The success of a pathogen is not to kill its host but to infect the host in a way that it helps to transfer and hence propel the pathogen further. The host has its own mechanisms to contain the infection, like low pH (acidic pH in the phagolysosomes is crucial for the hydrolytic activity of the enzymes), temperature (fever is a common symptom due to a lot of infections), and inflammation. All this is well mediated by the host immune system.
As Mtb is inhaled by a healthy individual, it is phagocytosed by the macrophages and dendritic cells in the lung alveoli. Macrophages, a part of the innate immunity, play a major role in killing and containing Mtb. Of the many bacteria inhaled, macrophages are able to kill some, while the others replicate
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A pro-inflammatory response triggered by infected macrophages causes recruitment of the mononuclear cells at the site of infection. The T-cells interact with the macrophages and activate them by releasing the cytokine, IFN-. Activated macrophages are more efficient at killing Mtb. At this stage of infection, antigen presentation also activates B-cells which produce antibodies against Mtb. A consolidated mass of infected host cells and immune cells forms a granuloma. The granuloma consists of infected macrophages, foamy macrophages that contain stored oil droplets which serve as the bacterial nutrition, T-cells, B-cells in the earlier stages. When the bacillary load becomes static, the infection is said to be “latent”. Early stages of granuloma formation also witnesses vascularisation and supply of blood through newly developed blood capillaries. The granuloma is lined by epithelial cells and fibrous tissue in the later stages. The core of the granuloma is hypoxic (Vandiviere et al., 1956; Via et al., 2008). Granulomas can be resolved due to the action of immune system. With suppression of the immune system due to ageing, HIV infection or malnutrition, the containment of the bacteria
Neutrophils and wandering macrophages (originating form monocytes) were most likely the WBCs that phagocytized the tissues and pathogens early in Ed's infection. They gather at sites of infection or inflammation by means of emigration. They are
All pathogens need a source of food to provide them with a source of energy and nutrients they need to multiply. Often they get it from the body of the infected individual.
Overwhelming, deleterious host immune response to an infection due to release of chemicals to fight the infection 2• 1
capsulatum must overcome numerous in vivo microenvironmental challenges to cause disease. The immediate host response is the stimulation of the macrophage’s microbicidal properties: oxidative stress, acidic pH, degradative stress caused by hydrolytic enzymes present in the lysosome, and nutrient (zinc and iron) deprivation6,7. Despite the harsh intracellular environment of the macrophage, H. capsulatum has evolved various mechanisms to evade destruction by the macrophage8. Inhaled yeasts can travel via the lymph nodes to the liver and spleen and cause disseminated infection. There activated macrophages and other host components surround the infected cells forming a circular wall of aggregated inflammatory cells or granuloma6,9. The granuloma functions to inhibit H. capsulatum growth and replication by restricting access to oxygen and nutrients and exposing the fungi to acidic pH and other immune effectors10,11. However, the fungus within the granuloma may also benefit from this isolated microenvironment. The granuloma may provide shelter from destruction by the host, and can serve as the source from which surviving pathogens emerge during reactivation of latent
Infection is the invasion and growth of microorganisms such as bacteria, viruses, and parasites that are not normally present within the body. A prokaryotic cell is a simple cell that does not have a nucleus. One of the most common types of prokaryotic cells is a bacterium. Bacteria are differentiated by many factors including shape, chemical composition, nutritional requirements, biochemical activities, and sources of energy (Tortora 76). A patient with an infection in the upper respiratory system will need to have a sputum sample sent to the lab for further evaluation to determine the cause in order to accurately treat the infection. While many microorganisms can be the cause of infection,
(With the onset of infection the immune system is activated and signs of infection appear.)
pertussis exhibits a clear preference for ciliated cells and alveolar macrophages found in their human host, it is capable of forming colonies anywhere between the nasopharynx cavity and the lungs (3). Human nasopharynx creates a great environment for the bacteria to first colonize and infect (1). Bps polysaccharide is necessary for B. pertussis to form a biofilm in the nasopharynx, however it is not involved in the colonization of the lungs (1). The biofilms are the reason the bacteria is able to survive for such extended periods of time within the host (1). C-terminus of mature filamentous hemagglutinin mediates bacterial adherence to epithelial and macrophage-like cells of the host (2). It is necessary for colonization of the respiratory tract, these experiments were performed with rats using B. bronchiseptica, however it is believed that the rat models should also apply to B. pertussis
symptoms mainly caused by damage to the host by the organism itself, or by the host
A pathogen also known as an infectious agent, is an organism which causes illness or disease to its host. There are many different kinds of pathogens and the main ones are bacteria, fungi and virus. In this report I will be mentioning two pathogens which are caused by a particular bacteria, Mycobacterium Tuberculosis (MTB) and Whooping Cough. I will be explaining TB in detail and whooping cough briefly.
This condition of low granular white blood cells in the blood results in frequent and chronic bacterial infections of the skin, lungs, throat, etc. It can be genetic or obtained as it is in leukemia, for example. (Leukemia is
This is a project of curiosity, I don’t have a super personal connection with this project and I don’t have a huge driving factor in making this project. I simply have always wanted to know how diseases have evolved to infect eukaryotes and counteract the immune system. I’ve always been interested in anatomy and the immune system fascinates me, it’s proof of a deadly race between the human body and the organism that seek to use it for their own purposes.
If the immune system is unable to stop the infection, the bacterium will multiply and then spread to the bloodstream, after which the first signs of disease are observed in the form of fever. The bacterium penetrates further into the bone marrow, liver, and bile ducts, from which bacteria are excreted into the bowel movements. (Easmon 2003)
immune response. If the filtering function is unsuccessful, in the case of bacteria, septicaemia can
Immune granulomas are complex structures, typically composed of a central follicle made of tightly packed epithelioid cells and T lymphocytes surrounded by a ring of fibroblasts, and a peripheral loose area rich in lymphocytes. CD4+ T lymphocytes predominate within the follicle, whereas CD8+ T lymphocytes and B lymphocytes are present mainly in the peripheral area. Early fibrotic changes are sometimes present at the periphery of the granuloma [6]. Granulomatous inflammation occurs primarily along lymphatic tracks, which course along bronchovascular bundles and through interlobular septa [7].The mechanism by which the granulomas resolve has not been fully elucidated. However, it is generally assumed that apoptosis and the withdrawal of inflammatory cytokines are involved in the disappearance of granulomas
Pulmonary Mycobacterium avium complex (MAC) infection may represent the next major health concern for immunocompromised patients; however the exact pathogenesis remains largely unknown. Current therapy consists of combined antibiotic treatment but bacterial eradication is frequently unsuccessful and the appearance of macrolide-resistant non-tuberculous mycobacteria (NTM) strains is cause for concern. In other mycobacterial disease such as tuberculosis (TB), infected mononuclear cells secrete soluble factors capable of driving unopposed secretion of proteolytic enzymes from stromal cells, which appears to be a causative factor for matrix degradation and progressive cavitary lung disease. As the pathophysiology of pulmonary MAC