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Major concerns in the fisheries business are parasitic fish and bacterial infections. When it comes to aquatic life microbes are a regular occurrence. The majority of microbes are naturally occurring in water. Because of poor environmental conditions, limited nutrition, and inefficient fish husbandry practices, they only cause diseases. Some microbial infections occur in fresh water fish (Pseudomonas infection, Acinetobacter infections, bacterial gill diseases), in marine water (Vibriosis, Tenacibaculosis, streptococcal infections, bacterial skin diseases) and in brackish water (Red sea bream iridoviral disease (RSID, Lymphocystis disease (LCD). All these infections affect fish differently. Parasitic illnesses can cause epidemics in fish that are overcrowded or under other unnatural situations. A large number of fish species have been severely impacted by parasite and bacterial species. Some parasitic infections of fresh water are Renal Sphaerosporosis, due to leeches and nematodes, isopods and Gill Monogeneans; in amarine water are Microsporidiosis, Cryptocaryonosis and Brooklynelliosis and in brackish water are Diplostomum spathaceum metacercarial infections. Some preventive actions are done to control this problem. In this review there is a complete detail about parasite and bacterial infections and how they can be prevented.

Objective Lipoprotein(a)-hyperlipoproteinemia (Lp(a)-HLP) along with progressive cardiovascular disease has been approved as indication for regular lipoprotein apheresis (LA) in Germany since 2008. We aimed to study the long-term preventive effect of LA and to assess hypothetical clinical correlations of apolipoprotein(a) (apo(a)) by analyzing genotypes and phenotypes. Approach and Results This prospective observational multicenter study included 170 patients with Lp(a)-HLP and progressive cardiovascular disease (48.9 years median age at diagnosis) despite other cardiovascular risk factors, including low-density lipoprotein cholesterol had maximally been treated (mean baseline low-density lipoprotein cholesterol: measured, 2.56 mmol/L [98.9 mg/dL] and corrected, 1.72 mmol/L [66.3 mg/dL]). Patients were prospectively investigated during a 5-year period about annual incidence rates of cardiovascular events. In addition, apo(a) isoforms and polymorphisms at the apo(a) gene (LPA) were characterized. One hundred fifty-four patients (90.6%) completed 5 years of follow-up. Mean Lp(a) concentration before commencing regular LA was 108.1 mg/dL. This was reduced by a single LA treatment by 68.1% on average. Significant decline of the mean annual cardiovascular event rate was observed from 0.580.53 2 years before regular LA to 0.11 +/- 0.15 thereafter (P<0.0001); 95.3% of patients expressed at least 1 small apo(a) isoform. Small apo(a) isoform (35.2%) carrying phenotypes were not tagged by single-nucleotide polymorphisms rs10455872 or rs3798220. Conclusions Results of 5 years of prospective follow-up confirm that LA has a lasting effect on prevention of cardiovascular events in patients with Lp(a)-HLP. Patients clinically selected by progressive cardiovascular disease were characterized by a highly frequent expression of small apo(a) isoforms. Only Lp(a) concentration seemed to comprehensively reflect Lp(a)-associated cardiovascular risk, however.

OBJECTIVE: Lipoprotein(a)-hyperlipoproteinemia (Lp(a)-HLP) along with progressive cardiovascular disease has been approved as indication for regular lipoprotein apheresis (LA) in Germany since 2008. We aimed to study the long-term preventive effect of LA and to assess hypothetical clinical correlations of apolipoprotein(a) (apo(a)) by analyzing genotypes and phenotypes.APPROACH AND RESULTS: This prospective observational multicenter study included 170 patients with Lp(a)-HLP and progressive cardiovascular disease (48.9 years median age at diagnosis) despite other cardiovascular risk factors, including low-density lipoprotein cholesterol had maximally been treated (mean baseline low-density lipoprotein cholesterol: measured, 2.56 mmol/L [98.9 mg/dL] and corrected, 1.72 mmol/L [66.3 mg/dL]). Patients were prospectively investigated during a 5-year period about annual incidence rates of cardiovascular events. In addition, apo(a) isoforms and polymorphisms at the apo(a) gene (LPA) were characterized. One hundred fifty-four patients (90.6%) completed 5 years of follow-up. Mean Lp(a) concentration before commencing regular LA was 108.1 mg/dL. This was reduced by a single LA treatment by 68.1% on average. Significant decline of the mean annual cardiovascular event rate was observed from 0.58±0.53 2 years before regular LA to 0.11±0.15 thereafter (P<0.0001); 95.3% of patients expressed at least 1 small apo(a) isoform. Small apo(a) isoform (35.2%) carrying phenotypes were not tagged by single-nucleotide polymorphisms rs10455872 or rs3798220.CONCLUSIONS: Results of 5 years of prospective follow-up confirm that LA has a lasting effect on prevention of cardiovascular events in patients with Lp(a)-HLP. Patients clinically selected by progressive cardiovascular disease were characterized by a highly frequent expression of small apo(a) isoforms. Only Lp(a) concentration seemed to comprehensively reflect Lp(a)-associated cardiovascular risk, however.

LPA is the major locus controlling Lp(a) plasma levels which vary extensively within and across populations and are associated with coronary heart disease. Identified causal genetic polymorphisms, including the KIV-2 CNV and other sequence variants, explain only a fraction of the variation in Lp(a) levels attributable to the LPA locus. Therefore additional sequence variation in LPA is expected to explain more of the observed variation in Lp(a) levels. One region of LPA not yet fully screened for such sequence variants is the KIV-2 CNV. Some variants in this region have been reported by the large re-sequencing projects but for those variants any data on the Lp(a) levels and the KIV-2 CNV size are missing. In one projects of this thesis, coding regions of the KIV 2 CNV were screened in individuals from six different populations (Gabonese Bantu, South African Bantu, Khoi San, Egyptians, Hong Kong Chinese and Austrians). LPA alleles of each individual were separated by PFGE and used for batchwise amplification of PCR fragments specific for the two exons of KIV-2. Despite a restricted sample size (in total 90 alleles) and limited sensitivity of the screening method used, several synonymous and non-synonymous variants as well as two previously unreported splice site variants were identified. Most of these variants were detected in African alleles. Among the variants found, an African specific acceptor splice site variant (K422 6T>G) associated with small KIV-2 CNV size was present in all African populations at high population frequencies (10% to 40%). This variant appears to be associated with low Lp(a) levels than expected considering the KIV-2 CNV size of the alleles carrying it. In contrast to the frequent African specific acceptor splice site variant, a rare donor splice site variant (K421 +1G>A) was found which was shared among Africans and Europeans and associated with non-detectable Lp(a). In Asians, only the synonymous variants that define the KIV 2 type B and typ, LPA is the major locus controlling Lp(a) plasma levels which vary extensively within and across populations and are associated with coronary heart disease. Identified causal genetic polymorphisms, including the KIV-2 CNV and other sequence variants, explain only a fraction of the variation in Lp(a) levels attributable to the LPA locus. Therefore additional sequence variation in LPA is expected to explain more of the observed variation in Lp(a) levels. One region of LPA not yet fully screened for such sequence variants is the KIV-2 CNV. Some variants in this region have been reported by the large re-sequencing projects but for those variants any data on the Lp(a) levels and the KIV-2 CNV size are missing. In one projects of this thesis, coding regions of the KIV 2 CNV were screened in individuals from six different populations (Gabonese Bantu, South African Bantu, Khoi San, Egyptians, Hong Kong Chinese and Austrians). LPA alleles of each individual were separated by PFGE and used for batchwise amplification of PCR fragments specific for the two exons of KIV-2. Despite a restricted sample size (in total 90 alleles) and limited sensitivity of the screening method used, several synonymous and non-synonymous variants as well as two previously unreported splice site variants were identified. Most of these variants were detected in African alleles. Among the variants found, an African specific acceptor splice site variant (K422 6T>G) associated with small KIV-2 CNV size was present in all African populations at high population frequencies (10% to 40%). This variant appears to be associated with low Lp(a) levels than expected considering the KIV-2 CNV size of the alleles carrying it. In contrast to the frequent African specific acceptor splice site variant, a rare donor splice site variant (K421 +1G>A) was found, by Asma Noureen, Kumulative Dissertation aus zwei Artikeln, Dissertation Medical University of Innsbruck 2015

LPA is the major locus controlling Lp(a) plasma levels which vary extensively within and across populations and are associated with coronary heart disease. Identified causal genetic polymorphisms, including the KIV-2 CNV and other sequence variants, explain only a fraction of the variation in Lp(a) levels attributable to the LPA locus. Therefore additional sequence variation in LPA is expected to explain more of the observed variation in Lp(a) levels. One region of LPA not yet fully screened for such sequence variants is the KIV-2 CNV. Some variants in this region have been reported by the large re-sequencing projects but for those variants any data on the Lp(a) levels and the KIV-2 CNV size are missing. In one projects of this thesis, coding regions of the KIV 2 CNV were screened in individuals from six different populations (Gabonese Bantu, South African Bantu, Khoi San, Egyptians, Hong Kong Chinese and Austrians). LPA alleles of each individual were separated by PFGE and used for batchwise amplification of PCR fragments specific for the two exons of KIV-2. Despite a restricted sample size (in total 90 alleles) and limited sensitivity of the screening method used, several synonymous and non-synonymous variants as well as two previously unreported splice site variants were identified. Most of these variants were detected in African alleles. Among the variants found, an African specific acceptor splice site variant (K422 6T>G) associated with small KIV-2 CNV size was present in all African populations at high population frequencies (10% to 40%). This variant appears to be associated with low Lp(a) levels than expected considering the KIV-2 CNV size of the alleles carrying it. In contrast to the frequent African specific acceptor splice site variant, a rare donor splice site variant (K421 +1G>A) was found which was shared among Africans and Europeans and associated with non-detectable Lp(a). In Asians, only the synonymous variants that define the KIV 2 type B and typ, LPA is the major locus controlling Lp(a) plasma levels which vary extensively within and across populations and are associated with coronary heart disease. Identified causal genetic polymorphisms, including the KIV-2 CNV and other sequence variants, explain only a fraction of the variation in Lp(a) levels attributable to the LPA locus. Therefore additional sequence variation in LPA is expected to explain more of the observed variation in Lp(a) levels. One region of LPA not yet fully screened for such sequence variants is the KIV-2 CNV. Some variants in this region have been reported by the large re-sequencing projects but for those variants any data on the Lp(a) levels and the KIV-2 CNV size are missing. In one projects of this thesis, coding regions of the KIV 2 CNV were screened in individuals from six different populations (Gabonese Bantu, South African Bantu, Khoi San, Egyptians, Hong Kong Chinese and Austrians). LPA alleles of each individual were separated by PFGE and used for batchwise amplification of PCR fragments specific for the two exons of KIV-2. Despite a restricted sample size (in total 90 alleles) and limited sensitivity of the screening method used, several synonymous and non-synonymous variants as well as two previously unreported splice site variants were identified. Most of these variants were detected in African alleles. Among the variants found, an African specific acceptor splice site variant (K422 6T>G) associated with small KIV-2 CNV size was present in all African populations at high population frequencies (10% to 40%). This variant appears to be associated with low Lp(a) levels than expected considering the KIV-2 CNV size of the alleles carrying it. In contrast to the frequent African specific acceptor splice site variant, a rare donor splice site variant (K421 +1G>A) was found, by Asma Noureen, Kumulative Dissertation aus zwei Artikeln, Dissertation Medical University of Innsbruck 2015