Clostridium and Neisseria Bacterias and Their Types

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Clostridium and Neisseria Bacterias and Their Types Essay

All bacterial species are divided into two main groups that are gram-positive and gram-negative. Such division is possible with the help of Gram’s methods based on the evaluation of the physical and chemical properties of bacteria’s cell walls and the detection of peptidoglycan (Ward, 2016). Clostridium is a Gram-positive bacterium. Such bacterium is defined as an obligate anaerobe that could produce endospores and can be classified into more than 100 species in regards to the nature of pathogens in cells. Clostridium and Neisseria Bacterias and Their Types Essay.

Among the well-known types of clostridium, there are clostridium difficile, clostridium botulinum, clostridium tetani, and Clostridium sordellii. For example, clostridium difficile is the bacterium that causes antibiotic-associated diarrhea (Ward, 2016) and serious cases of colitis that could be fatal for hospitalized patients (Carton, Daly, & Ramani, 2007). It is a spore-forming bacterium that can survive on various environmental surfaces for a long period.

Therefore, if patients are symptomatic, they are hospitalized and isolated in separate rooms where the risk of crossing this infection turns out to be minimal. As a rule, people, who have the risks of having this bacterium, should be treated during the next ten days with metronidazole or vancomycin (Ward, 2016). Clostridium botulinum aims at producing neurotoxin botulinum that leads to the possibility of having flaccid paralytic among humans (both adults and infants) or animals.

Clostridium tetani is another type of bacterium under consideration that leads to the cases of tetanus in people. It looks like a match through a microscope. As well as other types, clostridium tetanus is a rod-shaped anaerobe. Finally, there is Clostridium sordellii, a rare anaerobe that causes such diseases as pneumonia, arthritis, or even some fatal cases that occur after abortions. The list of clostridium bacteria is far from being full. Still, these types are the most frequent and dangerous for people today.

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Neisseria is another large genus of bacteria that cause the development of various infections in the organism. It is the Gram-negative bacteria that look like coffee beans under the microscope. The chosen genus has two main types of this bacterium: Neisseria gonorrhea and Neisseria meningitides. It is possible to guess the main peculiarity of Neisseria gonorrhea with ease. Such a bacterium causes gonorrhea and various sexually transmitted infections (Ward, 2016).

As a rule, the main area of this infection is the urogenital tract. Therefore, men, who get this bacterium, may suffer from penile discharge, and women, who get Neisseria gonorrhea, suffer from severe pelvic pain or some vaginal discharge. Neisseria gonorrhoeae are usually in pairs and can be grown in laboratories. They are dangerous for people. Still, the majority of diseases caused by the presence of this bacterium in the organism can be treated with special antibiotics.

Antibiotics can also be used to treat people with Neisseria meningitides. This gram-negative bacterium has a circular form and is formed in pairs. People, who carry this type of bacterium, are under a threat of having a meningococcal disease or even sepsis that can be a serious life threat. Neisseria meningitides may be spread through the exchange of saliva when people kiss or when kids chew the same things. Also, it can be spread respiratory when people sneeze or cough. In the majority of cases, all types of bacteria are dangerous for people. Sometimes, the organism is ready to fight against Neisseria with the help of antibiotics. Clostridium and Neisseria Bacterias and Their Types Essay.Sometimes, the symptoms are hard to observe, and people lose a lot of time to comprehend what kind of bacterium could cause a disease.

References
Carton, J., Daly, R., & Ramani, P. (2007). Clinical pathology. New York, NY: Oxford University Press.

Ward, D. (2016). Microbiology and infection prevention and control for nursing students. Thousand Oaks, CA: Learning Matters.

In the previous section, we explained that some pathogens are more virulent than others. This is due to the unique virulence factorsproduced by individual pathogens, which determine the extent and severity of disease they may cause. A pathogen’s virulence factors are encoded by genes that can be identified using molecular Koch’s postulates. When genes encoding virulence factors are inactivated, virulence in the pathogen is diminished. In this section, we examine various types and specific examples of virulence factors and how they contribute to each step of pathogenesis.

Virulence Factors for Adhesion
As discussed in the previous section, the first two steps in pathogenesis are exposure and adhesion. Recall that an adhesin is a protein or glycoprotein found on the surface of a pathogen that attaches to receptors on the host cell. Adhesins are found on bacterial, viral, fungal, and protozoan pathogens. One example of a bacterial adhesin is type 1 fimbrial adhesin, a molecule found on the tips of fimbriae of enterotoxigenic E. coli (ETEC). Recall that fimbriae are hairlike protein bristles on the cell surface. Type 1 fimbrial adhesin allows the fimbriae of ETEC cells to attach to the mannose glycans expressed on intestinal epithelial cells. Table 1 lists common adhesins found in some of the pathogens we have discussed or will be seeing later in this chapter.

Table 1. Some Bacterial Adhesins and Their Host Attachment Sites
Pathogen Disease Adhesin Attachment Site
Streptococcus pyogenes Strep throat Protein F Respiratory epithelial cells
Streptococcus mutans Dental caries Adhesin P1 Teeth
Neisseria gonorrhoeae Gonorrhea Type IV pili Urethral epithelial cells
Enterotoxigenic E. coli (ETEC) Traveler’s diarrhea Type 1 fimbriae Intestinal epithelial cells
Vibrio cholerae Cholera N-methylphenylalanine pili Intestinal epithelial cells
CLINICAL FOCUS: PANKAJ, PART 3
This example continues Pankaj’s story that started in Characteristics of Infectious Disease and How Pathogens Cause Disease.

The presence of bacteria in Pankaj’s blood is a sign of infection, since blood is normally sterile. There is no indication that the bacteria entered the blood through an injury. Instead, it appears the portal of entry was the gastrointestinal route. Based on Pankaj’s symptoms, the results of his blood test, and the fact that Pankaj was the only one in the family to partake of the hot dogs, the physician suspects that Pankaj is suffering from a case of listeriosis.

Listeria monocytogenes, the facultative intracellular pathogen that causes listeriosis, is a common contaminant in ready-to-eat foods such as lunch meats and dairy products. Once ingested, these bacteria invade intestinal epithelial cells and translocate to the liver, where they grow inside hepatic cells. Listeriosis is fatal in about one in five normal healthy people, and mortality rates are slightly higher in patients with pre-existing conditions that weaken the immune response. A cluster of virulence genes encoded on a pathogenicity island is responsible for the pathogenicity of L. monocytogenes. These genes are regulated by a transcriptional factor known as peptide chain release factor 1 (PrfA).Clostridium and Neisseria Bacterias and Their Types Essay. One of the genes regulated by PrfA is hyl, which encodes a toxin known as listeriolysin O (LLO), which allows the bacterium to escape vacuoles upon entry into a host cell. A second gene regulated by PrfA is actA, which encodes for a surface protein known as actin assembly-inducing protein (ActA). ActA is expressed on the surface of Listeria and polymerizes host actin. This enables the bacterium to produce actin tails, move around the cell’s cytoplasm, and spread from cell to cell without exiting into the extracellular compartment.

Pankaj’s condition has begun to worsen. He is now experiencing a stiff neck and hemiparesis (weakness of one side of the body). Concerned that the infection is spreading, the physician decides to conduct additional tests to determine what is causing these new symptoms.

What kind of pathogen causes listeriosis, and what virulence factors contribute to the signs and symptoms Pankaj is experiencing?
Is it likely that the infection will spread from Pankaj’s blood? If so, how might this explain his new symptoms?
We’ll conclude Pankaj’s example later on this page.

Bacterial Exoenzymes and Toxins as Virulence Factors
After exposure and adhesion, the next step in pathogenesis is invasion, which can involve enzymes and toxins. Many pathogens achieve invasion by entering the bloodstream, an effective means of dissemination because blood vessels pass close to every cell in the body. The downside of this mechanism of dispersal is that the blood also includes numerous elements of the immune system. Clostridium and Neisseria Bacterias and Their Types Essay. Various terms ending in –emia are used to describe the presence of pathogens in the bloodstream. The presence of bacteria in blood is called bacteremia. Bacteremia involving pyogens (pus-forming bacteria) is called pyemia. When viruses are found in the blood, it is called viremia. The term toxemia describes the condition when toxins are found in the blood. If bacteria are both present and multiplying in the blood, this condition is called septicemia.

Figure 1. This patient has edema in the tissue of the right hand. Such swelling can occur when bacteria cause the release of pro-inflammatory molecules from immune cells and these molecules cause an increased permeability of blood vessels, allowing fluid to escape the bloodstream and enter tissue.

Patients with septicemia are described as septic, which can lead to shock, a life-threatening decrease in blood pressure (systolic pressure <90 mm Hg) that prevents cells and organs from receiving enough oxygen and nutrients. Some bacteria can cause shock through the release of toxins (virulence factors that can cause tissue damage) and lead to low blood pressure. Gram-negative bacteria are engulfed by immune system phagocytes, which then release tumor necrosis factor, a molecule involved in inflammation and fever. Tumor necrosis factor binds to blood capillaries to increase their permeability, allowing fluids to pass out of blood vessels and into tissues, causing swelling, or edema(Figure 1). With high concentrations of tumor necrosis factor, the inflammatory reaction is severe and enough fluid is lost from the circulatory system that blood pressure decreases to dangerously low levels. This can have dire consequences because the heart, lungs, and kidneys rely on normal blood pressure for proper function; thus, multi-organ failure, shock, and death can occur. Clostridium and Neisseria Bacterias and Their Types Essay.

Exoenzymes
Some pathogens produce extracellular enzymes, or exoenzymes, that enable them to invade host cells and deeper tissues. Exoenzymes have a wide variety of targets. Some general classes of exoenzymes and associated pathogens are listed in Table 2. Each of these exoenzymes functions in the context of a particular tissue structure to facilitate invasion or support its own growth and defend against the immune system. For example, hyaluronidase S, an enzyme produced by pathogens like Staphylococcus aureus, Streptococcus pyogenes, and Clostridium perfringens, degrades the glycoside hylauronan (hyaluronic acid), which acts as an intercellular cement between adjacent cells in connective tissue (Figure 2). This allows the pathogen to pass through the tissue layers at the portal of entry and disseminate elsewhere in the body (Figure 2).

Table 2. Some Classes of Exoenzymes and Their Targets
Class Example Function
Glycohydrolases Hyaluronidase S in Staphylococcus aureus Degrades hyaluronic acid that cements cells together to promote spreading through tissues
Nucleases DNAse produced by S. aureus Degrades DNA released by dying cells (bacteria and host cells) that can trap the bacteria, thus promoting spread
Phospholipases Phospholipase C of Bacillus anthracis Degrades phospholipid bilayer of host cells, causing cellular lysis, and degrade membrane of phagosomes to enable escape into the cytoplasm
Proteases Collagenase in Clostridium perfringens Degrades collagen in connective tissue to promote spread
a) A diagram of epithelial cells that are connected along their membranes. Hyaluronidases enter at these connection points. B) after the hyaluronidases break down the connections between the cells, bacteria can flow through the openings.
Figure 2. (a) Hyaluronan is a polymer found in the layers of epidermis that connect adjacent cells. (b) Hyaluronidase produced by bacteria degrades this adhesive polymer in the extracellular matrix, allowing passage between cells that would otherwise be blocked.

Pathogen-produced nucleases, such as DNAse produced by S. aureus, degrade extracellular DNA as a means of escape and spreading through tissue.Clostridium and Neisseria Bacterias and Their Types Essay. As bacterial and host cells die at the site of infection, they lyse and release their intracellular contents. The DNA chromosome is the largest of the intracellular molecules, and masses of extracellular DNA can trap bacteria and prevent their spread. S. aureus produces a DNAse to degrade the mesh of extracellular DNA so it can escape and spread to adjacent tissues. This strategy is also used by S. aureus and other pathogens to degrade and escape webs of extracellular DNA produced by immune system phagocytes to trap the bacteria.

Enzymes that degrade the phospholipids of cell membranes are called phospholipases. Their actions are specific in regard to the type of phospholipids they act upon and where they enzymatically cleave the molecules. The pathogen responsible for anthrax, B. anthracis, produces phospholipase C. When B. anthracis is ingested by phagocytic cells of the immune system, phospholipase C degrades the membrane of the phagosome before it can fuse with the lysosome, allowing the pathogen to escape into the cytoplasm and multiply. Phospholipases can also target the membrane that encloses the phagosome within phagocytic cells. As described earlier in this chapter, this is the mechanism used by intracellular pathogens such as L. monocytogenes and Rickettsia to escape the phagosome and multiply within the cytoplasm of phagocytic cells. The role of phospholipases in bacterial virulence is not restricted to phagosomal escape. Many pathogens produce phospholipases that act to degrade cell membranes and cause lysis of target cells. These phospholipases are involved in lysis of red blood cells, white blood cells, and tissue cells.

Bacterial pathogens also produce various protein-digesting enzymes, or proteases. Proteases can be classified according to their substrate target (e.g., serine proteases target proteins with the amino acid serine) or if they contain metals in their active site (e.g., zinc metalloproteases contain a zinc ion, which is necessary for enzymatic activity).

One example of a protease that contains a metal ion is the exoenzyme collagenase. Collagenase digests collagen, the dominant protein in connective tissue. Collagen can be found in the extracellular matrix, especially near mucosal membranes, blood vessels, nerves, and in the layers of the skin. Similar to hyaluronidase, collagenase allows the pathogen to penetrate and spread through the host tissue by digesting this connective tissue protein. The collagenase produced by the gram-positive bacterium Clostridium perfringens, for example, allows the bacterium to make its way through the tissue layers and subsequently enter and multiply in the blood (septicemia). C. perfringens then uses toxins and a phospholipase to cause cellular lysis and necrosis. Once the host cells have died, the bacterium produces gas by fermenting the muscle carbohydrates. The widespread necrosis of tissue and accompanying gas are characteristic of the condition known as gas gangrene (Figure 3).

A diagram of a tube labeled lumen of blood vessel lined by cells labeled endothelial cells. Outside he cells is dense irregular connective tissue. Collagenase is shown as small dots that break up the connections between the cells. A micrograph of the dense connective tissue shows many red lines making a meshwork.
Figure 3. The illustration depicts a blood vessel with a single layer of endothelial cells surrounding the lumen and dense connective tissue (shown in red) surrounding the endothelial cell layer. Collagenase produced by C. perfringensdegrades the collagen between the endothelial cells, allowing the bacteria to enter the bloodstream. (credit illustration: modification of work by Bruce Blaus; credit micrograph: Micrograph provided by the Regents of University of Michigan Medical School © 2012)

Two types of cell death are apoptosis and necrosis. Visit this website to learn more about the differences between these mechanisms of cell death and their causes.
Toxins
In addition to exoenzymes, certain pathogens are able to produce toxins, biological poisons that assist in their ability to invade and cause damage to tissues. The ability of a pathogen to produce toxins to cause damage to host cells is called toxigenicity.

Toxins can be categorized as endotoxins or exotoxins. The lipopolysaccharide (LPS) found on the outer membrane of gram-negative bacteria is called endotoxin (Figure 4). During infection and disease, gram-negative bacterial pathogens release endotoxin either when the cell dies, resulting in the disintegration of the membrane, or when the bacterium undergoes binary fission. Clostridium and Neisseria Bacterias and Their Types Essay. The lipid component of endotoxin, lipid A, is responsible for the toxic properties of the LPS molecule. Lipid A is relatively conserved across different genera of gram-negative bacteria; therefore, the toxic properties of lipid A are similar regardless of the gram-negative pathogen.Clostridium and Neisseria Bacterias and Their Types Essay. In a manner similar to that of tumor necrosis factor, lipid A triggers the immune system’s inflammatory response (see Inflammation and Fever). If the concentration of endotoxin in the body is low, the inflammatory response may provide the host an effective defense against infection; on the other hand, high concentrations of endotoxin in the blood can cause an excessive inflammatory response, leading to a severe drop in blood pressure, multi-organ failure, and death.

A long chain of O antigens is drawn as various geometric shapes in a long row. Next is a core; a shorter region of similar shapes. Next is 2 circles labeled lipid A. Each of these has 2 or 3 long wavy lines projecting from them.
Figure 4. Lipopolysaccharide is composed of lipid A, a core glycolipid, and an O-specific polysaccharide side chain. Lipid A is the toxic component that promotes inflammation and fever.

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A classic method of detecting endotoxin is by using the Limulus amebocyte lysate (LAL) test. In this procedure, the blood cells (amebocytes) of the horseshoe crab (Limulus polyphemus) is mixed with a patient’s serum. The amebocytes will react to the presence of any endotoxin. This reaction can be observed either chromogenically (color) or by looking for coagulation (clotting reaction) to occur within the serum. An alternative method that has been used is an enzyme-linked immunosorbent assay (ELISA) that uses antibodies to detect the presence of endotoxin.

Unlike the toxic lipid A of endotoxin, exotoxins are protein molecules that are produced by a wide variety of living pathogenic bacteria. Although some gram-negative pathogens produce exotoxins, the majority are produced by gram-positive pathogens. Exotoxins differ from endotoxin in several other key characteristics, summarized in Table 4. In contrast to endotoxin, which stimulates a general systemic inflammatory response when released, exotoxins are much more specific in their action and the cells they interact with. Each exotoxin targets specific receptors on specific cells and damages those cells through unique molecular mechanisms. Endotoxin remains stable at high temperatures, and requires heating at 121 °C (250 °F) for 45 minutes to inactivate. By contrast, most exotoxins are heat labile because of their protein structure, and many are denatured (inactivated) at temperatures above 41 °C (106 °F). As discussed earlier, endotoxin can stimulate a lethal inflammatory response at very high concentrations and has a measured LD50 of 0.24 mg/kg. By contrast, very small concentrations of exotoxins can be lethal. For example, botulinum toxin, which causes botulism, has an LD50 of 0.000001 mg/kg (240,000 times more lethal than endotoxin). Clostridium and Neisseria Bacterias and Their Types Essay.

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