Taura syndrome virus (TSV) which belongs to the family Dicistroviridae is the causative agent of TS. With a diameter of 32 nm, the virion is a naked (without an envelope) icosahedron. TSV’s genetic material consists of 10,205 nucleotides of positive-sense, single-stranded RNA (+ssRNA). TSV’s genome has two open reading frames (ORFs): ORF 1, which codes for non-structural proteins, and ORF 2, which contains TSV structural protein sequences such as capsid proteins (Mari et al., 2002). Studies conducted on the TSV using molecular tools indicated that a single virus strain was behind the first TSV pandemic in American (Ecuador) aquaculture farms from 1991-1992. However, when cDNA sequences of TSV capsid protein 2 (CP2) were compared (Tang and Lightner, 2005), four different genetic variants of TSV were discovered (Wertheim et al., 2009). TS has caused a huge loss to the global shrimp aquaculture industry and has been reported in the Middle East, America, and Asia. The spread of TS was mainly due to the transfer of live broodstocks across regional and international borders (Walker and Mohan, 2009; Lightner, 2011).

With a cumulative death rate of 40-90%, L. vannamei is one of the most vulnerable species to TSV. TS has been reported in this species at post-larvae (PL), juvenile, and adult stages of its life cycle (Ochoa et al., 2020). This virus is also known to infect other varieties of shrimps such as Penaeus stylirostris and Penaeus setiferus. In addition, experiments on PL and juveniles of Penaeus japonicus, P. monodon, Penaeus duorarum, Fenneropenaeus chinensis, Penaeus aztecus and Penaeus schmitti were also reported to be prone to TSV. The viral replication of TSV is in the cytoplasm of the host cell (Ganjoor, 2015). TS occurs in shrimps in three phases. In the peracute/acute phase, the shrimps are more likely to die, and is characterized by the showing of tail fan, pale reddish color in pleopods, softening of coats and hollow intestines. Individuals that survive this phase will go through the regeneration process, which begins with multifocal melanoid lesions. In the chronic infectious phase, the shrimp remains persistently infected with subclinical infections. The TSV is spread to susceptible shrimps by contaminated water and horizontal transmission via cannibalism of diseased, moribund or dead shrimps. It is also hypothesized that TSV can be vertically transmitted, although this is yet to be experimentally validated. Furthermore, the aquatic insect, water boatman Trichocorixa reticulata (Guerin-Meneville, 1857), has been identified as a TSV vector (Dhar et al., 2004). Since the mid-1990s, various research and commercial breeding programs have employed TSV specific pathogen resistance (SPR¹) selective breeding to combat TSV disease, significantly decreasing its incidence (Sookruksawong et al., 2013). Notably, between 1999 and 2004, there were no TSV outbreaks reported in Colombian shrimp farms, demonstrating the effectiveness of a TSV-resistant breeding program where 100% of the raised shrimp were TSV-SPR¹.

WSD is a serious disorder caused by WSSV that causes rapid death, most notably in juvenile shrimp. WSSV is an enveloped virus of the genus Whispovirus with double-stranded DNA (dsDNA) and a genome size of 290 to 305 Kbp on average. The size of the genome of isolates from various geographical regions varies, indicating genetic instability that might lead to alterations in virulence (Ganjoor, 2015).

WSSV is widely regarded as one of the most serious threats to the shrimp aquaculture sector (Flegel and Alday-Sanz, 1998). Between 1990 and 1994, the first WSD outbreak was observed in Taiwan and Japan, in P. japonicus (Zhu et al., 2019). In 1999, WSSV was discovered in the United States and Latin America, inflicting massive losses in L. vannamei and P. stylirostris aquaculture. Subsequently, infections were discovered in P. indicus, P. setiferus, F. chinensis, P. merguiensis, and P. monodon, as well. The geographical spread of WSSV became a severe threat to shrimp farming in Asia and America. This restricted the import requirements for shrimp broodstocks in different countries with a ban on animal imports from regions with viral infection (Sangamaheswaran and Jeyaseelan, 2001; Citarasu et al., 2006; Zhang et al., 2006).

Significant signs of acute WSD include a sudden drop in food intake, lethargy, and loosened cuticles with white spots 0.5 to 2.0 mm wide, visible beneath the carapace. In some cases, infected shrimp may exhibit a pink to reddish-brown color due to increased chromatophores. Additionally, white spots are occasionally observed in infected P. vannamei from America. WSSV can infect mesodermal and ectodermal cells, such as the subcuticular epithelium, in various crustacean species, leading to inconsistent mortality rates. The virus spreads through vertical and horizontal transmission, including cannibalism of infected dead shrimp and water-borne pathways. Furthermore, WSSV can reach uncontaminated areas via organisms exposed to contaminated effluents from shrimp farms. Vectors or reservoirs of WSSV include aquatic insect larvae, invertebrates, and copepods (Ganjoor, 2015).

Yellow head virus (YHV) genotype 1 is the causative agent of YHD. YHV is a rod-shaped, enveloped virus with +ssRNA, belonging to the family Roniviridae (Ganjoor, 2015). When tissues infected with YHV were observed under transmission electron microscopy (TEM), vesicles encapsulating virions were observed in the cytoplasm, and in the intracellular spaces. These virions were reported to have a diameter of approximately 40-50 nm and 150-200 nm in length (Walker and Mohan, 2009; Lightner, 2011). First cases of YHV were reported in Thailand in 1990 in a P. monodon culture, and eventually was spread widely in cultured shrimps all over the country (Cowley et al., 2000). Subsequently, YHD has been reported in cultured shrimps in Malaysia, Sri Lanka, India, Taiwan, Indonesia, Vietnam, and Mexico (Mohan et al., 1998; Wang and Chang, 2000; Walker and Mohan, 2009). Apart from P. monodon, other susceptible species to YHD include L. vannamei, L. stylirostris, P. styliferus, Macrobrachium sintangense and Macrobrachium lanchesteri (Ganjoor, 2015).

There are now eight recognized genotypes of YHV (Arulmoorthy et al., 2020). Gill associated virus (GAV) is the genotype 2, recognized as the Australian strain of YHV, belonging to the genus Okavirus in Roniviridae (Spann et al., 1997). GAV is a rod-shaped, enveloped, positive-strand RNA nidovirus (Cowley et al., 1999; Cowley and Walker, 2002). Infections caused by genotypes 3 to 6 were reported in P. monodon in Asia, Australia, and East Africa with no associated disease symptoms (Lee D et al, 2022). Furthermore, genotypes 7 and 8 were reported recently in diseased P. monodon (Mohr et al., 2015) and F. chinensis (Liu et al., 2014).

YHD in Asian intensive cultivation systems are considered as a dangerous P. monodon disease. However, YHV has also been reported to infect other species such as P. aztecus, P. duorarum, P. japonicus, L. vannamei, P. setiferus, and P. stylirostris (Stentiford et al., 2009). Although there is a higher chance for YHD-associated mass mortality in early to juvenile stages of shrimps, there is a chance that individuals in late post larval stages may also die due to infection (Limsuwan, 1991).

As the name “Yellowhead” implies, one of the major characteristics of this disease is yellowish or bleached appearance of the cephalothorax. Other gross signs include high feeding rates followed by a cessation in feed intake, and the presence of moribund shrimp along the pond’s edge (Stentiford et al., 2009; Walker and Mohan, 2009). Moreover, a reddish discoloration is observed in infected shrimps. Although GAV infection is identified as less severe due to low mortality, YHV can infect and cause necrosis in ectodermal and mesodermal tissue, especially in lymphoid organ and gills (Walker and Mohan, 2009). YHV is spread via horizontal transmission by cannibalism of moribund and weak shrimp, and vertical transmission by survivors of the disease, which suffer from persistent subclinical infections (Stentiford et al., 2009; Lightner et al., 2012).

IHHN is caused by IHHNV, which belongs to the family Parvoviridae. This virus is 22 nm in diameter, making it the smallest known virus to infect penaeid shrimps. IHHNV is a nonenveloped icosahedral virus with single-stranded DNA of 3.9 kb (Mari et al., 1993; Lightner et al., 2012; Ganjoor, 2015). IHHNV was first discovered in L. vannamei and P. stylirostris in America in the early 1980s, which then rapidly spread to Central America, Brazil, Mexico, Peru, Philippines, Thailand, Indonesia, Singapore, Malaysia (Lightner, 1996a) Australia (Krabsetsve et al., 2004), China (Arulmoorthy et al., 2020) and India (Rai et al., 2009).

Molecular testing identified significant variation within the IHHNV isolates from Asia (Tang et al., 2003; Krabsetsve et al., 2004; Tang and Lightner, 2006). However, American isolates showed lower sequence variation (99.6 to 100% identity) (Tang and Lightner, 2002) and 99.8% sequence identity to IHHNV isolates from the Philippines (Tang et al., 2003 ). Based on molecular and epidemiology studies of this virus, three different genotypes were identified: (I) Southeast Asia; (II) America/Philippines; and (III) East Africa, Madagascar, Mauritius, and Australia (Lightner, 1996a; Tang and Lightner, 2002; Tang et al., 2003; Lightner, 2011). The host species P. monodon and L. vannamei were only susceptible to IHHNV-I and IHHNV-II. Studies show that genetically diverse cultures of P. monodon belonging to the Indo-Pacific region carried an IHHNV-III DNA fragment in their genome, which prevented infection by the genotype III (Duda and Palumbi, 1999; Tang and Lightner, 2006).

In P. stylirostris, IHHNV can cause high mortality and low virulence in juvenile shrimps and adults, respectively (Motte et al., 2003). Gross signs of this viral infection in P. stylirostris include reduced food intake, changes in behavior, stunted growth, and appearance of white or buff-colored spots (these spots appear different from the white spots observed in WSSV-infected shrimps). These spots are often observed in the cuticular epidermis of the shrimp, making it appear mottled. In moribund shrimps of P. stylirostris and P. monodon suffering from the terminal stage of the infection, the mottled appearance changes to a bluish color with opaqueness in the abdomen (Brock and Lightner, 1990; Lightner, 1996a). In L. vannamei, “Runt-deformity syndrome” (RDS) is observed, which can be characterized by reduced growth and deformed cuticles (Duda and Palumbi, 1999). RDS in juvenile shrimps can also be distinguished by a bent or malformed rostrum, wrinkly antennal flagella, roughness and the appearance of ‘bubble-heads’ on the cuticles (Kalagayan et al., 1991; Browdy et al., 1993; Carr et al., 1996; Lightner, 1996a; Motte et al., 2003).

IHHNV infects the ectodermal and mesodermal tissues such as gills, hypodermis, connective tissues, nerve cord, lymphoid organs, and antennal gland (Lightner, 2011). This virus is spread via horizontal transmission through cannibalism and contaminated water (Lightner, 1996a), and vertical transmission through infected eggs (Motte et al., 2003).

IMN is a novel viral infection caused by the Infectious myonecrosis virus (IMNV), which belongs to the Totiviridae family. IMNV is a non-enveloped icosahedral virus of 40 nm in size. The genome of this virus consists of a single double-stranded RNA (dsRNA) of 7,560 bp (Ganjoor, 2015). Two ORFs are present in the IMNV genome. ORF1 codes for capsid proteins and RNA-binding proteins, while putative RNA-dependent RNA polymerase is encoded by the second ORF (Poulos et al., 2006).

IMNV was initially discovered in L. vannamei of northeast Brazil in the year 2002, and later spread to countries in southeast Asia, including India and Indonesia (Senapin et al., 2007; Sahul Hameed et al., 2017). Genome sequencing analysis showed a 99.6% nucleotide sequence identity between the IMNV genomes from Brazil and Indonesia. This suggests that IMNV may have been transferred to Indonesia from Brazil in 2006 (Arulmoorthy et al., 2020).

IMNV can lead to cumulative mortality ranging from 40% to 70%. Experiments have demonstrated that P. stylirostris, Fenneropenaeus subtilis, and P. monodon can also be infected with IMNV, with shrimps at both juvenile and subadult stages being more susceptible (Arulmoorthy et al., 2020). Apart from increased mortality, lethargy, loss of coordination, and reduced food intake are gross signs of IMN. Furthermore, infected shrimps may appear at the water surface throughout the day and may exhibit necrotic regions in striated muscles that appears red (Nur’aini, 2009). In the acute phase of IMN, coagulative muscle necrosis can be observed with oedema of infected muscles, leading to fluid retention between muscle fibers and infiltration of hemocytes. The infection may further lead to hypertrophy due to lymphoid organ spheroids (LOSs) that generally appear in heart, gills, ventral nerve cord, and areas proximal to antennal gland tubules. LOS lesions are extremely consistent with IMNV lesions that are associated with acute, or chronic stages of the infection (Arulmoorthy et al., 2020). Primary target areas of IMNV include, striated muscles, hemocytes, lymph organ parenchyma cells, and connective tissues (Tang et al., 2005). IMNV is spread via horizontal transmission through cannibalism of the infected shrimps and contaminated water (Poulos et al., 2006; Lightner, 2011).

MBD is caused by a rod-shaped, enveloped virus which is known as Monodon baculovirus (MBV). This virus belongs to the Baculoviridae family and has circular dsDNA, with a genome size between 80 and 160 Kbp (Mari et al., 1993; Ganjoor, 2015). The first cases of MBD were discovered in 1977 in P. monodon shrimp farms in Taiwan. Subsequently it spread to other countries such as Australia, Philippines, China, Malaysia, Indonesia, Sri Lanka, South Africa, and USA. MBV is also known as P. monodon singly enveloped nuclear polyhedrosis virus (PmSNPV). Apart from MBV, two SNPV strains have been reported. They are the plebejus baculovirus and benettae baculovirus (Arulmoorthy et al., 2020).

Although the primary host species of MBV is P. monodon, multiple cases have been reported from other species including Macrobrachium rosenbergii, Penaus penicillatus, Penaeus semisulcatus, Metapenaeus ensus, P. merguiensis, Penaeus esculentus, L. vannamei, and Penaeus kerathurus (Lightner et al., 1987; Doubrovsky et al., 1988; Lightner, 1988; Chen et al., 1989; Colorni, 1989; Vijayan et al., 1995; Lightner, 1996a, 1996; Rajendran et al., 2012). The most susceptible individuals for MBV are larval and juvenile shrimps. However, the disease has been observed in all developmental stages of P. monodon (Brock and Lightner, 1990). This viral infection causes anorexia, subsequent retarded growth (Ganjoor, 2015), lethargy, and fouling of the surface with darkened appearance. Moreover, when compared to healthy individuals, the infected shrimps are smaller. MBV targets the anterior midgut and the hepatopancreas (Lightner, 1993). The virus spreads through horizontal transmission via the fecal oral route (Chen et al., 1992).

NHP is a bacterial disease caused by Hepatobacter penai, a bacterium like Rickettsia. This is a Gram-negative, dimorphic bacterium found in the cytoplasm of infected hepatopancreatic cells. The rod-shaped rickettsia-like body (0.35-0.9 μm) is the most common form. The spiral (helical) form (0.25 x 2-3.5 μm) possesses eight flagella at the basal apex (Lightner et al., 1992). The first cases of NHP were discovered in L. vannamei cultures in Texas, in the year 1985. Later in 1993, a similar disease surfaced in Peru, which was later confirmed as NHP through molecular diagnostic methods such as polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) (Loy et al., 1996). The isolates were further analyzed to have morphologies that are extremely similar, to be considered as identical. With a cumulative prevalence of 39.3%, Latin American countries have reported the highest number of NHP cases (Cuéllar-Anjel et al., 2018). NHP caused mass mortality in countries such as Peru, Costa Rica, Venezuela, Mexico, Panama, and Brazil. In the year 2006, Mexico also encountered an NHP outbreak (del Río-Rodríguez et al., 2006). NHP disease is more likely to occur in regions with high water temperature (29-35°C) and salinity (30-40 ppt) (Lightner, 1996a).

Primary host species susceptible to NHP are F. aztecus, L. vannamei, F. californiensis, P. setiferus, and P. stylirostris. The gross signs of NHP consists of reduced food consumption, slow growth, anorexia, softened shells, flaccid bodies, and expanded chromatophores, along with fouling of the body surface (Lightner, 1996a). NHP generally occurs in hepatopancreatic cell types (Lightner et al., 2012) and can be spread via horizontal transmission through cannibalism of infected tissue (Vincent et al., 2004).

Vibriosis is one of the major diseases that affect shrimp aquaculture farms and has been associated with mortality of shrimp cultures around the globe. Vibriosis is caused by Gram-negative bacteria, and multiple species may be associated with the disease. In this regard, species that have caused vibriosis include Vibrio harveyi, Vibrio alginolyticus, Vibrio splendidus, and Vibrio parahaemolyticus. These bacteria belonging to the Vibrionaceae family, have caused mortality in P. monodon larvae in shrimp farms. It has been demonstrated that only some isolates of V. harveyi have shown to possess virulence, indicating molecular and genetic variation. The over-intensification of shrimp aquaculture may have been associated with the emergence of vibriosis, as the disease has been known to occur in shrimps in stressful conditions (Ishimaru et al., 1995; Lavilla-Pitogo and de la Pena, 1998).

V. harveyi is a luminous bacterium, hence it is visible in infected shrimps at nighttime. Gross signs of this disease include reduced growth rate, lethargy, opaque muscles, and presence of patches (Karunasagar et al., 1994). Furthermore, necrosis of the appendages, gut emptiness, and expansion of chromatophores can also be observed in vibriosis-infected larvae (Chandrakala and Priya, 2017).

AHPND is a bacterial disease which is recognized as a major threat to shrimp aquaculture (Tran et al., 2013). In 2009, China reported an outbreak in shrimp cultures which was diagnosed as AHPND (Nunan et al., 2014). Subsequently, Malaysia, Philippines, Mexico, Vietnam, Thailand (Shinn et al., 2018), Bangladesh (Eshik et al., 2017), and the United States (Dhar et al., 2019) also encountered AHPND outbreaks which caused huge losses to their shrimp aquaculture productivity.

AHPND is caused by strains of V. parahaemolyticus, which are highly omnipresent, opportunistic, marine bacteria (Tran et al., 2013). The Gram-negative bacteria belonging to the family Vibrionaceae, contains the plasmid pVa1, which causes virulence. This plasmid carries transposons, binary toxin genes and conjugate transfer genes. This indicates that it is possible for plasmid transfer to other strains of this bacteria or other species (Lee et al., 2015).

This bacterium infects the shrimp by colonizing the gut (Tran et al., 2013; Lai et al., 2015). The pVa1 plasmid then expresses the binary toxins that invade the hepatopancreas (Prachumwat et al., 2019) and trigger shedding of the epithelial cell lining of the tubule (Tran et al., 2013). This makes the hepatopancreas appear pale. The severity of the disease can be influenced by the gut microbiota of the shrimp. When infected, the bacterial communities residing in the gut and hepatopancreas are exposed to an imbalance in their local distribution, known as dysbiosis (Chen et al., 2017). On the other hand, the host can gain protection against the pathogen by the enrichment of certain bacterial species (Yu et al., 2018).

Penaeid shrimp species that have been identified as highly susceptible hosts to AHPND-causing bacteria include L. vannamei and P. monodon (Tran et al., 2013; Zorriehzahra and Banaederakhshan, 2015). Gross signs of infected shrimps include exhibition of shrunken and pale hepatopancreas, gut emptying, low feed intake, swimming spirally, and sluggishness (Zorriehzahra and Banaederakhshan, 2015). This disease is spread via horizontal transmission through co-habituation or ingestion of the pathogen. In this regard, cannibalism of infected and dead shrimp, fecal-oral transmission, and feed pellets colonized by the bacteria can also spread AHPND (Tang et al., 2020).

Larval mycosis is a fungal disease caused by Haliphthoros philippinensis, Lagenidium callinectes, Sirolpidium sp., and Lagenidium sp. This disease can affect P. monodon eggs, larvae, and post-larvae. In shrimps infected by Lagenidium, vesicles with zoospores of high motility are formed at the end of the discharge tube, invading the host. On the other hand, when affected by Haliphthoros, vesicles are not formed, but long discharge tubes are observed. In contrast, Sirolpidium infection results in short discharge tubes, and vesicles do not form either (Baticados et al., 1990).

Significant signs of infection include whitish appearance, weakness and high risk of death. Moreover, the mortality rate may reach 100% within 2 days. The inner tissue of the individual is replaced by the zoospores, with discharge tubes protruding out from the body. If the egg is infected, they are prevented from hatching and respiratory difficulties are observed in infected larvae (Baticados et al., 1990).

Fusariosis is caused by Fusarium spp., such as Fusarium solani, which are opportunistic soil fungi that have been reported to infect penaeid shrimps. Cases of fusariosis has been found in P. californiensis, L. vannamei and P. stylirostris from Mexico (Lightner et al., 1979). Moreover, cultivated P. japonicus shrimps from Japan and France have also been affected by this disease (Bian and Egusa, 1981; Criado-Fornelio et al., 1988). Gross signs of this infection include large melanized lesions on cephalothorax and abdomen, with degradation and ulceration of cuticles (Colorni, 1989). Moreover, fungal hyphae can also be observed in infected tissue, under a light microscope (Karunasagar et al., 2004).

Microsporidiosis is caused by an endoparasite, Microsporidia. This protozoan has been shown to infect shrimps belonging to the species P. indicus, P. monodon, and P. merguiensis. Generally causing infection in juveniles and adult shrimps, the infected regions can be characterized by an opaque white appearance. The pathogen is known to form spores in infected tissue and may lead to white ovaries, which can cause sterility in spawners. Though the infection rate was estimated to be as low as < 10%, Microsporidia have been known to be extremely pathogenic (Baticados et al., 1990).

Gregarine disease is caused by gregarine, which are usually present in the gut of penaeid shrimps. They can infect P. monodon shrimps at larval, post larval, juvenile, and adult stages. When gregarines are prevalent, they can interfere with functions of the hepatopancreatic duct, such as particle infiltration. Gregarine infection rates up to 94% have been reported in shrimp cultures (Baticados et al., 1990).