The 's Immune System Of Relapsing Fever Borrelia Species

“Bacterial illness is a result of complex interactions between bacteria and the host. During evolution, humans developed many ways to protect themselves against bacterial pathogens. On the other hand, bacteria have developed strategies to evade, subvert or circumvent these defenses” (Sousa, 2003) “One of the most important characteristics of bacterial pathogenicity is the various strategies developed by prokaryotic organisms to use host molecules for their own benefit” (Sousa, 2003). “To accomplish this, bacteria have evolved elaborate control mechanisms to turn genes on and off, varying the transcriptional activator or

Instead of being recognized and attacked by T cells, bacteria are recognized and attacked by complement proteins. “Complement proteins assist in bacterial killing via three pathways, the classical complement pathway, the alternative complement pathway or the lectin pathway. The first steps of the classical complement pathway require the binding of antibodies to the surface of the target bacterium” (Immune, 2016). At this point, the antibodies are handled by protein complexes which bind to the surface of the invader (much the same as the process of T cells in viruses). In other words, the body goes through a similar reaction of identifying and then attempting to destroy the invader, including the formation of a membrane attack complex. “MAC can insert into the cell membrane of Gram-negative, but not Gram-positive, bacteria. There, it produces pores that allow the entry of membrane damaging molecules, such as lysozyme, and makes the bacterium susceptible to osmotic lysis” (Immune,

Dworkin MS, Schwan TG, Anderson DE, Borchardt SM. Tick-Borne Relapsing Fever. Infectious disease clinics of North America. 2008;22(3):449-viii. doi:10.1016/j.idc.2008.03.006.

It is a small, fastidious gram-negative bacteria that easily invades respiratory tract producing a number of antigens and toxins such as pertussis toxin (PT), tracheal cytotoxin, filamentous hemagglutin and pertactin that binds and destroys the pharyngeal epithelial cells (Centers of Disease Control and Prevention, Bordatella Pertussis, p 206). As a result, triggers the immune system response. B. Pertussis portal of entry is through the mouth, nose and throat and it is primarily transmitted through direct contact with respiratory droplets with an infected individual or aerosol droplets and rarely fomites (Brunner & Suddarth 2010, p. 2149). Bordatella pertussis is a human disease and adolescents and adults are the main reservoirs (CDC, p. 206). The disease has high infectivity, high pathogenicity and low virulence.

Borrelia burgdorferi was first diagnosed as Lyme disease in 1982 when the bacteria were isolated by the Centers for Disease Control and Prevention. The spirochete has been in the United States and Europe for many years but had gone un-diagnosed because of the limited medical knowledge. It is named after the leading American bacteriologist, Willy Burgdorfer, after his extensive research between the arachnid vectors and the human host was acknowledged. He studied many different diseases caused by animals, but the discovery of Lyme disease gained him recognition around the world. There are many tick-borne diseases, but Lyme disease is the number one tick-borne disease in America. The number of diagnoses has increased significantly in the last

Abstract: Ixodes scapularis and Ixodes pacificus are the two species of blacklegged ticks that act as vectors of transmission of the spirochete bacterium Borrelia burgdorferi to small mammals or human host, which cause Lyme disease in humans, also known as Lyme borreliosis (cdc.gov 2016; Qiu et al. 2002). After the pathogen’s initial entry through the skin, it proliferates in the blood and cerebrospinal fluid; Borrelia burgdorferi has also been seen in much smaller quantities in the following locations: ‘myocardium, retina, muscle, bone, spleen, liver, meninges, and brain’, which is the primary cause of more severe secondary symptoms of untreated infection (cdc.gov 2016; Steere 2004).

-B2 was Gram positive cocci that seemed to cluster and also showed no growth on the EMB plates.

In 1981, a spirochetal bacterium was discovered in a nymphal tick, Ixodes scapularis and named Borrelia burgdorferi. This species has now been divided into multiple species, three of which cause human infection. Agents belonging to the eubacterial phylum of spirochetes, which are bacteria shaped like corkscrews and are actively motile, cause Lyme borrelioses, also called Lyme disease. As discovered from its sequenced genome, B. burgdorferi depends entirely on its host for nutrients. Another unique characteristic of these bacteria is that it does not require iron for growth in vitro, which helps the parasite overcome a common host response of limiting iron. This pathogen causes infection not through toxins but through migrating through the

One way in which an infectious agent can evade immune surveillance is by altering its antigens; this is particularly important for extracellular pathogens, against which the principal defense is the production of antibody against their surface structures. There are three ways in which antigenic variation can occur. First, many infectious agents exist in a wide variety of antigenic types. There are, for example, 84 known types of Streptococcus pneumoniae, an important cause of bacterial pneumonia. Each type differs from the others in the structure of its polysaccharide capsule. The different types are distinguished by serological tests and so are often known as serotypes. Infection with one serotype of such an organism can lead to type-specific immunity, which protects against reinfection with that type but not with a different serotype. Thus, from the point of view of the adaptive immune system, each serotype of S. pneumoniae represents a distinct organism. The result is that essentially the same pathogen can cause disease many times in the same

Yersinia is a gram-negative bacteria causing plague pandemics in humans. They are facultative intracellular organisms that can very efficiently survive and replicate inside cells (1). They cause fatal plague and have destroyed millions of lives since 541 A.D (2). This review will highlight how these organisms subvert the immune system. It will elaborate on all the mechanisms and proteins utilized for the same. The main are the Yops or Yersinia outer proteins. But, there are other factors as

Yersinia pestis (Y. pestis), a gram-negative, non-motile facultative intracellular bacterium is responsible for the bubonic plague in humans (Smiley 2008). The bacterium uses the Rodent flea Xenopsylla cheopis as a vector to gain entry into a new host. (Butler 2009). The bacterium forms of an aggregative biofilm on the spicules of the proventriculus in the flea (Butler 2009). This blockage on the proventriculus causes the flea to behave as if it is starving continuously biting and try to feed (Butler 2009). Through this cycle of feeding, the transmission of the infected blood from the flea’s stomach enables the new host to be infected through its skin (Butler 2009).

the adaptive immune response to B. burgdorferi evokes both T-cell-independent and T-cell-dependent B cell responses. Furthermore, a recent study shows

The exact mechanism of this is unknown however there have been several hypotheses. B. burgdorferi has been shown to have the ability to form cyst-like forms, almost entering latency, in which they can hide from the immune response as well as evade antibiotic treatment (Brorson & Brorson, 1997). In their study, Gruntar et al. (2001) found that Borrelia garinii are particularly resilient as they can return to its motile state even after freeze then thawing the cysts. Another theory states that the inflammatory response may cause permanent damage to neurons therefore causing symptoms of pain, fatigue and malaise months after initial infection (Hildenbrand et al.,

Virulence Factors: The most important virulence factor of S. aureus is the specific surface proteins that allow the organism to attach to host proteins. The surface proteins of this bacterium allow it to attach to host proteins such as laminin and fibronectin, which form the extracellular matrix of epithelial and endothelial cells. S. aureus also produces a number of membrane damaging toxins that allow the organism to further invade and harm the host, of which the alpha- toxin is the most well studied and is the protein responsible for septic shock. The alpha- toxin is a protein that binds to a specific receptor in platelets and monocytes in humans, forming pores that eventually destroy the cell.

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