Nucleolin is a protein that in humans is encoded by the NCL gene.[5][6]
https://en.wikipedia.org/wiki/Nucleolin
RAC-alpha serine/threonine-protein kinase is an enzyme that in humans is encoded by the AKT1 gene. This enzyme belongs to the AKT subfamily of serine/threonine kinases that contain SH2 (Src homology 2b-like) protein domains.[5] It is commonly referred to as PKB, or by both names as "Akt/PKB".
https://en.wikipedia.org/wiki/AKT1
Anaplastic lymphoma kinase (ALK) also known as ALK tyrosine kinase receptor or CD246 (cluster of differentiation 246) is an enzyme that in humans is encoded by the ALK gene.[5][6]
https://en.wikipedia.org/wiki/Anaplastic_lymphoma_kinase
Adenine /ˈædɪnɪn/ (A, Ade) is a nucleobase (a purine derivative). It is one of the four nucleobases in the nucleic acid of DNA that are represented by the letters G–C–A–T. The three others are guanine, cytosine and thymine. Its derivatives have a variety of roles in biochemistry including cellular respiration, in the form of both the energy-rich adenosine triphosphate(ATP) and the cofactors nicotinamide adenine dinucleotide (NAD), flavin adenine dinucleotide (FAD) and Coenzyme A. It also has functions in protein synthesis and as a chemical component of DNA and RNA.[2] The shape of adenine is complementary to either thymine in DNA or uracil in RNA.
The adjacent image shows pure adenine, as an independent molecule. When connected into DNA, a covalent bond is formed between deoxyribose sugar and the bottom left nitrogen (thereby removing the existing hydrogen atom). The remaining structure is called an adenine residue, as part of a larger molecule. Adenosine is adenine reacted with ribose, as used in RNA and ATP; deoxyadenosine is adenine attached to deoxyribose, as used to form DNA.
adenosine triphosphate(ATP) and the cofactors nicotinamide adenine dinucleotide (NAD),
https://en.wikipedia.org/wiki/Adenine
Nucleobases, also known as nitrogenous bases or often simply bases, are nitrogen-containing biological compounds that form nucleosides, which, in turn, are components of nucleotides, with all of these monomersconstituting the basic building blocks of nucleic acids. The ability of nucleobases to form base pairs and to stack one upon another leads directly to long-chain helical structures such as ribonucleic acid (RNA) and deoxyribonucleic acid (DNA).
https://en.wikipedia.org/wiki/Nucleobase
Nucleosides are glycosylamines that can be thought of as nucleotides without a phosphate group. A nucleoside consists simply of a nucleobase (also termed a nitrogenous base) and a five-carbon sugar (ribose or 2'-deoxyribose) whereas a nucleotide is composed of a nucleobase, a five-carbon sugar, and one or more phosphate groups. In a nucleoside, the anomeric carbon is linked through a glycosidic bond to the N9 of a purine or the N1 of a pyrimidine. Examples of nucleosides include cytidine, [ alcohol group (-CH2-OH) to produce nucleotides. Nucleotides are the molecular building-blocks of DNA and RNA.
https://en.wikipedia.org/wiki/Nucleoside
https://www.genome.gov/genetics-glossary/Base-Pair
https://seer.cancer.gov/seertools/hemelymph/51f6cf57e3e27c3994bd5363/?q=cytoid#
T. pallidum's lack of either tricarboxylic acid cycle or oxidative phosphorylation results in minimal metabolic activity.[3]
Treponema pallidum
https://en.wikipedia.org/wiki/Treponema_pallidum
Syphilis is a sexually transmitted infection caused by the bacterium Treponema pallidum subspecies pallidum.[3] The signs and symptoms of syphilis vary depending in which of the four stages it presents (primary, secondary, latent, and tertiary).[1] The primary stage classically presents with a single chancre (a firm, painless, non-itchy skin ulceration usually between 1 cm and 2 cm in diameter) though there may be multiple sores.[1] In secondary syphilis, a diffuse rash occurs, which frequently involves the palms of the hands and soles of the feet.[1] There may also be sores in the mouth or vagina.[1] In latent syphilis, which can last for years, there are few or no symptoms.[1] In tertiary syphilis, there are gummas (soft, non-cancerous growths), neurological problems, or heart symptoms.[2] Syphilis has been known as "the great imitator" as it may cause symptoms similar to many other diseases.[1][2]
https://en.wikipedia.org/wiki/Syphilis
Dark-field microscopy (also called dark-ground microscopy) describes microscopy methods, in both light and electron microscopy, which exclude the unscattered beam from the image. As a result, the field around the specimen (i.e., where there is no specimen to scatter the beam) is generally dark.
https://en.wikipedia.org/wiki/Dark-field_microscopy
Successful long-term cultivation of T. pallidum subspecies pallidum in a tissue culture system has been reported in 2018.[13]
T. pallidum's outer membrane has the most contact with host cells and contains few transmembrane proteins, limiting antigenicity while its cytoplasmic membrane is covered in lipoproteins.[3][10] The outer membrane's treponemal ligands main function is attachment to host cells, with functional and antigenic relatedness between ligands.[11] The genus Treponema has ribbons of cytoskeletal cytoplasmic filaments that run the length of the cell just underneath the cytoplasmic membrane. They are composed of the intermediate filament-like protein CfpA (cytoplasmic filament protein A). Although the filaments may be involved in chromosome structure and segregation or cell division, their precise function is unknown.[12][10]
It revealed that T. pallidum relies on its host for many molecules provided by biosynthetic pathways, and that it is missing genes responsible for encoding key enzymes in oxidative phosphorylation and the tricarboxylic acid cycle.
The clinical features of syphilis, yaws, and bejel occur in multiple stages that affect the skin. The skin lesions observed in the early stage last for weeks or months. The skin lesions are highly infectious, and the spirochetes in the lesions are transmitted by direct contact. The lesions regress as the immune response develops against T. pallidum. The latent stage that results lasts a lifetime in many cases. In a minority of cases, the disease exits latency and enters a tertiary phase, in which destructive lesions of skin, bone, and cartilage ensue. Unlike yaws and bejels, syphilis in its tertiary stage often affects the heart, eyes, and nervous system as well.[6]
The incubation period for a T. p. pallidum infection is usually around 21 days, but can range from 10 to 90 days.[24]
T. pallidum was first microscopically identified in syphilitic chancres by Fritz Schaudinn and Erich Hoffmann at the Charité in Berlin in 1905.[25]
Bacterial diseases due to gram negative non-proteobacteria (BV4)
https://en.wikipedia.org/wiki/Treponema_pallidum
It was found that this is due to 5% of T. pallidum's genes coding for transport genes.[16]
transport gene viral plasmid or non-transporter acquisition etc., injury by insecticide-pesticide-gen/mod-etc.. no transporter required for nutrient human phosphate (rf atp triphos), proton, frags, prion, comp, virus particle, electron, photon, phonon, particle, particle transform, energy transform (particle to wave, low potential energy storage dormancy), etc.. protein or channel or transport gene outcome protein or circumstance may be signaling, sensory, adherance micro, etc.. for sustainability one particle per one year, dormancy variable capacity onset. capacity to activate function, trigger particle. hemolysins for release of cellular content, transcription with rna/dna/etc., acidification reduce non-self/agranulocyte/etc., granulocyte acidification melt biofilm inclined fungus-bact nutrient prov increase, iron sulfur facilitate chemical state change to permit self-energizement (no need for further energy), etc.. 1.14Mbp comp exp. wave synchronization, inversion, interference, fielding, gamma, etc.. small pox, syphilius, yellow fever, malaria, equine infectious anemia, worm or virus, measles mumps rubellaes, siv, polio, hiv, zoonotics, prison inhumane experimentation bred families (pus eater layng, etc.), tettany toxins production clostridium sym, malariae, highly infective leukemia virus type 1, etc.. usually deep sewer worms. special worm, probably modified or stolen.
Advisory do not tort the parasite. Very advanced, old, 1000 and 50.50 rat.
Antigenicity is the capacity of a chemical structure (either an antigen or hapten) to bind specifically with a group of certain products that have adaptive immunity: T cell receptors or antibodies (a.k.a. B cell receptors). Antigenicity was more commonly used in the past to refer to what is now known as immunogenicity, and the two are still often used interchangeably. However, strictly speaking, immunogenicity refers to the ability of an antigen to induce an adaptive immune response. Thus an antigen might bind specifically to a T or B cell receptor, but not induce an adaptive immune response. If the antigen does induce a response, it is an 'immunogenic antigen', which is referred to as an immunogen.
References[edit]
- Cruse, Julius M.; Lewis, Robert E. (1998). Atlas of Immunology. Boca Raton: CRC Press. ISBN 978-0849394898.
| Phylum: | Spirochaetes |
| Order: | Spirochaetales |
Pathogenic Leptospira
- Leptospira alstonii Smythe et al. 2013 ["Leptospira alstoni" Haake et al. 1993]
- Leptospira interrogans (Stimson 1907) Wenyon 1926 emend. Faine and Stallman 1982 ["Spirochaeta interrogans" Stimson 1907; "Spirochaeta nodosa" Hubener & Reiter 1916; "Spirochaeta icterohaemorrhagiae" Inada et al. 1916; "Spirochaeta icterogenes" Uhlenhuth & Fromme 1916; "Leptospira icteroides" Noguchi 1919]
- Leptospira kirschneri Ramadass et al. 1992
Non-pathogenic Leptospira
- Leptospira biflexa (Wolbach and Binger 1914) Noguchi 1918 emend. Faine and Stallman 1982 ["Spirochaeta biflexa" Wolbach & Binger 1914; "Ancona ancona"; "Canela canela"; "Jequitaia jequitaia"]
- Members of Leptospira are also grouped into serovars according to their antigenic relatedness. There are currently over 200 recognized serovars. A few serovars are found in more than one species of Leptospira.
 | |
| Scanning electron micrograph of Leptospira interrogans |
The outer membrane contains a variety of lipoproteins and transmembrane outer membrane proteins.[15] As expected, the protein composition of the outer membrane differs when comparing Leptospira growing in artificial medium with Leptospira present in an infected animal.[16][17][18] Several leptospiral outer membrane proteins have been shown to attach to the host extracellular matrix and to factor H. These proteins may be important for adhesion of Leptospira to host tissues and in resisting complement, respectively.[19][20][21]
Leptospira have a Gram-negative-like cell envelope consisting of a cytoplasmic and outer membrane. However, the peptidoglycan layer is associated with the cytoplasmic rather than the outer membrane, an arrangement that is unique to spirochetes. The two flagella of Leptospira extend from the cytoplasmic membrane at the ends of the bacterium into the periplasmic space and are necessary for the motility of Leptospira.[14]Louse-borne relapsing fever[edit]
Along with Rickettsia prowazekii and Bartonella quintana, Borrelia recurrentis is one of three pathogens of which the body louse (Pediculus humanus humanus) is a vector.[4] Louse-borne relapsing fever is more severe than the tick-borne variety.[citation needed]
Louse-borne relapsing fever occurs in epidemics amid poor living conditions, famine and war in the developing world.[5] It is currently prevalent in Ethiopia and Sudan.[citation needed]
Mortality rate is 1% with treatment and 30–70% without treatment. Poor prognostic signs include severe jaundice, severe change in mental status, severe bleeding and a prolonged QT interval on ECG.[citation needed]
Lice that feed on infected humans acquire the Borrelia organisms that then multiply in the gut of the louse. When an infected louse feeds on an uninfected human, the organism gains access when the victim crushes the louse or scratches the area where the louse is feeding. B. recurrentis infects the person via mucous membranes and then invades the bloodstream. No non-human, animal reservoir exists.[citation needed]
https://en.wikipedia.org/wiki/Relapsing_fever#Louse-borne_relapsing_fever
Relapsing fever is a vector-borne disease caused by infection with certain bacteria in the genus Borrelia,[1] which is transmitted through the bites of lice or soft-bodied ticks (genus Ornithodoros).[2]
https://en.wikipedia.org/wiki/Relapsing_fever#Louse-borne_relapsing_fever
Borrelia recurrentis is a species of Borrelia, a spirochaete bacterium associated with relapsing fever.[1][2] B. recurrentis is usually transmitted from person to person by the human body louse.[3] Since the 1800s, the body louse has been known as its only known vector.[4]
B. recurrentis DNA was found in 23% of head lice from patients with louse-borne relapsing fever in Ethiopia. Whether head lice can transmit these bacteria from one person to another remains to be determined.[4]
It is notable for its ability to alter the proteins expressed on its surface, which causes the "relapsing" characteristic of relapsing fever.[5]
https://en.wikipedia.org/wiki/Borrelia_recurrentis
The phylum "Bacteroidetes" is composed of three large classes of Gram-negative, nonsporeforming, anaerobic or aerobic, and rod-shaped bacteria that are widely distributed in the environment, including in soil, sediments, and sea water, as well as in the guts and on the skin of animals.
Although some Bacteroides spp. can be opportunistic pathogens, many "Bacteroidetes" are symbiotic species highly adjusted to the gastrointestinal tract. Bacteroides are highly abundant in intestines, reaching up to 1011 cells g−1 of intestinal material. They perform metabolic conversions that are essential for the host, such as degradation of proteins or complex sugar polymers. "Bacteroidetes" colonize the gastrointestinal already in infants, as non-digestible oligosaccharides in mother milk support the growth of both Bacteroides and Bifidobacterium spp. Bacteroides spp. are selectively recognized by the immune system of the host through specific interactions.[3]
https://en.wikipedia.org/wiki/Bacteroidetes
Fusobacteria are obligately anaerobic non-sporeforming Gram-negative bacilli. Since the first reports in the late nineteenth century, various names have been applied to these organisms, sometimes with the same name being applied to different species. More recently, not only have there been changes to the nomenclature, but also attempts to differentiate between species which are believed to be either pathogenic or commensal or both. Because of their asaccharolytic nature, and a general paucity of positive results in routine biochemical tests, laboratory identification of the fusobacteria has been difficult. However, the application of novel molecular biological techniques to taxonomy has established a number of new species, together with the subspeciation of Fusobacterium necrophorum and F. nucleatum, and provided new methods for identification. The involvement of fusobacteria in a wide spectrum of human infections causing tissue necrosis and septicaemia has long been recognised, and, more recently, their importance in intra-amniotic infections, premature labour and tropical ulcers has been reported.
Since the first reports of fusobacteria in the late nineteenth century, the variety of species names has led to some confusion within the genera Fusobacterium and Leptotrichia. However, newer methods of investigation have led to a better understanding of the taxonomy, with the description of several new species of fusobacteria. Among the new species described are F. ulcerans from tropical ulcers, and several species from the oral cavity. Subspeciation of the important species F. necrophorum and F. nucleatumhas also been possible. It is probable that the taxonomy of the fusobacteria may be further developed in the future.[2]
https://en.wikipedia.org/wiki/Fusobacteria
Streptobacillus moniliformis is a non-motile, Gram-negative rod-shaped bacterium that is a member of the family Leptotrichiaceae.[2] The genome of S. moniliformis is one of two completed sequences of the order Fusobacteriales.[3] Its name comes from the Greek word streptos for "curved" or "twisted", and the Latin words bacillus meaning "small rod" and moniliformisfor "necklace".[4] S. moniliformis is microaerophilic, requiring less oxygen than is present in the atmosphere for its growth.[5]
https://en.wikipedia.org/wiki/Streptobacillus_moniliformis
Fusobacterium polymorphum is a bacterium that has been isolated from the gingival crevice in humans, and has been implicated in the immunopathology of periodontal disease. It has also been isolated in guinea pigs in research studies.[1]
https://en.wikipedia.org/wiki/Fusobacterium_polymorphum
Fusobacterium nucleatum is an oral bacterium, commensal to the human oral cavity, that plays a role in periodontal disease. This organism is commonly recovered from different monocultured microbial and mixed infections in humans and animals. It is a key component of periodontal plaque due to its abundance and its ability to coaggregate with other bacteria species in the oral cavity.[1][2]
https://en.wikipedia.org/wiki/Fusobacterium_nucleatum
Lemierre's syndrome refers to infectious thrombophlebitis of the internal jugular vein.[2] It most often develops as a complication of a bacterial sore throat infection in young, otherwise healthy adults. The thrombophlebitis is a serious condition and may lead to further systemic complications such as bacteria in the blood or septic emboli.
Lemierre's syndrome occurs most often when a bacterial (e.g., Fusobacterium necrophorum) throat infection progresses to the formation of a peritonsillar abscess. Deep in the abscess, anaerobic bacteria can flourish. When the abscess wall ruptures internally, the drainage carrying bacteria seeps through the soft tissue and infects the nearby structures. Spread of infection to the nearby internal jugular vein provides a gateway for the spread of bacteria through the bloodstream. The inflammation surrounding the vein and compression of the vein may lead to blood clot formation. Pieces of the potentially infected clot can break off and travel through the right heart into the lungs as emboli, blocking branches of the pulmonary artery that carry blood with little oxygen from the right side of the heart to the lungs.
Sepsis following a throat infection was described by Schottmuller in 1918.[3] However, it was André Lemierre, in 1936, who published a series of 20 cases where throat infections were followed by identified anaerobic sepsis, of whom 18 died.[4]
https://en.wikipedia.org/wiki/Lemierre%27s_syndrome
Fusobacterium necrophorum is a species of bacteria responsible for Lemierre's syndrome and other medical problems.
https://en.wikipedia.org/wiki/Fusobacterium_necrophorum
Prevotella intermedia (formerly Bacteroides intermedius) is a gram-negative, obligate anaerobic pathogenic bacterium involved in periodontal infections, including gingivitis and periodontitis, and often found in acute necrotizing ulcerative gingivitis. It is commonly isolated from dental abscesses, where obligate anaerobes predominate. P. intermedia is thought to be more prevalent in patients with noma. [1]
P. intermedia use steroid hormones as growth factors, so their numbers are higher in pregnant women.[citation needed] It has also been isolated from women with bacterial vaginosis.[2]
https://en.wikipedia.org/wiki/Prevotella_intermedia
Porphyromonas gingivalis belongs to the phylum Bacteroidetes and is a nonmotile, Gram-negative, rod-shaped, anaerobic, pathogenic bacterium. It forms black colonies on blood agar.
It is found in the oral cavity, where it is implicated in periodontal disease,[1] as well as in the upper gastrointestinal tract, the respiratory tract and the colon. It has been isolated from women with bacterial vaginosis.[2]
Collagen degradation observed in chronic periodontal disease results in part from the collagenase enzymes of this species. It has been shown in an in vitro study that P. gingivalis can invade human gingival fibroblasts and can survive in the presence of antibiotics.[3] P. gingivalis invades gingival epithelial cells in high numbers, in which case both bacteria and epithelial cells survive for extended periods of time. High levels of specific antibodies can be detected in patients harboring P. gingivalis.
P. gingivalis infection has been linked to Alzheimer's disease[4] and rheumatoid arthritis. It contains the enzyme peptidyl-arginine deiminase, which is involved in citrullination.[5] Patients with rheumatoid arthritis have increased incidence of periodontal disease;[6]antibodies against the bacterium are significantly more common in these patients.[7]
P. gingivalis is divided into K-serotypes based upon capsular antigenicity of the various types.[8] These serotypes have been the drivers of observations regarding bacterial cell to cell interactions to the associated serotype-dependent immune response and risk with pancreatic cancer.[9][10]
https://en.wikipedia.org/wiki/Porphyromonas_gingivalis
Porphyromonadaceae is a family of bacteria.[1][2]
https://en.wikipedia.org/wiki/Porphyromonadaceae
Capnocytophaga canimorsus is a fastidious, slow-growing, Gram-negative rod of the genus Capnocytophaga.[1][2] It is a commensal bacterium in the normal gingival flora of canine and feline species, but can cause illness in humans. Transmission may occur through bites, licks, or even close proximity with animals.[3] C. canimorsus generally has low virulence in healthy individuals,[4]but has been observed to cause severe, even grave, illness in persons with pre-existing conditions.[5] The pathogenesis of C. canimorsus is still largely unknown, but increased clinical diagnoses have fostered an interest in the bacillus. Treatment with antibiotics is effective in most cases, but the most important yet basic diagnostic tool available to clinicians remains the knowledge of recent exposure to canines or felines.[3]
https://en.wikipedia.org/wiki/Capnocytophaga_canimorsus
Tannerella forsythia is an anaerobic, Gram-negative bacterial species of the Cytophaga-Bacteroidetes family. It has been implicated in periodontal diseases and is a member of the red complex of periodontal pathogens.[1][2] T. forsythia was previously named Bacteroides forsythus and Tannerella forsythensis.[3][4][5][6]
Tannerella forsythia was discovered by and named after Dr. Anne Tanner who works at The Forsyth Institute located in Cambridge, Massachusetts.[citation needed]
T. forsythia has been identified in atherosclerotic lesions. Lee et al. found that infecting mice with T. forsythia induced foam cell formation and accelerated the formation of atherosclerotic lesions.[7] It has also been isolated from women with bacterial vaginosis.[8] The presence of oral T. forsythia has been found to be associated with an increased risk of esophageal cancer.[9]
https://en.wikipedia.org/wiki/Tannerella_forsythia
girardia, gardenerellas, chalimidyaes, spiders, spirals, dental oral mucosal bacteria (to bone nervous), spiral and bone teeth, cholera, typhus, ricketts, scurvy, rickettesia, etc..
Bacteroides fragilis is an obligately anaerobic, Gram-negative, rod-shaped bacterium. It is part of the normal microbiota of the human colon and is generally commensal,[1][2] but can cause infection if displaced into the bloodstream or surrounding tissue following surgery, disease, or trauma.[3]
https://en.wikipedia.org/wiki/Bacteroides_fragilis
Chlamydia trachomatis (/kləˈmɪdiə trəˈkoʊmətɪs/), commonly known as chlamydia,[2] is a bacterium that causes chlamydia, which can manifest in various ways, including: trachoma, lymphogranuloma venereum, nongonococcal urethritis, cervicitis, salpingitis, pelvic inflammatory disease. C. trachomatis is the most common infectious cause of blindness and the most common sexually transmitted bacterium.[3]
Different types of C. trachomatis cause different diseases. The most common strains cause disease in the genital tract, while other strains cause disease in the eye or lymph nodes. Like other Chlamydia species, the C. trachomatis life cycle consists of two morphologically distinct life stages: elementary bodies and reticulate bodies. Elementary bodies are spore-like and infectious, whereas reticulate bodies are in the replicative stage and are seen only within host cells.
https://en.wikipedia.org/wiki/Chlamydia_trachomatis
Trachoma is an infectious disease caused by bacterium Chlamydia trachomatis.[2] The infection causes a roughening of the inner surface of the eyelids.[2] This roughening can lead to pain in the eyes, breakdown of the outer surface or cornea of the eyes, and eventual blindness.[2] Untreated, repeated trachoma infections can result in a form of permanent blindness when the eyelids turn inward.[2]
The bacteria that cause the disease can be spread by both direct and indirect contact with an affected person's eyes or nose.[2] Indirect contact includes through clothing or flies that have come into contact with an affected person's eyes or nose.[2] Children spread the disease more often than adults.[2] Poor sanitation, crowded living conditions, and not enough clean water and toilets also increase spread.[2]
Efforts to prevent the disease include improving access to clean water and treatment with antibiotics to decrease the number of people infected with the bacterium.[2] This may include treating, all at once, whole groups of people in whom the disease is known to be common.[3] Washing, by itself, is not enough to prevent disease, but may be useful with other measures.[5] Treatment options include oral azithromycin and topical tetracycline.[3] Azithromycin is preferred because it can be used as a single oral dose.[6] After scarring of the eyelid has occurred, surgery may be required to correct the position of the eyelashes and prevent blindness.[2]
Globally, about 80 million people have an active infection.[4] In some areas, infections may be present in as many as 60–90% of children.[2] Among adults, it more commonly affects women than men – likely due to their closer contact with children.[2] The disease is the cause of decreased vision in 2.2 million people, of whom 1.2 million are completely blind.[2] Trachoma is a public health problem in 44 countries across Africa, Asia, and Central and South America, with 136.9 million people at risk.[2] It results in US$8 billion of economic losses a year.[2] It belongs to a group of diseases known as neglected tropical diseases.[4]
https://en.wikipedia.org/wiki/Trachoma
Chlamydia pneumoniae is a species of Chlamydia, an obligate intracellular bacterium[2] that infects humans and is a major cause of pneumonia. It was known as the Taiwan acute respiratory agent (TWAR) from the names of the two original isolates – Taiwan (TW-183) and an acute respiratory isolate designated AR-39.[3] Briefly, it was known as Chlamydophila pneumoniae, and that name is used as an alternate in some sources.[4] In some cases, to avoid confusion, both names are given.[5]
C. pneumoniae has a complex life cycle and must infect another cell to reproduce; thus, it is classified as an obligate intracellular pathogen. The full genome sequence for C. pneumoniae was published in 1999.[6] It also infects and causes disease in koalas, emerald tree boas (Corallus caninus), iguanas, chameleons, frogs, and turtles.
The first known case of infection with C. pneumoniae was a case of conjunctivitis in Taiwan in 1950. There are no known cases of C. pneumoniae in human history before 1950. This atypical bacterium commonly causes pharyngitis, bronchitis, coronary artery disease and atypical pneumonia in addition to several other possible diseases.[7][8]
https://en.wikipedia.org/wiki/Chlamydia_pneumoniae
Chlamydia psittaci is a lethal intracellular bacterial species that may cause endemic avian chlamydiosis, epizootic outbreaks in mammals, and respiratory psittacosis in humans. Potential hosts include feral birds and domesticated poultry, as well as cattle, pigs, sheep, and horses. C. psittaci is transmitted by inhalation, contact, or ingestion among birds and to mammals. Psittacosis in birds and in humans often starts with flu-like symptoms and becomes a life-threatening pneumonia. Many strains remain quiescent in birds until activated by stress. Birds are excellent, highly mobile vectors for the distribution of chlamydia infection, because they feed on, and have access to, the detritus of infected animals of all sorts.
C. psittaci in birds is often systemic, and infections can be inapparent, severe, acute, or chronic with intermittent shedding.[2][3][4]C. psittaci strains in birds infect mucosal epithelial cells and macrophages of the respiratory tract. Septicaemia eventually develops and the bacteria become localized in epithelial cells and macrophages of most organs, conjunctiva, and gastrointestinal tracts. It can also be passed in the eggs. Stress will commonly trigger onset of severe symptoms, resulting in rapid deterioration and death. C. psittaci strains are similar in virulence, grow readily in cell culture, have 16S rRNA genes that differ by <0.8%, and belong to eight known serotypes. All should be considered to be readily transmissible to humans.
C. psittaci serovar A is endemic among psittacine birds and has caused sporadic zoonotic disease in humans, other mammals, and tortoises. Serovar B is endemic among pigeons, has been isolated from turkeys, and has also been identified as the cause of abortion in herds of dairy cattle. Serovars C and D are occupational hazards for slaughterhouse workers and for people in contact with birds. Serovar E isolates (known as Cal-10, MP or MN) have been obtained from a variety of avian hosts worldwide and, although they were associated with the 1920s–1930s outbreak in humans, a specific reservoir for serovar E has not been identified. The M56 and WC serovars were isolated during outbreaks in mammals. Many C. psittaci strains are susceptible to bacteriophages.
https://en.wikipedia.org/wiki/Chlamydia_psittaci
Lyme disease, also known as Lyme borreliosis, is a vector-borne disease caused by the Borrelia bacterium which is spread by ticks in the genus Ixodes.[2][6][7] The most common sign of infection is an expanding red rash, known as erythema migrans, that appears at the site of the tick bite about a week after it occurred.[1] The rash is typically neither itchy nor painful.[1] Approximately 70–80% of infected people develop a rash.[1] Other early symptoms may include fever, headache and tiredness.[1] If untreated, symptoms may include loss of the ability to move one or both sides of the face, joint pains, severe headaches with neck stiffness, or heart palpitations, among others.[1] Months to years later, repeated episodes of joint pain and swelling may occur.[1] Occasionally, people develop shooting pains or tingling in their arms and legs.[1] Despite appropriate treatment, about 10 to 20% of people develop joint pains, memory problems, and tiredness for at least six months.[1][8]
Lyme disease is transmitted to humans by the bites of infected ticks of the genus Ixodes.[9] In the United States, ticks of concern are usually of the Ixodes scapularis type, and must be attached for at least 36 hours before the bacteria can spread.[10][11] In Europe, Ixodes ricinus ticks may spread the bacteria more quickly.[11][12] In North America, the bacteria Borrelia burgdorferi, B. bissettiae, and B. mayonii cause Lyme disease.[2][13][7] In Europe and Asia, Borrelia afzelii, Borrelia garinii, B. spielmanii, and 4 other species also cause of the disease.[2] The disease does not appear to be transmissible between people, by other animals, or through food.[10] Diagnosis is based upon a combination of symptoms, history of tick exposure, and possibly testing for specific antibodies in the blood.[3][14] Blood tests are often negative in the early stages of the disease.[2] Testing of individual ticks is not typically useful.[15]
Prevention includes efforts to prevent tick bites by wearing clothing to cover the arms and legs, and using DEET or picaridin-based insect repellents.[2][6] Using pesticides to reduce tick numbers may also be effective.[2] Ticks can be removed using tweezers.[16] If the removed tick was full of blood, a single dose of doxycycline may be used to prevent development of infection, but is not generally recommended since development of infection is rare.[2] If an infection develops, a number of antibiotics are effective, including doxycycline, amoxicillin, and cefuroxime.[2]Standard treatment usually lasts for two or three weeks.[2] Some people develop a fever and muscle and joint pains from treatment which may last for one or two days.[2] In those who develop persistent symptoms, long-term antibiotic therapy has not been found to be useful.[2][17]
Lyme disease is the most common disease spread by ticks in the Northern Hemisphere.[18] It is estimated to affect 300,000 people a year in the United States and 65,000 people a year in Europe.[2][19] Infections are most common in the spring and early summer.[2] Lyme disease was diagnosed as a separate condition for the first time in 1975 in Lyme, Connecticut.[20] It was originally mistaken for juvenile rheumatoid arthritis.[21] The bacterium involved was first described in 1981 by Willy Burgdorfer.[22] Chronic symptoms following treatment are well described and are known as "post-treatment Lyme disease syndrome" (PTLDS).[17] PTLDS is different from chronic Lyme disease, a term no longer supported by the scientific community and used in different ways by different groups.[17][23] Some healthcare providers claim that PTLDS is caused by persistent infection, but this is not believed to be true because no evidence of persistent infection can be found after standard treatment.[24] A vaccine for Lyme disease was marketed in the United States between 1998 and 2002, but was withdrawn from the market due to poor sales.[2][25][26] Research is ongoing to develop new vaccines.[2]
https://en.wikipedia.org/wiki/Lyme_disease
https://en.wikipedia.org/wiki/Leptospira
Taxonomy ID: 171 (for references in articles please use NCBI:txid171)
NCBI BLAST name: bacteria
Rank: genus
Genetic code: Translation table 11 (Bacterial, Archaeal and Plant Plastid)
- Lineage( full )
- cellular organisms; Bacteria; Spirochaetes; Spirochaetia; Leptospirales; Leptospiraceae
G66
https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=171
- Althouse BM, Hébert-Dufresne L (October 2014). "Epidemic cycles driven by host behaviour". Journal of the Royal Society, Interface. 11 (99): 20140575. doi:10.1098/rsif.2014.0575. PMC 4235258. PMID 25100316.
https://en.wikipedia.org/wiki/Treponema_pallidum
Table 11 is used for Bacteria, Archaea, prokaryotic viruses and chloroplast proteins. As in the standard code, initiation is most efficient at AUG. In addition, GUG and UUG starts are documented in Archaea and Bacteria (Kozak 1983, Fotheringham et al. 1986, Golderer et al. 1995, Nolling et al. 1995, Sazuka & Ohara 1996, Genser et al. 1998, Wang et al. 2003). In E. coli, UUG is estimated to serve as initiator for about 3% of the bacterium's proteins (Blattner et al. 1997). CUG is known to function as an initiator for one plasmid-encoded protein (RepA) in Escherichia coli (Spiers and Bergquist, 1992). In addition to the NUG initiations, in rare cases Bacteria can initiate translation from an AUU codon as e.g. in the case of poly(A) polymerase PcnB and the InfC gene that codes for translation initiation factor IF3 (Polard et al. 1991, Liveris et al. 1993, Sazuka & Ohara 1996, Binns & Masters 2002). The internal assignments are the same as in the standard code though UGA codes at low efficiency for Trp in Bacillus subtilis and, presumably, in Escherichia coli (Hatfiled and Diamond, 1993).
https://www.ncbi.nlm.nih.gov/Taxonomy/taxonomyhome.html/index.cgi?chapter=cgencodes#SG11
| Leptospira ognonensis Lineage: Bacteria[31753]; Spirochaetes[307]; Leptospirales[80]; Leptospiraceae[79]; Leptospira[66]; Leptospira ognonensis[1] |
https://www.ncbi.nlm.nih.gov/genome/78288
| Leptospira perdikensis Lineage: Bacteria[31753]; Spirochaetes[307]; Leptospirales[80]; Leptospiraceae[79]; Leptospira[66]; Leptospira perdikensis[1] |
https://www.ncbi.nlm.nih.gov/genome/78276
| Leptospira saintgironsiae Lineage: Bacteria[31753]; Spirochaetes[307]; Leptospirales[80]; Leptospiraceae[79]; Leptospira[66]; Leptospira saintgironsiae[1] |
https://www.ncbi.nlm.nih.gov/genome/74150
LIC20035 of Leptospira interrogans was characterized as a surface exposed adhesin that binds host extracellular matrix components. Orthologs appear restricted to the genus Leptospira. Member proteins average about 430 residues in length, much of which consists of repeats. All members are predicted lipoproteins.
FEATURES Location/Qualifiers source 1..428 /organism="Leptospira sp. B5-022" /db_xref="taxon:1242992" Protein 1..428 /product="LIC20035 family adhesin" /calculated_mol_wt=47970 Region 136..391 /region_name="YwqK" /note="Antitoxin component YwqK of the YwqJK toxin-antitoxin module [Defense mechanisms]; COG2849" /db_xref="CDD:225405" ORIGIN 1 mkkilstavs islligcsst svvenkgkaa efqilepnir vekfketfnl kaegpvklec
https://www.ncbi.nlm.nih.gov/Structure/cdd/cddsrv.cgi?uid=411195
Leptospira kirschneriTaxonomy ID: 29507 (for references in articles please use NCBI:txid29507)NCBI BLAST name: bacteria Rank: species Genetic code: Translation table 11 (Bacterial, Archaeal and Plant Plastid) |
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Comments and References:
 | Ramadass P et al. (1992) Ramadass, P., Jarvis, B.D., Corner, R.J., Penny, D., and Marshall, R.B. "Genetic characterization of pathogenic Leptospira species by DNA hybridization." Int. J. Syst. Bacteriol. (1992) 42:215-219. https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=29507&lvl=3&lin=f&keep=1&srchmode=1&unlock
Comments and References:
External Information Resources (NCBI LinkOut) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=29507&lvl=3&lin=f&keep=1&srchmode=1&unlock
Above. Porcelain and the Tramps - Transparent
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