Intracellular evasion strategies of fish pathogenic bacteria: a comprehensive review of immune subversion mechanisms

Introduction

The aquatic immune landscape represents a sophisticated and evolutionary vital defence network composed of both innate and adaptive components designed to protect fish from a constant barrage of environmental pathogens (Uribe et al., 2011) [1] . Because fish inhabit an aquatic medium dense with microorganisms, physical and mucosal barriers including the skin, gills, and gut epithelia serve as the crucial first line of defence, utilizing continuous mucus sloughing, lysozymes, and antimicrobial peptides to trap and neutralize invaders before entry (Sahoo et al., 2021) [2] . If pathogens successfully breach these superficial layers, they encounter innate cellular defences driven by professional phagocytes such as macrophages and neutrophils, which home in on conserved pathogen-associated molecular patterns (PAMPs) to execute phagocytosis and generate reactive oxygen and nitrogen species (Smith et al., 2019) [3] . Concurrently, this innate response coordinates with the slower-evolving adaptive immune system mediated by specialized lymphocytes and Major Histocompatibility Complex (MHC) molecules to establish long-term specific immunity and immunological protection across mucosal surfaces (Salinas, 2015) [4] . The intracellular niche presents a distinct evolutionary battleground characterized by a fundamental divergence between extracellular pathogens and facultative or obligate intracellular bacteria (Storrs et al., 2020). While extracellular microbes reside and multiply in host tissue fluids and blood plasma vulnerable to circulating antibodies, complement proteins, and phagocytic clearance intracellular pathogens breach host cell membranes to establish residency within the host cytoplasm or specialized vacuoles (Ramakrishnan, 2012) [5] . Prominent aquatic pathogens such as Piscirickettsia salmonis, Mycobacterium species, and Francisella noatunensis have adapted to this protected intracellular milieu, circumventing humoral defenses and utilizing host cellular machinery to shield themselves from direct immune recognition (Fryer & Hedrick, 2003; Mauel et al., 2007) [6] . Building upon this compartmentalized dynamic, the scope of this review centres on highlighting how these sophisticated fish pathogens subvert host immune cells, effectively transforming primary defenders into se cure safe havens for replication and dissemination (Holden et al., 2016). Rather than succumbing to the oxidative and enzymatic arsenal of professional phagocytes like macrophages and neutrophils, intracellular bacterial strains actively manipulate host cell signalling pathways, suppress phagolysosome maturation, and evade apoptosis (Vázquez et al., 2018) [7] . Understanding these multi-faceted subversion tactics is critical for decoding the pathogenesis of chronic aquatic diseases and designing targeted therapeutics capable of piercing the host cell membrane to eradicate hidden bacterial reservoirs (Casadevall, 2008) [8] .

Invasion strategies: gaining entry into host cells

Receptor-mediated recognition and uptake represent the critical first step wherein intracellular fish pathogens exploit the host cell's own surface machinery to gain entry (Takeuchi et al., 2010) [9] . Rather than relying solely on accidental engulfment, pathogenic bacteria actively engage host pattern recognition receptors (PRRs) such as Tolllike receptors (TLRs) and C-type lectin receptors (CLRs) along with specialized surface proteins on fish macrophages and neutrophils to trigger targeted receptor-mediated endocytosis (Medzhitov, 2009) [10] . By mimicking normal host ligands or displaying surface adhesins, these bacteria manipulate intracellular signalling pathways to promote their own uptake while simultaneously dampening the initial inflammatory response that would normally sound the alarm (Casadevall, 2008) [8] . Furthermore, successful intracellular invaders like Piscirickettsia salmonis and Mycobacterium species subvert complement receptors and scavenger receptors on teleost phagocytes, ensuring they are quietly internalized without triggering the full oxidative burst typically associated with traditional phagocytic clearance (Vázquez et al., 2018) [7] . Active invasion mechanisms rely heavily on the deployment of specialized secretion systems such as Type III, Type IV, or Type VI Secretion Systems which act as molecular syringes to inject bacterial effector proteins directly into the cytosol of fish phagocytes (Green et al., 2016) [11] . These translocated bacterial effectors manipulate host cytoskeletal dynamics, membrane trafficking, and signal transduction cascades, actively forcing non-phagocytic cells to engulf the bacteria or subverting the normal internalization process of professional phagocytes to secure a protected intracellular niche (Costa et al., 2015) [12] . By commandeering these host pathways, pathogens like Francisella and other aquatic intracellular bacteria can cross epithelial barriers and manipulate vesicular transport to prevent early host defence responses (Brodsky et al., 2017) [13] . Complementing this direct molecular hijacking, these pathogens specifically target professional phagocytes primarily macrophages and neutrophils which are designed to destroy foreign invaders, turning them into primary entry points and Trojan horses for systemic dissemination (Flannagan et al., 2009) [14] . Although these immune cells normally rely on their powerful microbicidal arsenal to neutralize pathogens, intracellular fish bacteria exploit the phagocytic uptake mechanism to bypass extracellular clearance and gain direct access to the nutrient-rich intracellular environment (Rosenberger et al., 2003) [15] . By surviving and multiplying within these frontline defenders, the bacteria effectively subvert the host's primary cellular defense network, leading to chronic infections that are exceptionally difficult for the fish's immune system to clear (Ramakrishnan, 2012) [5] .

Subversion of innate immunity and intracellular survival tactics

To successfully survive inside teleost host cells, intracellular bacterial pathogens must overcome a sequence of hostile intracellular defences, beginning with the prevention of phagolysosome fusion (Kinchen et al., 2008) [16] . By actively modifying the membrane characteristics of the bacteria-containing vacuole, pathogens such as Mycobacterium species and Piscirickettsia salmonis secrete specific effector molecules that interfere with normal vesicular trafficking, blocking the recruitment of proton pumps and essential hydrolytic enzymes necessary to acidify the compartment and degrade the invader (Russell, 2011) [17] . This active arrest ensures that the pathogen resides within a non-fusogenic, protected niche where it can safely establish early infection without being exposed to the lethal degradative environment of a mature lysosome. Beyond merely avoiding lysosomal degradation, certain intracellular fish pathogens employ an aggressive strategy by escaping the vascular membrane altogether to replicate freely within the host cell cytoplasm (Cossart et al., 2004) [18] . Drawing parallels from well-documented terrestrial mammalian infection models, aquatic pathogens utilize specialized pore-forming proteins, phospholipases, or secretion systems to disrupt the membrane of the containing phagosome, enabling direct access to the nutrient-rich cytosolic milieu (Ray et al., 2009) [19] . This cytosolic localization provides an unrestricted environment for rapid bacterial multiplication, shielding the organisms from remaining vesicular defences and facilitating direct actin-based motility to spread to adjacent cells without re-entering the extracellular space. Even within these protected intracellular compartments, bacteria must continuously contend with the host's lethal antimicrobial arsenal, driving the evolution of sophisticated mechanisms to resist oxidative and nitrosative stress (Fang, 2004) [20] . Upon phagocytic entry, fish macrophages and neutrophils unleash a powerful oxidative burst, generating toxic reactive oxygen species (ROS) and reactive nitrogen species (RNS) designed to damage microbial DNA, lipids, and proteins (Bogdan et al., 2000) [21] . To counteract this, intracellular fish pathogens deploy high levels of antioxidant enzymes-such as superoxide dismutase, catalases, and peroxidases-that effectively neutralize these free radicals, allowing the bacteria to persist indefinitely inside professional phagocytes.

Evasion of adaptive immunity and immune modulation

Interference with Antigen Processing and Presentation: To successfully establish chronic infections, intracellular fish pathogens must extend their evasion tactics beyond initial cellular entry and survival by directly disrupting the adaptive arm of the immune system through the interference of antigen processing and presentation (Blumenthal et al., 2002) [22] . By downregulating or mislocalizing Major Histocompatibility Complex (MHC) class I and class II molecules on the surface of infected teleost antigen-presenting cells, these bacteria effectively mask their presence and block the subsequent activation of naive and memory T-cells (Rrapi et al., 2017) [23] . This targeted suppression prevents the host from mounting a robust, cell-mediated adaptive response, allowing the pathogen to persist undetected within the host tissues for extended periods.

Cytokine Modulation:

Complementing this receptor-level masking, intracellular fish pathogens actively manipulate the host's chemical signaling network via precise cytokine modulation to dampen the overall inflammatory response (Redd et al., 2006) [24] . Pathogens achieve this by stimulating the production of anti-inflammatory cytokines like interleukin-10 (IL-10) while simultaneously suppressing pro-inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), thereby creating a localized immunosuppressive microenvironment that deactivates nearby macrophages and NK cells (Oide et al., 2008) [25] . This chemical hijacking ensures that the host immune system remains pacified, preventing the recruitment of additional immune cells that could otherwise compromise the intracellular bacterial niche.

Induction of Apoptosis vs. Necrosis: Intracellular fish pathogens exert tight control over host cell fate by manipulating cell death pathways, balancing the induction of apoptosis versus necrosis to suit their replication cycle (Roulston et al., 1999) [26] . During early and mid-stages of infection, many intracellular bacteria secrete anti-apoptotic effector proteins that delay host cell death, maximizing the window of time available for intracellular replication and nutrient acquisition (Wyllie, 2010) [27] . Conversely, once intracellular resources are exhausted, the bacteria can actively trigger rapid host cell lysis or necrosis, releasing progeny into the extracellular matrix to invade and infect neighbouring cells.

Major intracellular bacterial pathogens in fish (case studies)

Piscirickettsia salmonis: Among intracellular aquatic pathogens, Piscirickettsia salmonis stands out as the primary model of facultative intracellular persistence in salmonids, responsible for Piscirickettsiosis (salmon rickettsial septicemia), which causes severe economic losses in global aquaculture (Fryer et al., 2003) [6] . This bacterium specifically targets teleost macrophages and epithelial cells, where it replicates within cytoplasmic vacuoles by subverting normal vesicular trafficking and evading the host's innate immune clearance mechanisms (Rozas et al., 2014) [28] . The study of P. salmonis has provided foundational insights into how facultative in-tracellular bacteria establish systemic chronic infections across economically vital farmed fish species (Cvitanich et al., 1991) [29] . Mycobacterium species: In parallel, Mycobacterium species such as Mycobacterium marinum and Mycobacterium fortuitum exemplify chronic intracellular persistence in teleost fish through the hallmark formation of granulomas (Ramakrishnan, 2012) [5] . Following uptake by professional phagocytes, these pathogenic mycobacteria arrest phagolysosome maturation and reside indefinitely within epithelioid cells and macrophages, eventually recruiting lymphocytes and surrounding tissue to form organized, multi-layered granulomatous structures (Rawlings et al., 2007) [30] . This enclosed microenvironment protects the bacteria from systemic host immunity, resulting in chronic, lifelong infections characterized by granulomatous lesions in visceral organs like the spleen, kidney, and liver (Aalma et al., 2018) [31] . Francisella: Francisella and various Rickettsia-like organisms (RLOs) have emerged as critical intracellular challenges facing modern global aquaculture (Birkbeck et al., 2015) [32] . Pathogens such as Francisella noatunensis infect a wide range of farmed and wild fish species, causing francisellosis, which similarly manifests as severe granulomatous disease and high mortality rates (Hestnes et al., 2010) [33] . The continuous emergence of these intracellular RLOs underscores the expanding geographical footprint and epidemiological threat of intracellular bacterial infections, necessitating enhanced biosecurity and targeted immunological research (Ostland et al., 2006) [34] . Table 1 below represents some of the studies reported intracellular bacterial pathogens in different fishes.

Challenges in treatment and control

Standard extracellular antibiotic treatments frequently fail against intracellular fish pathogens due to the formidable antibiotic barrier posed by host cell membranes and specialized vacuolar compartments (Piddock, 2006) [35] . Many conventionally administered hydrophilic or low-lipid-soluble antibiotics are unable to efficiently penetrate the hydrophobic plasma membranes of teleost phagocytes or maintain active therapeutic concentrations within the intracellular milieu where the bacteria reside (Lemaire et al., 2007) [36] . Furthermore, even if an antibiotic successfully enters the host cell, the acidic environment of the phagosome or the active efflux pumps of the pathogen can neutralize the drug, leaving intracellular bacterial reservoirs completely protected from pharmacological clearance (Straubinger et al., 2014) [37] . Overcoming these persistent infections also introduces significant vaccination hurdles, primarily demanding the stimulation of robust cell-mediated immunity (CMI) rather than relying solely on conventional humoral (antibody) responses (Plant et al., 2011) [38] . Because intracellular pathogens hide safely within host cells away from circulating antibodies and complement proteins, traditional antibody-based vaccines often fail to confer adequate protection against intracellular bacterial challenges (Gomez et al., 2013) [39] . Consequently, nextgeneration prophylactic strategies must focus on activating cytotoxic T-lymphocytes and enhancing macrophage microbicidal effector functions to effectively clear infected host cells and achieve long-term adaptive immunity in aquaculture species (Vassallo & Standing, 2019).

Future perspectives and conclusion

Despite significant advancements in understanding fish immunology, critical gaps remain in our current knowledge regarding fish-specific molecular cross-talk during intracellular bacterial infections. While much of the foundational signaling pathways have been inferred from mammalian models, the precise ligand-receptor interactions, teleostspecific transcription factors, and the nuanced biochemical cross-talk between intracellular pathogens (such as Piscirickettsia salmonis or Mycobacterium species) and host teleost cells require much deeper investigation. Unraveling these species-specific signaling mechanisms is essential for identifying unique vulnerability points in pathogen survival that can be therapeutically exploited.

To bridge these knowledge gaps and overcome current treatment failures, future efforts must focus on the development of novel control strategies tailored for aquaculture. These innovative approaches include targeted immunostimulants to boost macrophage microbicidal activity, intracellular-penetrating therapeutics capable of crossing host cell membranes to reach secluded bacterial reservoirs, and advanced vaccines designed to elicit robust cell-mediated immunity (CMI) rather than relying solely on traditional antibody production.

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