Wolbachia And Its Effects On The Reproductive Ability Of Its Host And Cause Re Productive Parasitism

Some phages infect bacteria to destroy them, which is called lysic lifestyle, while other phages infect bacteria and stay dormant inside them for a while, which is referred to as a lysogenic lifestyle. A phage infects the bacteria cell by injecting its genetic material into the bacteria’s cytoplasm. This allows the bacteria synthesis process to start making the phage’s genetic code instead of its own. Once the bacteria have made enough phages to handle, the walls will break and release all of the phage that was created. The phages that were made are now resetting the process and beginning again by infecting the other near bacteria by injecting their genetic material once again. Those phages that stay within the bacteria and not burst the bacteria will continue to reproduce the phages own genetic code. (Griffiths,

5 drops of chloroform were added to the mixture and incubated at room temperature for 15 minutes to kill, and lyse the bacteria cells which allows all the unadsorbed phages to be accounted for when determining the titer of unadsorbed phage with susceptible bacteria, E. Coli B. (Biology Dept.). 0.1 ml of E.coli B was added to the 10 fold dilution. Using soft agar technique, the unadsorbed phage were plated. After incubation, the titer of unadsorbed phage was determined by counting the number of plaques on the plate from the infection of single E. coli cells in the assay tube by a free phage particle before

Rickettsia rickettsii is the small, aerobic gram-negative bacterium that is the cause Rocky Mountain spotted fever in humans (and other vertebrates). They are obligate, intracellular bacteria that range in size form 0.2x0.5 µm to 0.3x2.0µm. Rickettsia belong to the phylum alpha-protobacteria, which are capable of growing in low levels of nutrients, and have a long generation time relative to other gram negative bacteria such as Escherichia coli. In humans rickettsiae preferentially reside in the nucleus or cytoplasm of cells lining small to medium size blood vessels.

Prokaryotes are ubiquitous, successfully adapting to diverse environments as well as developing symbiotic relationships with host organisms (Lengeler, Drews, & Schlegel, 1999). Prokaryotes may have both autotrophic and heterotrophic characteristics. A cyanobacteria is photosynthetic, commonly called blue-green algae, and may produce toxins (Crayton, 1993). Bacteria are most commonly associated in the general

The genome of E. coli 0157:H7 was recently sequenced and contains 1,387 new genes absent in non pathogenic strains. Analysis of the genome suggests that there are a variety of potential virulence genes that have yet to be explored, including fimbrial and other adhesions, secretion systems, and toxins. Many of the virulence genes are similar to those associated with pathogenesis in Salmonella and Shigella. Most of them are found on pathogenicity islands from viral DNA that is transmitted to the bacteria through the activity of a lysogenic phage. The two most important toxins, Stx1 and Stx2 (for shiga-toxin) are found on such islands and are composed of 5 B subunits surounding an active A component, which is transported into the cell after the

14 Davis B, Waldor M (2003). "Filamentous phages linked to virulence of Vibrio cholerae". Curr Opin Microbiol. 6 (1): 35–42. doi:10.1016/S1369-5274(02)00005-X. PMID 12615217.

rOmpA and rOmpA proteins are found across various strains of rickettsia rickettsii bacteria and play a role in pathogenesis through adhesion and invasion. It is noted that due to a premature stop codon, rOmpA is not produced in the avirulent strains of the rickettsia rickettsii bacteria and thus, it is thought that OmpA may play a role in virulence. This hypothesis was tested by inserting an isogenic ompA mutant – to create a premature stop codon – into a guinea pig infected with the highly virulent Shelia Smith strain. It was evident that this did not affect the duration or severity of illness versus the control guinea pig. From these findings it was concluded, and as the title of the article states, “the rickettsia rickettsii OmpA surface antigen does not diminish virulence in a mammalian model

The bacteria, Yersinia pestis, is encoded with two specific plasmids that aid in the transfer and survival of the bacteria, especially in the wild. Both of these plasmids must be present on the bacteria for full virulence of the organism. The largest of the extrachromosomal elements, with typical strains of ~100 kb, is the Murine toxin plasmid (pFra), a capsule protein. pFra is characterized by two specific factors: FI capsular protein antigen and YMT. The second plasmid, Pesticin plasmid named pPla after the plasminogen activator, happens to be the smallest of the plasmids. The bacteriocin (pesticin;Pst) and the bilanolysin and coagulase activities are found to be connected with one another and aids the former organism of Yersinia in the invasion of "the host from peripheral sites" (Carniel 41). After the bacteria is injected through a bite of the rat flea, Yersinia pestis affects the immune system similar to the bacterial agent, Bacillis anthracis. By having a Type III secretion system, the bacteria are able to find "a means ? to target virulence factors directly at host cells". The common Yersinia encoded plasmid molecule, pYV (or pLcr), found on the bacteria specifically aids in the injection of cytotoxic proteins into the macrophages, preventing the

In the BIOL2202 bacteria genetics practical, our results can hardly discriminate which sex mechanism was employed by E.coli to revert back to prototroph as the donor(JC158) and recipient strands(AB1157) were added into a Erlenmeyer flask and mixed together to facilitate conjugation. Besides, the reversion could also be attributed to transformation due to unknown transforming factors which somehow mutated the gene back to wild type configuration. When mixing began, both transformation and cell conjugation were possible, thus it was hard to differentiate which mechanism that ultimately leads to the appearance of prototroph.

For millions of years’ bacteria have been surviving to their environments and been at war against other microorganism. This wars have lead them to creating an unstoppable arsenal of weapons they can use to survive. Unlike virus that need a host cell to survive, bacteria can survive anywhere since they can share their DNA with each other. This allows bacteria to survive in places like radioactive waste, zero oxygen environments, and even in absolute darkness. Unlike human beings who are born with a specific genetic code, bacteria have the capability of changing that code. Bacteria have three methods of evolving themselves in order to survive the harsh is of conditions. The three methods are called horizontal gene transfer. The first is Transformation, but some pathologists call it the “Funeral Grab”.

Naegleria Fowleri is a free living ameba found in high temperature, fresh water environments. Although rare, this ameba can travel through the nasal mucosa to the brain and cause primary amoebic meningoencephalitis (PAM). The three stages of life for N. Fowleri include the cyst, trophozoite, and flagellate stage. The only stage the ameba is able to infect humans in is the trophozoite stage in which it feeds off of organic molecules such as brain tissue; When food source is scarce or temperatures are too cold the ameba will return to the cyst stage. The cyst consisting of a thickened cell membrane, nucleus, cytoplasm, mitochondria and vacuoles allow for the ameba to survive

A group of wollies lives in the Amazon rainforest where they survive altogether. Not only their abilities are unique but also their unity in the group. Whatever, they do or intend to do they know everything about each other. They are telepathic and a leader of the group connect all of them together at one time like a group call on social media. So far, wollies are serving with air around them. They don't need anything but air as energy resources.

Vibrio fischeri is a Gram-negative bacterium that served as the model organism in this experiment. We isolated only the luxAB portion of the entire lux operon and inserted it into the pGEM vector plasmid to transcribe the luciferase enzyme required for bioluminescence. Within the lux operon, luxAB is responsible for producing subunits that form luciferase, which oxidizes the aldehyde made by luxCDE into the reduced flavin-mononucleotide FMNH2 and results in the production of light known as bioluminescence[6]. The luxI gene that is also present on the operon produces the “autoinducer which interacts with a regulator, LuxR, [and] activates transcription of the lux operon at high-cell density” to induce bioluminescence[4]. This interaction between the products of luxI and luxR is known as quorum sensing and serves as an evolutionary purpose in the symbiotic relationship with Euprymna scolopes, a type of squid that contains the light organ where the bacteria resides[6].

Pathogenic L. monocytogenes go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. The bacterium is first phagocytosed by these cells and secretes a pore-forming toxin called listeriolysin, which allows the bacterium to escape from the phagosome. All virulent strains of L. monocytogenes synthesize and secrete listeriolysin. Phospholipase A and B are other virulence factors that facilitate escape of L. monocytogenes from the phagosome. Once out of the phagosome L. monocytogenes is capable of rapid division in the cytoplasm, evading the immune response and moving throughout the cytoplasm from cell to cell. L. monocytogenes is well known for its ability to propel itself like a rocket through the cell cytoplasm. This is the result of the bacterium’s ability to polymerize actin filaments at its tail end. Actin is arranged in subunits to form microfilaments that are capable of directing cell movement. L. monocytogenes accomplishes cell motility through a virulence factor called ActA that takes advantage of normal actin polymerization going on in the cell. The ActA protein shares sequence homology with a protein called WASP that is found in virtually all eukaryotic cells. WASP is responsible for recognizing and

The bacterium evolved by loosing its genes converting it from a free-living microbe into a pathogen. It needs the host’s nutrients in order to survive. The bacterium latches itself onto the host epithelial cells by a 160 kDa type 1 pilli. The pilli, located on a specific organelle on the polar region of the