-102

[8] Jia Z, Tang S, Luo W, Hai Y. Water quality improvement through five

constructed serial wetland cells and its implication on nonpoint-source pollution control. Hydrological Sciences Journal. 2016;**61**(16):2946-2956. DOI: 10.1080/02626667.2016.1171323

[9] Zalewski M. Ecohydrology—The use of ecological and hydrological processes for sustainable management of water resources. Hydrological Sciences Journal. 2002;**47**:825-834

[10] Bodin H. Wastewater treatment in constructed wetlands: Effects of vegetation, hydraulics and data analysis methods [PhD thesis]. Sweden: Linkoping UniversityAccession No. 1509; 2013

[11] Konnerup D, Koottatep T, Brix H. Treatment of domestic wastewater in tropical subsurface flow constructed wetlands planted with *Canna and Heliconia*. Ecological Engineering. 2009; **35**(2):248-257

[12] Mangangka IR. Role of hydraulic factors in constructed wetland and bioretention basin treatment performance [PhD thesis]. Australia: Queensland University of Technology; 2013

[13] Rousseau DPL, Vanrolleghemb PA, De Pauwa N. Model-based design of horizontal subsurface flow constructed treatment wetlands: A review. Water Research. 2004;**38**:1484-1493

[14] Ellis JB, Shutes RBE, Revitt DM. Guidance Manual for Constructed Wetlands. Research Development Technical Report No. P2-159/TR2. Bristol, UK: Environment Agency; 2003

[15] Vymazal J. Constructed wetlands for wastewater treatment. Water. 2010;**2**: 530-549. DOI: 10.3390/w2030530

[16] Kadlec RH, Wallace SD. Treatment Wetlands. 2nd ed. Boca Raton, New York, USA: CRC Press; 2009

**Author details**

*Inland Waters - Dynamics and Ecology*

**68**

Sani Dauda Ahmed1,2\*, Sampson Kwaku Agodzo1 and Kwaku Amaning Adjei1

1 Regional Water and Environmental Sanitation Centre Kumasi (RWESCK), Kwame Nkrumah University of Science and Technology, Kumasi, Ghana

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

2 National Water Resources Institute, Kaduna, Nigeria

\*Address all correspondence to<EMAIL_ADDRESS>
provided the original work is properly cited.

[17] Vymazal J. Emergent plants used in free water surface constructed wetlands: A review. Ecological Engineering. 2013; **61**(Part B):582-592. 1-11. DOI: 10.1016/j. ecoleng.2013.06.023

[18] Westerhoff P, Sharif F, Halden R, Herckes P, Krajmalnik-Brown R. Constructed wetlands for treatment of organic and engineered nanomaterial contaminants of emerging concerns. In: Web Report No: 4334. Denver, USA: Water Research Foundation (WRF); 2014

[19] Mitsch WJ, Day W. Restoration of wetlands in the Mississippi–Ohio– Missouri (MOM) river basin: Experience and needed research. Ecological Engineering*.* 2006;**26**:55-69. DOI: 10.1016/j.ecoleng.2005.09.005

[20] Verhoeven JTA, Arheimer B, Yin C, Hefting MM. Regional and global concerns over wetlands and water quality. Trends in Ecology and Evolution. 2006;**21**(2):96-103

[21] Meybeck M, Kimstach V, Helmer R. Strategies for water quality assessment. In: Chapman D, editor. Water Quality Assessments—A Guide to Use of Biota, Sediments and Water in Environmental Monitoring. 2nd ed. Cambridge, Great Britain: UNESCO/WHO/UNEP University Press; 1996

[22] Kimwaga RJ, Mwegoha WJS, Mahenge A, Nyomora AM, Lugali LG. Factors for success and failures of constructed wetlands in sanitation service chain. In: Dissemination of the Sustainable Wastewater Technology of Constructed Wetlands in Tanzania (VLIR Research Project). 2013

[23] USEPA. (U.S. Environmental Protection Agency) Constructed Wetlands for Treatment of Municipal Wastewater Manual (EPA 625/R-99/ 010). Cincinnati, OH: U.S. EPA; 2000

[24] Economopoulou MA, Tsihrintzis VA. Design methodology of free water surface constructed wetlands. Water Resources Management*.* 2004;**18**: 541-565

[32] Ajmal M, Khan TA, Kim T. A CNbased ensembled hydrological model for enhanced watershed runoff prediction. Water. 2016;**8**(20):1-17. DOI: 10.3390/

*DOI: http://dx.doi.org/10.5772/intechopen.92119*

*Designing River Diversion Constructed Wetland for Water Quality Improvement*

performance using the advection diffusion equation. WIT Transactions on Ecology and the Environment. 2008;

**109**(IV):363-371. DOI: 10.2495/

[41] Stairs DB. Flow characteristics of constructed wetlands: Tracer studies of the hydraulic regime [MSc thesis]. USA: Oregon State University; 1993. pp. 81

[42] Crites RW, Tchobanoglous G. Small

Management Systems. New York, NY:

Middlebrooks EJ. Natural Systems for Waste Management and Treatment. 2nd ed. New York, USA: McGraw-Hill, Inc.;

[44] Kadlec RH, Knight RL. Treatment Wetlands. Boca Raton, USA: Lewis

[45] Kadlec RH. The inadequacy of firstorder treatment wetland models. Ecological Engineering. 2000;**15**:105-119

[46] Kayombo S, Mbwette TSA, Katima JHY, Ladegaard N, Jorgensen SE. Waste stabilization ponds and constructed wetlands design manual. Tanzania, Dar Es Salaam: UNEP-IETC with the Danish International Development Agency

[47] Kadlec RH, Reddy KR. Temperature effects in treatment wetlands. Water Environment Research. 2001;**73**(5):

[49] Mitchell C, McNevin D. Alternative analysis of BOD removal in subsurface flow constructed wetlands employing

[48] Kivaisi AK. The potential for constructed wetlands for wastewater treatment and reuse in developing countries: A review. Ecological Engineering. 2001;**16**:545-560

and Decentralized Wastewater

McGraw Hill Co.; 1998

[43] Reed SC, Crites RW,

1995

Publishers; 1996

(Danida); 2005

543-557

WM080381

[33] Duran-Barroso P, Gonzalez J, Valdes JB. Sources of uncertainty in the NRCS model: Recognition and solution. Hydrological Processes. 2017;**31**(22):1-9.

[34] Yuan Y, Nie W, McCutcheon SC, Taguas EV. Initial abstraction and curve numbers for semiarid watersheds in southeastern Arizona. Hydrological Processes. 2012;**28**(3):1-11. DOI:

[35] WMO (World Meteorological Organization). Manual on Stream Gauging: Volume II—Computation of Discharge (WMO-No. 1044). Geneva, Switzerland: World Meteorological Organization (WMO); 2010

[36] Lenhart C, Gordon B, Gamble J, Current D, Ross N, Herring L, et al. Design and hydrologic performance of a tile drainage treatment wetland in Minnesota, USA. Water. 2016;**8**(549):

[37] Guven A, Aytek A, Azamathulla H. A practical approach to formulate stage– discharge relationship in natural rivers. Neural Computation and Application. 2012;**23**(3-4):873-880. DOI: 10.1007/

[38] Dottori F, Martina MLV, Todini E. A dynamic rating curve approach to indirect discharge measurement. Hydrology and Earth System Sciences

Discussions. 2009;**6**:859-896

[39] Biggs BJF. Hydraulic habitat of plants in streams. Regulated River Resource and Management. 1996;**12**:

[40] Popov V, Ahmed S, Qureshi MI. Simulation of constructed wetland

1-19. DOI: 10.3390/w8120549

s00521-012-1011-5

131-144

**71**

DOI: 10.1002/hyp.11305

10.1002/hyp9592

w8010020

[25] Chapman D, Kimstach V. Selection of water quality variables. In: Chapman D, editor. Water Quality Assessments—A Guide to Use of Biota, Sediments and Water in Environmental Monitoring. 2nd ed. Cambridge, Great Britain: UNESCO/WHO/UNEP University Press; 1996

[26] Ashbolt NJ, Grabow WOK, Snozzi M. 13: Indicators of microbial water quality. In: Fretwell L, Bartram J, editors. Water Quality: Guidelines, Standards and Health (World Health Organization (WHO)). London, UK: IWA Publishing; 2001

[27] Miller J. Constructed Wetlands Technology Assessment and Design Guidance (Manual). USA: Iowa Department of Natural Resources (IDNR); 2007

[28] Gikas GD, Tsihrintzis VA. Municipal wastewater treatment using constructed wetlands. Water Utility Journal. 2014;**8**:57-65

[29] HTCKL (Humid Tropics Hydrology and Water Resources Centre). Technical Report on Constructed Wetland. The Regional Humid Tropics Hydrology and Water Resources Centre for Southern Asia and the Pacific. Malaysia, Kuala Lumpur: HTCKL; 2014

[30] Millhollon EP, Rodrigue PB, Rabb JL, Martin DF, Anderson RA, Dans DR. Designing a constructed wetland for the detention of agricultural runoff for water quality improvement. Journal of Environmental Quality. 2009;**38**: 2458-2467. DOI: 10.2134/jeq2008.0526

[31] WSUD (Water Sensitive Urban Design). Constructed wetlands (Engineering Guidelines) for Brisbane City. Australia, Brisbane City; Brisbane City Councils; 2005

*Designing River Diversion Constructed Wetland for Water Quality Improvement DOI: http://dx.doi.org/10.5772/intechopen.92119*

[32] Ajmal M, Khan TA, Kim T. A CNbased ensembled hydrological model for enhanced watershed runoff prediction. Water. 2016;**8**(20):1-17. DOI: 10.3390/ w8010020

[17] Vymazal J. Emergent plants used in free water surface constructed wetlands: A review. Ecological Engineering. 2013; **61**(Part B):582-592. 1-11. DOI: 10.1016/j.

*Inland Waters - Dynamics and Ecology*

free water surface constructed wetlands. Water Resources Management*.* 2004;**18**:

[25] Chapman D, Kimstach V. Selection

of water quality variables. In: Chapman D, editor. Water Quality Assessments—A Guide to Use of Biota, Sediments and Water in Environmental Monitoring. 2nd ed. Cambridge, Great Britain: UNESCO/WHO/UNEP

[26] Ashbolt NJ, Grabow WOK, Snozzi M. 13: Indicators of microbial water quality. In: Fretwell L, Bartram J, editors. Water Quality: Guidelines, Standards and Health (World Health Organization (WHO)). London, UK:

[27] Miller J. Constructed Wetlands Technology Assessment and Design Guidance (Manual). USA: Iowa Department of Natural Resources

[28] Gikas GD, Tsihrintzis VA.

Municipal wastewater treatment using constructed wetlands. Water Utility

[29] HTCKL (Humid Tropics Hydrology and Water Resources Centre). Technical Report on Constructed Wetland. The Regional Humid Tropics Hydrology and Water Resources Centre for Southern Asia and the Pacific. Malaysia, Kuala

[30] Millhollon EP, Rodrigue PB, Rabb JL, Martin DF, Anderson RA, Dans DR. Designing a constructed wetland for the detention of agricultural runoff for water

quality improvement. Journal of Environmental Quality. 2009;**38**: 2458-2467. DOI: 10.2134/jeq2008.0526

[31] WSUD (Water Sensitive Urban Design). Constructed wetlands (Engineering Guidelines) for Brisbane City. Australia, Brisbane City; Brisbane

University Press; 1996

IWA Publishing; 2001

(IDNR); 2007

Journal. 2014;**8**:57-65

Lumpur: HTCKL; 2014

City Councils; 2005

541-565

[18] Westerhoff P, Sharif F, Halden R, Herckes P, Krajmalnik-Brown R. Constructed wetlands for treatment of organic and engineered nanomaterial contaminants of emerging concerns. In: Web Report No: 4334. Denver, USA: Water Research Foundation (WRF); 2014

[19] Mitsch WJ, Day W. Restoration of wetlands in the Mississippi–Ohio– Missouri (MOM) river basin: Experience and needed research. Ecological Engineering*.* 2006;**26**:55-69. DOI: 10.1016/j.ecoleng.2005.09.005

[20] Verhoeven JTA, Arheimer B, Yin C, Hefting MM. Regional and global concerns over wetlands and water quality. Trends in Ecology and Evolution. 2006;**21**(2):96-103

[21] Meybeck M, Kimstach V, Helmer R. Strategies for water quality assessment. In: Chapman D, editor. Water Quality Assessments—A Guide to Use of Biota, Sediments and Water in Environmental Monitoring. 2nd ed. Cambridge, Great Britain: UNESCO/WHO/UNEP

University Press; 1996

[22] Kimwaga RJ, Mwegoha WJS, Mahenge A, Nyomora AM, Lugali LG. Factors for success and failures of constructed wetlands in sanitation service chain. In: Dissemination of the Sustainable Wastewater Technology of Constructed Wetlands in Tanzania (VLIR Research Project). 2013

[23] USEPA. (U.S. Environmental Protection Agency) Constructed Wetlands for Treatment of Municipal Wastewater Manual (EPA 625/R-99/ 010). Cincinnati, OH: U.S. EPA; 2000

Tsihrintzis VA. Design methodology of

[24] Economopoulou MA,

**70**

ecoleng.2013.06.023

[33] Duran-Barroso P, Gonzalez J, Valdes JB. Sources of uncertainty in the NRCS model: Recognition and solution. Hydrological Processes. 2017;**31**(22):1-9. DOI: 10.1002/hyp.11305

[34] Yuan Y, Nie W, McCutcheon SC, Taguas EV. Initial abstraction and curve numbers for semiarid watersheds in southeastern Arizona. Hydrological Processes. 2012;**28**(3):1-11. DOI: 10.1002/hyp9592

[35] WMO (World Meteorological Organization). Manual on Stream Gauging: Volume II—Computation of Discharge (WMO-No. 1044). Geneva, Switzerland: World Meteorological Organization (WMO); 2010

[36] Lenhart C, Gordon B, Gamble J, Current D, Ross N, Herring L, et al. Design and hydrologic performance of a tile drainage treatment wetland in Minnesota, USA. Water. 2016;**8**(549): 1-19. DOI: 10.3390/w8120549

[37] Guven A, Aytek A, Azamathulla H. A practical approach to formulate stage– discharge relationship in natural rivers. Neural Computation and Application. 2012;**23**(3-4):873-880. DOI: 10.1007/ s00521-012-1011-5

[38] Dottori F, Martina MLV, Todini E. A dynamic rating curve approach to indirect discharge measurement. Hydrology and Earth System Sciences Discussions. 2009;**6**:859-896

[39] Biggs BJF. Hydraulic habitat of plants in streams. Regulated River Resource and Management. 1996;**12**: 131-144

[40] Popov V, Ahmed S, Qureshi MI. Simulation of constructed wetland

performance using the advection diffusion equation. WIT Transactions on Ecology and the Environment. 2008; **109**(IV):363-371. DOI: 10.2495/ WM080381

[41] Stairs DB. Flow characteristics of constructed wetlands: Tracer studies of the hydraulic regime [MSc thesis]. USA: Oregon State University; 1993. pp. 81

[42] Crites RW, Tchobanoglous G. Small and Decentralized Wastewater Management Systems. New York, NY: McGraw Hill Co.; 1998

[43] Reed SC, Crites RW, Middlebrooks EJ. Natural Systems for Waste Management and Treatment. 2nd ed. New York, USA: McGraw-Hill, Inc.; 1995

[44] Kadlec RH, Knight RL. Treatment Wetlands. Boca Raton, USA: Lewis Publishers; 1996

[45] Kadlec RH. The inadequacy of firstorder treatment wetland models. Ecological Engineering. 2000;**15**:105-119

[46] Kayombo S, Mbwette TSA, Katima JHY, Ladegaard N, Jorgensen SE. Waste stabilization ponds and constructed wetlands design manual. Tanzania, Dar Es Salaam: UNEP-IETC with the Danish International Development Agency (Danida); 2005

[47] Kadlec RH, Reddy KR. Temperature effects in treatment wetlands. Water Environment Research. 2001;**73**(5): 543-557

[48] Kivaisi AK. The potential for constructed wetlands for wastewater treatment and reuse in developing countries: A review. Ecological Engineering. 2001;**16**:545-560

[49] Mitchell C, McNevin D. Alternative analysis of BOD removal in subsurface flow constructed wetlands employing

Monod kinetics. Water Research. 2001; **35**(5):1295-1303

[50] Wynn TM, Liehr SK. Development of a constructed subsurface-flow wetland simulation model. Ecological Engineering. 2001;**16**:519-536

[51] Economopoulou MA, Tsihrintzis VA. Design methodology and area sensitivity analysis of horizontal subsurface flow constructed wetlands. Water Resources Management. 2003;**17**(2):147-174

[52] Sarah KL. Natural treatment and onsite processes. Water Environmental Research. 2005;**77**(6):1389-1424

[53] Moreno-Mateos D, Pedrocchi C, Comin FA. Effects of wetland construction on water quality in a semiarid catchment degraded by intensive agricultural use. Ecological Engineering*.* 2010;**36**:631-639

[54] Bendoricchio G, Cin LD, Persson J. Guidelines for free water surface wetland design. EcoSys Bd. 2000;**8**: 51-91

[55] Steiner GR, Freeman RJ. Configuration and substrate design considerations for constructed wetlands wastewater treatment. In: Hammer DA, editor. Constructed Wetlands for Wastewater Treatment. Chelsea, USA: Lewis Publishers; 1989

[56] Persson J, Somes NLG, Wong THF. Hydraulics efficiency of constructed wetlands and ponds. Water Science and Technology. 1999;**40**:291-300

**73**

**Figure 1.**

*Maumee Bay State Park, Ohio, 2013 HAB. Source: Ref. [2].*

**Chapter 5**

**Abstract**

**1. Introduction**

The Tourism Impacts of Lake Erie

Nutrient loading and warming waters can lead to hazardous algal blooms (HABs). Policymakers require cost-effective valuation tools to help understand impacts and prioritize adaptation measures. This chapter evaluates the tourism impacts of HABs in Western Lake Erie based on HABs that occurred in 2011 and 2014, both through a unique temporal and spatial specification of HAB severity as

well as input/output analysis and decomposition of trips and profitability.

**Keywords:** hazardous algal blooms, HABs, nutrient loading, socioeconomic,

Attractive inland waters such as western Lake Erie can provide significant tourism services [1]. Hazardous algal blooms (HABs) that tend to result from warm water and nutrient loading result in murky and unpleasant water (**Figure 1**), potentially interrupting the \$12.9 billion tourism industry in the region and putting

Hazardous Algal Blooms

*Matthew Bingham and Jason Kinnell*

benefits transfer, Lake Erie, input/output, tourism

#### **Chapter 5**

Monod kinetics. Water Research. 2001;

*Inland Waters - Dynamics and Ecology*

[50] Wynn TM, Liehr SK. Development of a constructed subsurface-flow wetland simulation model. Ecological

Tsihrintzis VA. Design methodology and area sensitivity analysis of

horizontal subsurface flow constructed

[52] Sarah KL. Natural treatment and onsite processes. Water Environmental Research. 2005;**77**(6):1389-1424

[53] Moreno-Mateos D, Pedrocchi C, Comin FA. Effects of wetland

construction on water quality in a semiarid catchment degraded by intensive agricultural use. Ecological Engineering*.*

[54] Bendoricchio G, Cin LD, Persson J. Guidelines for free water surface wetland design. EcoSys Bd. 2000;**8**:

[56] Persson J, Somes NLG, Wong THF. Hydraulics efficiency of constructed wetlands and ponds. Water Science and

[55] Steiner GR, Freeman RJ. Configuration and substrate design considerations for constructed wetlands wastewater treatment. In: Hammer DA, editor. Constructed Wetlands for Wastewater Treatment. Chelsea, USA:

Lewis Publishers; 1989

Technology. 1999;**40**:291-300

Engineering. 2001;**16**:519-536

[51] Economopoulou MA,

wetlands. Water Resources Management. 2003;**17**(2):147-174

2010;**36**:631-639

51-91

**72**

**35**(5):1295-1303


**9.9 Regenerative approaches**

Regenerative procedures using a membrane and bone graft substitutes attempting to partially fill the bony defects caused by peri-implantitis can be successful [92].

**Figure 5.** *A case of peri-implantitis treated with bone augmentation.*


**5.4 Multiple regression models**

Multiple regression analyses are used when product pricing is required across an industry such as real estate pricing and marketing organizations in order to establish the impact of a campaign. It is a broader category of regressions that incorporates both linear and nonlinear regressions and uses explanatory variables to perform an analysis [14]. The main application of multiple regression algorithms in practical situations is social science research, the analysis of the behavior of a device, or in the insurance industry to estimate the worthiness of a claim. Multiple regression analysis was used to examine the factors that affected the outcome of a referendum in which the United Kingdom opted to leave the European Union. The research involved the application of multivariate regression analysis in which the Logistic (Logit) Model was combined with real data to determine the statistically significant factors that have an impact on the voting preference in a simultaneous manner, in addition to the odds ratio that supports Leave or Remain [15]. The results of the multiple regressions showed that the gender of voters, age, and level of education were statistically significant factors, while country of birth was a statistically insignificant factor.


*Postharvest Technology of Tamarind DOI: http://dx.doi.org/10.5772/intechopen.101096*

[15] reported drying tamarind pulp using foam mat drying with various foaming agents. Mesquite gum, ovalbumin, and a low molecular weight surface active blend were hydrated to 50% (w/w) solutions and applied to the samples single or in combination (**Figure 13**).