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To identify the potential zones for gold mineralization at the Felda Chiku 3, Gua Musang, Kelantan, East coast Malaysia, twenty-one (21) geophysical survey lines were conducted at the proposed mineral exploration site using the pole - dipole of the electrical resistivity and induced polarization arrays to get the maximum depth of 150 m with 400 m survey length. From the resistivity and chargeability concentration maps, the potential mineralized zones as delineated, was observed to be dominantly concentrated towards the southwest and northern part of the area. The 3D resistivity and chargeability slice model present low resistivity values and high chargeability values that are well correlated which is palpable especially at the depths of 25 m and 50 m respectively. The data showed that the potential mineralized zones are trending approximately north-south directions. Forty (40) drilling locations were proposed for follow-up drilling based on the resistivity and chargeability models.

Highlights • Development of a novel method to assess environmnetal hazards of industrial, and municipal wastes. • Application of the inverted RES2-D data using the Oasis Montaj to generate a rectangular prism model. • Using the rectangular prism model developed to estimate the volume of IWM and MSW materials. • Quantification of the leachate contaminant plumes flow from IWM and MSW for remediation., A novel methodological approach was developed to quantified the volume of industrial waste desposal (IWD) site, combined with municipal waste materials (MWM), through the integration of a non-invasive, fast, and less expenssive RES2-D Electrical Resistivity Technique (ERT), using Wenner-Schlumberger electrode array geophysical method with Oasis Montaj software. Underground water bearing structures, and the eco-system are being contaminated through seepage of the plumes emanating from the mixtures of the industrial waste materials (IWM), made of moist cemented soil with municipal solid wastes (MSW) dumped at the site. The distribution of the contiminant hazardous plumes emanating from the waste materials' mixtures within the subsurface structural lithological layers was clearly map and delineated within the near-surface structures, using the triplicate technique to collect samples of the soil with the waste mixtures, and the water analysis for the presence of dissolved ions. The deployed method helped to monitor the seepage of the contaminant leachate plumes to the groundwater aquifer units via the ground surface, through the subsurface stratum lithological layers, and hence, estimation of the waste materials' volume was possibly approximated to be 312,000 m3. In summary, the novel method adopted are as presented below:•The novel method is transferable, reproduce-able, and most importantly, it is unambiguous technique for the quantification of environmental, industrial and municipal waste materials.•It helps to map the distribution of the plumes emanating from the waste materials' mixtures within the subsurface structural lithological layers that was clearly delineated within the near-surface structures underlain the study site.•The procedure helped in the monitoring of leachate contaminants plumes seepages into the surface water bodies and the groundwater aquifer units, via the ground surface, through to the porous subsurface stratum lithological layers., Graphical abstract Image, graphical abstract

Industrial, and municipal wastes are part of the main sources of environmental hazards as well as groundwater and surface water pollutions. If not well composed, treated, and safely disposed, it could permeate through the subsurface lithologies by reaching down to the underground water aquifers, particularly in zones of unprotected aquifer units. Pollutants, most especially the landfills leachates that encompassed organic contaminants, ammonia, nitrates, total nitrogen, suspended solids, heavy metals and soluble inorganic salts, i.e., soluble nitrogen, sulphur compound, sulphate and chlorides, could posed undesirable environmental impacts due to inappropriate disposals that may give rise to gaseous fumes and leachate formations. An electrical resistivity geophysical technique utilizing the RES2D no-invasive, cost-effective and rapid method of data collection was integrated with the 3D Oasis Montaj software to approximate the volume of the generated rectangular prism model of the contaminants delineated from mixtures of the industrial, and municipal wastes plumes to be 312,000 m 3.

The Transient Electro-Magnetic (TEM) geophysical technique was deployed to map and characterized the subsurface of Pahang River Basin along the East Coast Peninsula Malaysia. The data aimed at differentiating between the massive zones and the weak zones within the region, to also assess and differentiate the subsurface structures and comes up with recommendations for policy decision, formulation and plans on the flooding impact, surface water and groundwater managements, in addition to other environmental related issues ravaging the area. The data presented in this paper, showed the properties of the subsurface rocks underlain the region as beneficial to the Agriculturists; Climatologists; Engineers; Environmentalists; Geoscientists, Hydrologists and Policy formulation officers. The TEM data collection utilized a 100 m x 100 m single loop coil for both the Transmitter (Tx) loop and the Receiver (Rx) loop to produce a total surface area coverage of 10,000 m2 per survey line along a single profile. The total area covered in the data extended across an average area of 30 km x 40 km in parts of Maran, Temerloh and Jerantut districts, within the State of Pahang, East Coast, Peninsula Malaysia. The conductivity data recorded varied from -20 mS/m to about 440 mS/m at a maximum depth of about 375 m. On the other hand, the resistivity data recorded varied from 0 Oh-m to about 1000 Oh-m. The information derived from the data are intended for potential abstraction by the Malaysian Groundwater Management Board; the Department of Mineral and Geoscience; Department of Irrigation and Drainage; the Pahang State Water Board, and the Department of Agriculture.

Data on the micrometeorological parameters and Energy Fluxes at an intertidal zone of a Tropical Coastal Ocean was carried out on an installed eddy covariance instruments at a Muka head station in the north-western end of the Pinang Island (5°28’06’’N, 100°12’01’’E), Peninsula Malaysia. The vast source of the supply of energy and heat to the hydrologic and earth׳s energy cycles principally come from the oceans. The exchange of energies via air-sea interactions is crucial to the understanding of climate variability, energy, and water budget. The turbulent energy fluxes are primary mechanisms through which the ocean releases the heat absorbed from the solar radiations to the environment. The eddy covariance (EC) system is the direct technique of measuring the micrometeorological parameters which allow the measurement of these turbulent fluxes in the time scale of half-hourly basis at 20 Hz over a long period. The data being presented is the comparison of the two-year seasonality patterns of monsoons variability on the measured microclimate variables in the southern South China Sea coastal area.

Graphical abstract, The southern South China coastal oceans within the South East Asian region are much lacking in the perception of the surface energy budget and evaporation over the ocean waters in response to climatic changes. The eddy covariance method was used to measure the energy fluxes, microclimate variables, and surface water temperature from November 2015 to October 2017 at the Straits of Malacca, South China Sea; Pulau Pinang, Malaysia, situated at latitude 5°28′06″N, and longitude 100°12′01″E. This work focused on the methodological approach to the air-sea energy fluxes data collection and analysis. In this regard, the method applied for the direct measurements and analysis of energy fluxes and other meteorological parameters in the site is considered and reported. • The paper summarizes the analysis of energy fluxes, microclimate variables, and surface water temperature data in a tropical coastal ocean station using the eddy covariance method. • The methodological approach illustrates the method of analysis applied in this study which can be compared and used for similar studies in other places. • The reproducible data analysis technique matches similar comparative methods such as Matlab and Python.

Publisher Summary This chapter summarizes the various strategies used by the microbes against the immune defenses of the host cell. Many infections that are restricted to body surfaces have short incubation periods, with less than a week between initial infection and disease onset. The microbe thus evades the immune response by completing its growth and shedding within a few days before the host deploys specific antibody and T cells. Immunological tolerance is another factor that reduces the immune response to a given antigen. There is commonly a degree of tolerance to a microorganism when infection occurs during fetal or early postnatal life. Tolerance to a given microorganism can also arise when large amounts of microbial antigen or antigen-antibody complexes are circulating in the body. If a microbial antigen is very similar to normal host antigens, the immune response to this antigen may be weak or absent, giving a degree of tolerance. A large variety of microorganisms causes immunosuppression in the infected host, i.e., the host shows a depressed immune response to antigens unrelated to those of the infecting microorganism. Some of the other strategies include, latent phase of the microbes, microbial presence in bodily sites inaccessible to the immune response, induction of inappropriate antibody and T-cell responses, antibodies mopped up by soluble microbial antigens, and antigenic variations.

Publisher Summary This chapter discusses the immunological factors associated in the recovery of host from infections. Antibody, T cells, natural killer cells, complement, phagocytes, and interferon are involved in the response to nearly all infections and, without any doubt, are together responsible for recovery. There is good evidence that T-cell-mediated immunity is of supreme importance in recovery from a variety of microbial infections. These are the infections in which the microorganism replicates intracellularly. Tissue responses in the host bear the hallmarks of T-cell involvement, the infiltrating cells consisting primarily of lymphocytes and macrophages. Inflammation, whether induced by immunological reactions, tissue damage or microbial products, plays a vital role in recovery from infection. Inflammation is necessary for the proper functioning of the immune defenses because it focuses all circulating antimicrobial factors onto the site of infection. Complement can carry out antimicrobial activities. However, there is little direct evidence that the antimicrobial activities of complement are in fact important in the body. Interferons also act on uninfected cells, binding to a cell surface receptor and activating a number of genes involved in immunity to viruses. Multimechanistic recovery is illustrated in the chapter and other issues, such as the role of temperature, tissue repair, and resistance to re-infection are discussed.

Publisher Summary This chapter describes several methods through which the microbes spread in the host body. Direct spread occurs to organs and tissues below the body surfaces, extending the focus of infection and sometimes accounting for striking complications. Several microbial factors – such as some soluble substances and enzymes – help in the promotion of direct spread. The spread of the microbes can also occur through lymphatics blood and various other pathways. Microbes in tissue fluids enter lymphatic capillaries rather than blood capillaries, and are transported to the nearest lymph node. A rich lymphatic network lies below the epithelium in the nasopharynx, mouth, and lung; microorganisms traversing these epithelia enter cervical and pulmonary lymph nodes. The blood is the most effective vehicle of all for the spread of microbes through the body, particularly the blood tissue junctions. In small vessels – such as capillaries and sinusoids – where blood flows slowly, there is an opportunity for the microorganism to be arrested and to establish infection in neighboring tissues. Some of the other pathways of microbial spread include cerebrospinal fluid (CSF), pleural and peritoneal cavities, and peripheral nerves.

Publisher Summary This chapter focuses on some of the host and microbial factors influencing susceptibility to disease. These factors include genetic factors in the microorganism, genetic factors in the host, hormonal factors, and stress. The microorganism's ability to infect a given host is genetically determined and many microorganisms infect only one particular host species. Pathogenicity or virulence is also a function of the microbial genome. Virulence is being increasingly recognized to depend on coordinated expression of numerous genes, whose products mediate adherence, antiphagocytic activity, immune evasion, production of toxins, etc. Susceptibility to infectious disease is always influenced and is sometimes determined by the genetic constitution of the host. Inflammation makes an important contribution to tissue damage and pathology in infectious disease and injected corticosteroids (or ACTH) have a pronounced anti-inflammatory effect; their therapeutic use in infectious diseases depending on a reduction in the inflammatory pathological components at sites of infection. Increased circulating levels of corticosteroid hormones are necessary for a successful host response to infectious disease. A host of miscellaneous factors, such as smoking, seasonal changes mental state, influence the course of infectious diseases.

Publisher Summary This chapter discusses the various factors that contribute to the failure of host defense mechanism in eliminating microbes. One way of looking at persistent infections is to regard them as failures of the host defense mechanisms which are designed to eliminate invading microorganisms from tissues. Persistent infections usually represent a secondary event, following on from an initial acute infection. In certain acute infections the patient appears to recover, but there is later a relapse. Many of the severe infections causing illness and death in communities (poliomyelitis, plague, yellow fever, cholera) are not persistent and the microorganisms are eliminated from the body after recovery. Persistent infections are often important from the microbe's point of view, enabling it to be maintained in small or isolated host communities. Persistent infections also generally present problems in the development of vaccines. They are becoming relatively more important, both for the individual and for the community, as the nonpersistent infections are eliminated by public health measures and by vaccination. Not only may they reactivate and cause troublesome infections in immunocompromised or immunosuppressed patients, but some of them can cause malignant tumors.

Publisher Summary This chapter provides an overview of various interspecies relationships, such as parasitic relations, symbiotic relations, and commensalism. However, the chapter is mainly concerned with the parasitic associations and pathogenicity of several microorganisms. Generalized infections, such as measles, tuberculosis, or typhoid are clearly examples of parasitism. A successful parasitic microbe, like all successful parasites, tends to get what it can from the infected host without causing too much damage. The concept of balanced pathogenicity is helpful in understanding infectious diseases, but many infections have not yet had time to reach this ideal state. It is the virulence and pathogenicity of microorganisms, their ability to kill and damage the host that makes them important to the physician or veterinarian. As molecular biological and immunological techniques are brought to bear on these problems, knowledge is steadily increasing beyond descriptive pathology to a more detailed understanding of host pathogen interactions at the cellular, genetic, and biochemical levels.

Publisher Summary Cell damage has profound effects if it is the endothelial cells of small blood vessels that are involved. When bacteria invade tissues, they almost inevitably cause some damage, and this is also true for fungi and protozoa. Cell and tissue damage are sometimes due to the direct local action of the microorganism and microbial toxins. They either interfere with the transcription, translation, and DNA synthesis or change the permeability of the cell membrane. Some of the indirect damage brought about by these microbes is through inflammation and immune responses. Host cells are destroyed or blood vessels injured as a direct result of the action of microbes or their toxins. Inflammatory materials are liberated from necrotic cells, whatever the cause of the necrosis. Also many bacteria themselves liberate inflammatory products and certain viruses cause living infected cells to release inflammatory mediators. The expression of the immune response necessarily involves a certain amount of inflammation, cell infiltration, lymph node swelling, even tissue destruction. Sometimes they are very severe, leading to serious disease or death, but at other times they play a minimal part in the pathogenesis of disease. Other indirect mechanisms of damage include stress, hemorrhage, placental infection, and tumors.

Publisher Summary These various immune responses of a host cell can be divided into antibody and the cell-mediated component. Pre-existing antigen-sensitive B lymphocytes encounter antigen via the immunoglobulin receptor. The antigen is internalized and processed via the exogenous pathway and presented in association with MHC class II molecules to activated T-helper cells. Each T or B cell is committed to respond to a particular epitope. The initial encounter with this epitope, whether in lymphoid tissues or elsewhere in the body, is a small-scale microscopical event. The purpose of the response, especially when the antigen is from an infecting microorganism, is to turn this microscopical event into a larger event as soon as possible, so that both antibody and T cells can be brought into action on a significant scale. Immune reactions are specifically triggered by T and B cells by virtue of their ability to recognize antigen in a highly specific manner. Macrophages and the dendritic cell family, by processing and presenting antigens, exercise a controlling influence at this stage, and are in close physical association with T and B cells. Macrophages, polymorphs, natural killer cells, and complement play an important part as effectors and amplifiers of the reaction in tissues.

Publisher Summary This chapter discusses the general principles of vaccines, its complications and side effects, and the development of new vaccines. Effective resistance to infection or disease depends on the vaccine having certain properties – such as inducing the right type of immune resistance, inducing an immune response in the right place, inducing an immune response to the right antigens, and immunity to toxins. Virulent microorganisms are inactivated to make killed vaccine. If inactivation has been incompletely carried out, vaccination introduces infection. Nonmicrobial antigens in vaccines can cause allergic responses. Large numbers of killed salmonellas are present in the vaccine for typhoid, and this vaccine therefore contains large amounts of endotoxin, which can present toxicity. Live vaccines often cause illness in children with immunodeficiencies. Several procedures for the development of synthetic peptides as vaccines also have been described. Successful new vaccines will come from encouraging laboratory advances in immunology and biotechnology and at the same time attending to practical problems, such as vaccine supply, quality testing, licensing, and financing.

This chapter discusses the various strategies employed by the microbes in response against host defense mechanisms. Phagocyte, the most important part of the host defense system, is equipped with a powerful array of antimicrobial weapons and lysosomal enzymes. A detailed description of the process of phagocytosis is provided in the chapter. Microorganisms that readily attract phagocytes, and are then ingested and killed by them, are by definition unsuccessful as they fail to cause a successful infection. Microbial factors that damage the host or actively promote the spread of infection are often called agressins. Such factors have a 'toxic' activity that is demonstrable in a suitable test system. In many instances, however, microbial factors inhibit the operation of host defense mechanisms without actually doing any damage. Microbial products that kill phagocytes may at lower concentrations interfere with their locomotion or their phagocytic activity, for instance, by inhibiting protein synthesis. Microorganisms can avoid the attentions of phagocytic cells by inhibiting chemotaxis, and as a result of this, the host is less able to focus polymorphs and macrophages into the exact site of infection. In case the particle is enclosed in a phagocytic vacuole, there are other methods of entry such as endocytosis.

This chapter discusses the events and responses that follow immediately after the entry of an organism in a host cell. The first activity that could be observed is the growth of the epithelial cells. At the site of entry into the body, microorganisms that are shed directly to the exterior multiply in the epithelial surface producing a spreading infection in the epithelium. Certain microorganisms spread through the body to reach susceptible target organs after free microorganism particles have entered vessels below the skin or intestinal epithelium. The infected host has a variety of defenses that operate without delay, before the immune response comes into action. However, many microbes have strategies for interfering with these defenses. After traversing the epithelial cell layer, a microorganism encounters the basement membrane. After reaching the subepithelial tissues they are exposed to three important host defense systems: the tissue fluids, the lymphatic system leading to the lymph nodes, and phagocytic cells. In addition to being able to resist host defense mechanisms, a pathogenic organism—be it an obligate intracellular, facultative intracellular, or extracellular pathogen—must also overcome the problem of obtaining essential nutrients if it is to be successful.

Publisher Summary This chapter focuses on some of the host and microbial factors influencing susceptibility to disease. These factors include genetic factors in the microorganism, genetic factors in the host, hormonal factors, and stress. The microorganism's ability to infect a given host is genetically determined and many microorganisms infect only one particular host species. Pathogenicity or virulence is also a function of the microbial genome. Virulence is being increasingly recognized to depend on coordinated expression of numerous genes, whose products mediate adherence, antiphagocytic activity, immune evasion, production of toxins, etc. Susceptibility to infectious disease is always influenced and is sometimes determined by the genetic constitution of the host. Inflammation makes an important contribution to tissue damage and pathology in infectious disease and injected corticosteroids (or ACTH) have a pronounced anti-inflammatory effect; their therapeutic use in infectious diseases depending on a reduction in the inflammatory pathological components at sites of infection. Increased circulating levels of corticosteroid hormones are necessary for a successful host response to infectious disease. A host of miscellaneous factors, such as smoking, seasonal changes mental state, influence the course of infectious diseases.

Publisher Summary These various immune responses of a host cell can be divided into antibody and the cell-mediated component. Pre-existing antigen-sensitive B lymphocytes encounter antigen via the immunoglobulin receptor. The antigen is internalized and processed via the exogenous pathway and presented in association with MHC class II molecules to activated T-helper cells. Each T or B cell is committed to respond to a particular epitope. The initial encounter with this epitope, whether in lymphoid tissues or elsewhere in the body, is a small-scale microscopical event. The purpose of the response, especially when the antigen is from an infecting microorganism, is to turn this microscopical event into a larger event as soon as possible, so that both antibody and T cells can be brought into action on a significant scale. Immune reactions are specifically triggered by T and B cells by virtue of their ability to recognize antigen in a highly specific manner. Macrophages and the dendritic cell family, by processing and presenting antigens, exercise a controlling influence at this stage, and are in close physical association with T and B cells. Macrophages, polymorphs, natural killer cells, and complement play an important part as effectors and amplifiers of the reaction in tissues.

Publisher Summary Cell damage has profound effects if it is the endothelial cells of small blood vessels that are involved. When bacteria invade tissues, they almost inevitably cause some damage, and this is also true for fungi and protozoa. Cell and tissue damage are sometimes due to the direct local action of the microorganism and microbial toxins. They either interfere with the transcription, translation, and DNA synthesis or change the permeability of the cell membrane. Some of the indirect damage brought about by these microbes is through inflammation and immune responses. Host cells are destroyed or blood vessels injured as a direct result of the action of microbes or their toxins. Inflammatory materials are liberated from necrotic cells, whatever the cause of the necrosis. Also many bacteria themselves liberate inflammatory products and certain viruses cause living infected cells to release inflammatory mediators. The expression of the immune response necessarily involves a certain amount of inflammation, cell infiltration, lymph node swelling, even tissue destruction. Sometimes they are very severe, leading to serious disease or death, but at other times they play a minimal part in the pathogenesis of disease. Other indirect mechanisms of damage include stress, hemorrhage, placental infection, and tumors.

Summary In summary, the encounter between the microorganism and the phagocytic cell is a central feature of infection and pathogenicity. Phagocytes are designed to ingest, kill and digest invaders, and the course of the infection depends on the success with which this is carried out. Virulent microorganisms have developed a great variety of devices for countering or avoiding the antimicrobial action of phagocytes. Although substances produced by or present on microbes may at first sight appear to have a useful function, not all will prove to be of practical importance in the infected host. Studies on microbial killing and digestion in phagocytes are still poorly understood, but it is important to conceive logically of the ways in which microorganisms can avoid being ingested, killed and digested. Most viruses do not infect phagocytes, and the exceptions do so by endocytosis or fusion, not phagocytosis.

Publisher Summary This chapter discusses the immunological factors associated in the recovery of host from infections. Antibody, T cells, natural killer cells, complement, phagocytes, and interferon are involved in the response to nearly all infections and, without any doubt, are together responsible for recovery. There is good evidence that T-cell-mediated immunity is of supreme importance in recovery from a variety of microbial infections. These are the infections in which the microorganism replicates intracellularly. Tissue responses in the host bear the hallmarks of T-cell involvement, the infiltrating cells consisting primarily of lymphocytes and macrophages. Inflammation, whether induced by immunological reactions, tissue damage or microbial products, plays a vital role in recovery from infection. Inflammation is necessary for the proper functioning of the immune defenses because it focuses all circulating antimicrobial factors onto the site of infection. Complement can carry out antimicrobial activities. However, there is little direct evidence that the antimicrobial activities of complement are in fact important in the body. Interferons also act on uninfected cells, binding to a cell surface receptor and activating a number of genes involved in immunity to viruses. Multimechanistic recovery is illustrated in the chapter and other issues, such as the role of temperature, tissue repair, and resistance to re-infection are discussed.

Publisher Summary This chapter provides an overview of various interspecies relationships, such as parasitic relations, symbiotic relations, and commensalism. However, the chapter is mainly concerned with the parasitic associations and pathogenicity of several microorganisms. Generalized infections, such as measles, tuberculosis, or typhoid are clearly examples of parasitism. A successful parasitic microbe, like all successful parasites, tends to get what it can from the infected host without causing too much damage. The concept of balanced pathogenicity is helpful in understanding infectious diseases, but many infections have not yet had time to reach this ideal state. It is the virulence and pathogenicity of microorganisms, their ability to kill and damage the host that makes them important to the physician or veterinarian. As molecular biological and immunological techniques are brought to bear on these problems, knowledge is steadily increasing beyond descriptive pathology to a more detailed understanding of host pathogen interactions at the cellular, genetic, and biochemical levels.

This chapter summarizes the various strategies used by the microbes against the immune defenses of the host cell. Many infections that are restricted to body surfaces have short incubation periods, with less than a week between initial infection and disease onset. The microbe thus evades the immune response by completing its growth and shedding within a few days before the host deploys specific antibody and T cells. Immunological tolerance is another factor that reduces the immune response to a given antigen. There is commonly a degree of tolerance to a microorganism when infection occurs during fetal or early postnatal life. Tolerance to a given microorganism can also arise when large amounts of microbial antigen or antigen-antibody complexes are circulating in the body. If a microbial antigen is very similar to normal host antigens, the immune response to this antigen may be weak or absent, giving a degree of tolerance. A large variety of microorganisms causes immunosuppression in the infected host, i.e., the host shows a depressed immune response to antigens unrelated to those of the infecting microorganism. Some of the other strategies include, latent phase of the microbes, microbial presence in bodily sites inaccessible to the immune response, induction of inappropriate antibody and T-cell responses, antibodies mopped up by soluble microbial antigens, and antigenic variations.

This chapter describes several methods through which the microbes spread in the host body. Direct spread occurs to organs and tissues below the body surfaces, extending the focus of infection and sometimes accounting for striking complications. Several microbial factors – such as some soluble substances and enzymes – help in the promotion of direct spread. The spread of the microbes can also occur through lymphatics blood and various other pathways. Microbes in tissue fluids enter lymphatic capillaries rather than blood capillaries, and are transported to the nearest lymph node. A rich lymphatic network lies below the epithelium in the nasopharynx, mouth, and lung; microorganisms traversing these epithelia enter cervical and pulmonary lymph nodes. The blood is the most effective vehicle of all for the spread of microbes through the body, particularly the blood tissue junctions. In small vessels – such as capillaries and sinusoids – where blood flows slowly, there is an opportunity for the microorganism to be arrested and to establish infection in neighboring tissues. Some of the other pathways of microbial spread include cerebrospinal fluid (CSF), pleural and peritoneal cavities, and peripheral nerves.