08-24-2021-0732 - Petersen Wade HIV-AIDS Stage V Toxoplasmosis and EIV - Swelling ref. bel. - infectivity potency increase
Equine infectious anemia or equine infectious anaemia (EIA), also known by horsemen as swamp fever, is a horse disease caused by a retrovirus (Equine infectious anemia virus) and transmitted by bloodsucking insects. The virus (EIAV) is endemic in the Americas, parts of Europe, the Middle and Far East, Russia, and South Africa. The virus is a lentivirus, like human immunodeficiency virus (HIV). Like HIV, EIA can be transmitted through blood, milk, and body secretions. Transmission is primarily through biting flies, such as the horse-fly and deer-fly.[1] The virus survives up to 4 hours in the vector. Contaminated surgical equipment and recycled needles and syringes, and bits[2] can transmit the disease. Mares can transmit the disease to their foals via the placenta. The risk of transmitting the disease is greatest when an infected horse is ill, as the blood levels of the virus are then highest.
Stages[edit]
Acute: The acute form is a sudden onset of the disease at full-force. Symptoms include high fever, anemia (due to the breakdown of red blood cells), weakness, swelling of the lower abdomen and legs, weak pulse, and irregular heartbeat. The horse may die suddenly.
Subacute: A slower, less severe progression of the disease. Symptoms include recurrent fever, weight loss, an enlarged spleen (felt during a rectal examination), anemia, and swelling of the lower chest, abdominal wall, penile sheath, scrotum, and legs.
Chronic: The horse tires easily and is unsuitable for work. The horse may have a recurrent fever and anemia, and may relapse to the subacute or acute form even several years after the original attack.
A horse may also not appear to have any symptoms, yet still tests positive for EIA antibodies. Such a horse can still pass on the disease. According to most veterinarians, horses diagnosed EIA positive usually do not show any sign of sickness or disease.
EIA may cause abortion in pregnant mares. This may occur at any time during the pregnancy if there is a relapse when the virus enters the blood. Most infected mares will abort, however some give birth to healthy foals. Foals are not necessarily infected.
Studies indicate that there are breeds with a tolerance to EIA.[3]
Recent studies in Brazil on living wild horses have shown that in the Pantanal, about 30% of domesticated and about 5.5% of the wild horses are chronically infected with EIA.[4]
The Coggins test (agar immunodiffusion) is a sensitive diagnostic test for equine infectious anemia developed by Dr. Leroy Coggins in the 1970s.
Currently, the US does not have an eradication program due to the low rate of incidence. However, many states require a negative Coggins test for interstate travel. In addition, most horse shows and events require a negative Coggins test. Most countries require a negative test result before allowing an imported horse into the country.
Horse owners should verify that all the horses at a breeding farm and or boarding facility have a negative Coggins test before using the services of the facility. A Coggins test should be done on an annual basis. Tests every 6 months are recommended if there is increased traveling.
https://en.wikipedia.org/wiki/Equine_infectious_anemia
MALARIA, BLOOD CELL PARASITE, SLUDGE BLUD ANEKS/ANEMIATION/ANEMETICS/DYSEQUILS/ETC.
LEUKEMIATION LEUKEMIA
ATROPHY OR HYPERTROPHY ANABOLIC OR CATABOLIC
INFECTIOUS OR NON INFECTIOUS
DESIGNER DISEASE OR NON DESIGNER; ANY EQUAL OR NO EQUAL TO DESIGNER
CL1 METHROXYTREATE/METHROX/Methotrexate/AMPHOTERIN/PTERINS/ETC.
LARGE DNA VIRUS WITH 100PSO, LENTIVIRIDAE, ETC.
TUBERCULOSIS BACILLUS THURIGS
MACROPHATE/MACROPHAGULANTS/PHAGE/PHAGULANT ETC., LEUKOCYTE, THYMUS, SPLEEN, BONE BONE BONE BONE BRAIN BONE EYE.
DISEASE REQ FOR SUSTENANCE, FRAGMENTATIVE CAPACITY, ESSENTIAL NUTRIENT FOR REGENERATION SPORULANTS, FANCY FUNGI, SCALE. TRANS CAP. ENV ANY. ANAEROBIC PHOSPHOR, NUCLEAR, PARTICULATE. ACID LOVING; POTENCY WITH ALKALIZATION SUSTENANCE BY N-FIELD to cat-t.
SEWER-WATER-CROP REACTIVE SYNERGISM; LEAD TOLERANCE; RADIOACTIVE HIGH TOLERANCE; SUSPENSION ENDURANCE; AEROSOL TRANSMISSION; SURVIVAL THROUGH PARTICULARIZATION/SCALE/SIZE (PARTICLE F-IM); ETC.
APE-DISE; MIDDLE EAST DIS RECEP-ACQ; INC PRISON MIXES. BROWN RECEPTION.
ENDOGENOUS RETROVIRAL CAPACITY; REACTIVATION OF DISEASE; INTERACTION SYNERGY WITH ENDOGEN VIRIDAE PRESENT PREEXISTANT; COASSIMILATION WITH AUGMENTATION CHANGE ACCRUUALS CHANGE INVERSION TOLERANCE ETC.
Liposomal amphotericin B was significantly more effective than amphotericin B deoxycholate for the treatment of moderate to severe disseminated histoplasmosis in patients with AIDS, with 88% and 64% of patients, respectively, having a successful response.
https://pubmed.ncbi.nlm.nih.gov/19275278/
Simian immunodeficiency virus (SIV) is a species of retrovirus that cause persistent infections in at least 45 species of African non-human primates.[1][2] Based on analysis of strains found in four species of monkeys from Bioko Island, which was isolated from the mainland by rising sea levels about 11,000 years ago, it has been concluded that SIV has been present in monkeys and apes for at least 32,000 years, and probably much longer.[3][4]
Virus strains from two of these primate species, SIVsmm in sooty mangabeys and SIVcpz in chimpanzees, are believed to have crossed the species barrier into humans, resulting in HIV-2 and HIV-1 respectively, the two human immunodeficiency viruses. The most likely route of transmission of HIV-1 to humans involves contact with the blood of chimps that are often hunted for bushmeat in Africa. Four subtypes of HIV-1 (M, N, O, and P) likely arose through four separate transmissions of SIV to humans, and the resulting HIV-1 group M strain most commonly infects people worldwide.[5][6] Therefore, it is theorized that SIV may have previously crossed the species barrier into human hosts multiple times throughout history, but it was not until recently, after the advent of modern transportation and global commuterism, that it finally took hold, spreading beyond localized decimations of a few individuals or single small tribal populations.
Unlike HIV-1 and HIV-2 infections in humans, SIV infections in their natural African simian non-human hosts appear in many cases to be non-pathogenic due to evolutionary adaptation of the hosts to the virus. Extensive studies in sooty mangabeys have established that SIVsmm infection does not cause any disease in these African primates, despite high levels of circulating virus. However, if the virus infects an Asian or Indian rhesus macaque, these non-African simian primates will also develop simian AIDS (SAIDS), as they, like humans (despite being an African-origin simian primate species), have not had a prolonged history with the virus.[7] A recent[when?] study of SIVcpz in wild living chimpanzees suggests that infected chimpanzees experience an AIDS-like illness similar to HIV-1 infected humans. The later stages of SIV infection turn into SAIDS, much as HIV infection turns into AIDS.
https://en.wikipedia.org/wiki/Simian_immunodeficiency_virus
Methotrexate (MTX), formerly known as amethopterin, is a chemotherapy agent and immune-system suppressant.[4] It is used to treat cancer, autoimmune diseases, and ectopic pregnancy and for medical abortions.[4] Types of cancers it is used for include breast cancer, leukemia, lung cancer, lymphoma, gestational trophoblastic disease, and osteosarcoma.[4] Types of autoimmune diseases it is used for include psoriasis, rheumatoid arthritis, and Crohn's disease.[4] It can be given by mouth or by injection.[4]
Common side effects include nausea, feeling tired, fever, increased risk of infection, low white blood cell counts, and breakdown of the skin inside the mouth.[4] Other side effects may include liver disease, lung disease, lymphoma, and severe skin rashes.[4] People on long-term treatment should be regularly checked for side effects.[4] It is not safe during breastfeeding.[4] In those with kidney problems, lower doses may be needed.[4] It acts by blocking the body's use of folic acid.[4]
Methotrexate was first made in 1947 and initially was used to treat cancer, as it was less toxic than the then current treatments.[7] In 1956 it provided the first cures of a metastatic cancer.[8] It is on the World Health Organization's List of Essential Medicines, the safest and most effective medicines needed in a health system.[9] Methotrexate is available as a generic medication.[4] In 2018, it was the 123rd most commonly prescribed medication in the United States, with more than 5 million prescriptions.[10][11]
https://en.wikipedia.org/wiki/Methotrexate
Caprine arthritis encephalitis virus (CAEV) is a retrovirus which infects goats and cross-reacts immunologicallywith HIV,[1] due to being from the same family of viruses.[2] CAEV cannot be transmitted to humans, including through the consumption of milk from an infected goat.[3] There is no evidence that CAEV can cure HIV in humans.[2][4]
CAEV is commonly transferred within the goat species by ingestion of colostrum or milk from an infected goat, and to a less extent, cross species CAEV transfer by sheep is possible.[3][5]
https://en.wikipedia.org/wiki/Caprine_arthritis_encephalitis_virus
Lentivirus is a genus of retroviruses that cause chronic and deadly diseases characterized by long incubation periods, in the human and other mammalian species.[1] The best known lentivirus is the human immunodeficiency virus (HIV), which causes AIDS. Lentiviruses are also hosted in apes, cows, goats, horses, cats, and sheep.[1]Recently, lentiviruses have been found in monkeys, lemurs, Malayan flying lemur (neither a true lemur nor a primate), rabbits, and ferrets. Lentiviruses and their hosts have worldwide distribution. Lentiviruses can integrate a significant amount of viral cDNA into the DNA of the host cell and can efficiently infect nondividing cells, so they are one of the most efficient methods of gene delivery.[2] Lentiviruses can become endogenous (ERV), integrating their genome into the host germline genome, so that the virus is henceforth inherited by the host's descendants.
https://en.wikipedia.org/wiki/Lentivirus
Jaagsiekte sheep retrovirus (JSRV) is a betaretrovirus which is the causative agent of a contagious lung cancer in sheep, called ovine pulmonary adenocarcinoma.
https://en.wikipedia.org/wiki/Jaagsiekte_sheep_retrovirus
The human T-lymphotropic virus, human T-cell lymphotropic virus, or human T-cell leukemia-lymphoma virus (HTLV) family of viruses are a group of human retroviruses that are known to cause a type of cancer called adult T-cell leukemia/lymphoma and a demyelinating disease called HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLVs belong to a larger group of primate T-lymphotropic viruses (PTLVs). Members of this family that infect humans are called HTLVs, and the ones that infect Old World monkeys are called Simian T-lymphotropic viruses (STLVs). To date, four types of HTLVs (HTLV-1, HTLV-2, HTLV-3, and HTLV-4) and four types of STLVs (STLV-1, STLV-2, STLV-3, and STLV-5) have been identified. HTLV types HTLV-1 and HTLV-2 viruses are the first retroviruses discovered. Both belong to the oncovirus subfamily of retroviruses and can transform human lymphocytes so that they are self-sustaining in vitro.[1] The HTLVs are believed to originate from interspecies transmission of STLVs. The HTLV-1 genome is diploid, composed of two copies of a single-stranded RNA virus whose genome is copied into a double-stranded DNA form that integrates into the host cell genome, at which point the virus is referred to as a provirus. A closely related virus is bovine leukemia virus BLV. The original name for HIV, the virus that causes AIDS, was HTLV-3.
https://en.wikipedia.org/wiki/Human_T-lymphotropic_virus
Visna virus (also known as Visna-maedi virus, Maedi-visna virus and Ovine lentivirus[1]) from the genusLentivirus and subfamily Orthoretrovirinae, is a "prototype"[2] retrovirus[3] that causes encephalitis and chronic pneumonitis in sheep.[4] It is known as visna when found in the brain, and maedi when infecting the lungs. Lifelong, persistent infections in sheep occur in the lungs, lymph nodes, spleen, joints, central nervous system, and mammary glands;[2][5] The condition is sometimes known as "ovine progressive pneumonia" (OPP), particularly in the United States,[1] or "Montana sheep disease".[6] White blood cells of the monocyte/macrophage lineage are the main target of visna virus.[7]
https://en.wikipedia.org/wiki/Visna-maedi_virus
Treponema pallidum is a spirochaete bacterium with various subspecies that cause the diseases syphilis, bejel, and yaws. It is transmitted only amongst humans.[1] It is a helically coiled microorganism usually 6–15 μm long and 0.1–0.2 μm wide.[2] T. pallidum's lack of either tricarboxylic acid cycle or oxidative phosphorylation results in minimal metabolic activity.[3] The treponemes have a cytoplasmic and an outer membrane. Using light microscopy, treponemes are visible only by using dark field illumination. Treponema pallidum consists of three subspecies, T. p. pallidum, T. p. endemicum, and T. p. pertenue, each of which has a distinct associated disease.[4]
https://en.wikipedia.org/wiki/Treponema_pallidum
Acute lymphoblastic leukemia (ALL) is a cancer of the lymphoid line of blood cells characterized by the development of large numbers of immature lymphocytes.[1] Symptoms may include feeling tired, pale skin color, fever, easy bleeding or bruising, enlarged lymph nodes, or bone pain.[1] As an acute leukemia, ALL progresses rapidly and is typically fatal within weeks or months if left untreated.[11]
In most cases, the cause is unknown.[2] Genetic risk factors may include Down syndrome, Li-Fraumeni syndrome, or neurofibromatosis type 1.[1] Environmental risk factors may include significant radiation exposure or prior chemotherapy.[1] Evidence regarding electromagnetic fields or pesticides is unclear.[4][6] Some hypothesize that an abnormal immune response to a common infection may be a trigger.[4] The underlying mechanism involves multiple genetic mutations that results in rapid cell division.[2] The excessive immature lymphocytes in the bone marrow interfere with the production of new red blood cells, white blood cells, and platelets.[1] Diagnosis is typically based on blood tests and bone marrow examination.[3]
ALL is typically treated initially with chemotherapy aimed at bringing about remission.[2] This is then followed by further chemotherapy typically over a number of years.[2] Treatment usually also include intrathecal chemotherapy since systemic chemotherapy can have limited penetration into the central nervous system and the central nervous system is a common site for relapse of acute lymphoblastic leukemia. [12][13]
Treatment can also include radiation therapy if spread to the brain has occurred.[2] Stem cell transplantation may be used if the disease recurs following standard treatment.[2] Additional treatments such as Chimeric antigen receptor T cell immunotherapy are being used and further studied.[2]
ALL affected about 876,000 people globally in 2015 and resulted in about 111,000 deaths.[14][10] It occurs most commonly in children, particularly those between the ages of two and five.[15][4] In the United States it is the most common cause of cancer and death from cancer among children.[2] ALL is notable for being the first disseminated cancer to be cured.[16] Survival for children increased from under 10% in the 1960s to 90% in 2015.[2] Survival rates remain lower for babies (50%)[17] and adults (35%).[8] According to the National Cancer Intelligence Network (NCIN), generally for people with ALL: around 70 out of 100 people (70%) will survive their leukemia for 5 years or more after they are diagnosed.
Rare mutations in ETV6 and PAX5 are associated with a familial form of ALL with autosomal dominant patterns of inheritance.[2]
https://en.wikipedia.org/wiki/Acute_lymphoblastic_leukemia
Acute myeloid leukemia (AML) is a cancer of the myeloid line of blood cells, characterized by the rapid growth of abnormal cells that build up in the bone marrow and blood and interfere with normal blood cell production.[1] Symptoms may include feeling tired, shortness of breath, easy bruising and bleeding, and increased risk of infection.[1] Occasionally, spread may occur to the brain, skin, or gums.[1] As an acute leukemia, AML progresses rapidly, and is typically fatal within weeks or months if left untreated.[1]
Risk factors include smoking, previous chemotherapy or radiation therapy, myelodysplastic syndrome, and exposure to the chemical benzene.[1] The underlying mechanism involves replacement of normal bone marrow with leukemia cells, which results in a drop in red blood cells, platelets, and normal white blood cells.[1] Diagnosis is generally based on bone marrow aspiration and specific blood tests.[3] AML has several subtypes for which treatments and outcomes may vary.[1]
The first-line treatment of AML is usually chemotherapy, with the aim of inducing remission.[1] People may then go on to receive additional chemotherapy, radiation therapy, or a stem cell transplant.[1][3]The specific genetic mutations present within the cancer cells may guide therapy, as well as determine how long that person is likely to survive.[3]
In 2015, AML affected about one million people, and resulted in 147,000 deaths globally.[4][5] It most commonly occurs in older adults.[2] Males are affected more often than females.[2] The five-year survival rate is about 35% in people under 60 years old and 10% in people over 60 years old.[3] Older people whose health is too poor for intensive chemotherapy have a typical survival of five to ten months.[3] It accounts for roughly 1.1% of all cancer cases, and 1.9% of cancer deaths in the United States.[2]
https://en.wikipedia.org/wiki/Acute_myeloid_leukemia
Tumor lysis syndrome is a group of metabolic abnormalities that can occur as a complication during the treatment of cancer,[1] where large amounts of tumor cells are killed off (lysed) at the same time by the treatment, releasing their contents into the bloodstream. This occurs most commonly after the treatment of lymphomas and leukemias. In oncology and hematology, this is a potentially fatal complication, and patients at increased risk for TLS should be closely monitored before, during, and after their course of chemotherapy.
Tumor lysis syndrome is characterized by high blood potassium (hyperkalemia), high blood phosphate (hyperphosphatemia), low blood calcium (hypocalcemia), high blood uric acid (hyperuricemia), and higher than normal levels of blood urea nitrogen (BUN) and other nitrogen-containing compounds (azotemia). These changes in blood electrolytes and metabolites are a result of the release of cellular contents of dying cells into the bloodstream from breakdown of cells. In this respect, TLS is analogous to rhabdomyolysis, with comparable mechanism and blood chemistry effects but with different cause. In TLS, the breakdown occurs after cytotoxic therapy or from cancers with high cell turnover and tumor proliferation rates. The metabolic abnormalities seen in tumor lysis syndrome can ultimately result in nausea and vomiting, but more seriously acute uric acid nephropathy, acute kidney failure, seizures, cardiac arrhythmias, and death.[2][3]
Treatment is first targeted at the specific metabolic disorder.
Acute kidney failure prior to chemotherapy. Since the major cause of acute kidney failure in this setting is uric acid build-up, therapy consists of rasburicase to wash out excessive uric acid crystals as well as a loop diuretic and fluids. Sodium bicarbonate should not be given at this time. If the patient does not respond, hemodialysis may be instituted, which is very efficient in removing uric acid, with plasma uric acid levels falling about 50% with each six-hour treatment.[citation needed]
Acute kidney failure after chemotherapy. The major cause of acute kidney failure in this setting is hyperphosphatemia, and the main therapeutic means is hemodialysis. Forms of hemodialysis used include continuous arteriovenous hemodialysis (CAVHD), continuous venovenous hemofiltration (CVVH), or continuous venovenous hemodialysis (CVVHD).
https://en.wikipedia.org/wiki/Tumor_lysis_syndrome
Human T-
https://rarediseases.info.nih.gov/diseases/9645/human-t-cell-leukemia-virus-type-1
FeLV is an enveloped RNA virus that belongs to the genus Gammaretrovirus of the family Retroviridae. FeLV infection remains an important cause of mortality in domestic cats through its ability to cause immune suppression, bone marrow disorders, and hematopoietic neoplasia. FeLV also causes disease in wild felids such as the highly endangered Iberian lynx.2
FeLV infection progresses more rapidly than FIV infection and is more pathogenic, so most cats that develop progressive infections ultimately die of FeLV-related disease. However, in contrast to FIV infection, many cats in the early state of FeLV infection regress to a permanent state of viral latency (“regressive infection”). It is possible that some cats, after exposure to a low dose of FeLV, may eliminate the infection altogether (“abortive infection”), although this appears to be a rare outcome. Regardless, a positive test result for FeLV infection in an apparently healthy cat does not always imply that FeLV-related disease and mortality will occur.
The structure of FeLV is similar to that of FIV, except that the capsid is icosahedral rather than cone shaped (Figure 22-1 ). There are three main subtypes of FeLV: FeLV-A, FeLV-B, and FeLV-C. Each subtype uses a different receptor to enter cells (Table 22-1 ). All cats infected with FeLV-B and FeLV-C are co-infected with FeLV-A, and only FeLV-A is transmitted between animals. FeLV-B and FeLV-C are more pathogenic than FeLV-A. FeLV-B arises through recombination of FeLV-A proviral DNA with endogenous FeLV sequences present in host cellular DNA.3 FeLV-C arises from accumulation of mutations or insertions in the env (SU) gene of FeLV-A.4., 5. The FeLV subtype influences the clinical expression of disease (see Table 22-1). For example, FeLV-C is associated with nonregenerative anemia. Even within an FeLV subtype, mutations in the SU and the LTR regions of the viral genome affect disease outcome.6., 7. An additional subtype, FeLV-T, has been associated with immunodeficiency.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7152252/
Feline leukemia virus (FeLV) is a retrovirus that infects cats. FeLV can be transmitted from infected cats when the transfer of saliva or nasal secretions is involved. If not defeated by the animal's immune system, the virus weakens the cat's immune system which can lead to diseases which can be lethal. Because FeLV is cat-to-cat contagious, FeLV+ cats should only live with other FeLV+ cats.
FeLV is categorized into four subgroups, A, B, C and T. An infected cat has a combination of FeLV-A and one or more of the other subgroups.[2][3] Symptoms, prognosis and treatment are all affected by subgroup.[2]
FeLV+ cats often have a shorter lifespan, but can still live "normal", healthy lives.[4]
Once the virus has entered the cat, there are six stages to a FeLV infection[citation needed]:
- Stage One: The virus enters the cat, usually through the pharynx where it infects the epithelial cells and infects the tonsilar B-lymphocytes and macrophages. These white blood cells then filter down to the lymph nodes and begin to replicate.
- Stage Two: The virus enters the blood stream and begins to distribute throughout the body.
- Stage Three: The lymphoid system (which produces antibodies to attack infected and cancerous cells) becomes infected, with further distribution throughout the body.
- Stage Four: The main point in the infection- where the virus can take over the body's immune system and cause viremia. During this stage the hemolymphatic system and intestines become infected.
If the cat's immune system does not fight off the virus, then it progresses to:
- Stage Five: The bone marrow becomes infected. At this point, the virus will stay with the cat for the rest of its life. In this phase, the virus replicates and is released four to seven days later in infected neutrophils, and sometimes lymphocytes, monocytes, and eosinophils (all white blood cells formed in the bone marrow).
- Stage Six: The cat's body is overwhelmed by infection and mucosal and glandular epithelial cells (tissue that forms a thin protective layer on exposed bodily surfaces and forms the lining of internal cavities, ducts, and organs) become infected. The virus replicates in epithelial tissues including salivary glands, oropharynx, stomach, esophagus, intestines, trachea, nasopharynx, renal tubules, bladder, pancreas, alveolar ducts, and sebaceous ducts from the muzzle.
https://en.wikipedia.org/wiki/Feline_leukemia_virus
Bacillus thuringiensis (or Bt) is a Gram-positive, soil-dwelling bacterium, the most commonly used biological pesticide worldwide. B. thuringiensis also occurs naturally in the gut of caterpillars of various types of moths and butterflies, as well on leaf surfaces, aquatic environments, animal feces, insect-rich environments, and flour mills and grain-storage facilities.[1][2] It has also been observed to parasitize other moths such as Cadra calidella—in laboratory experiments working with C. calidella, many of the moths were diseased due to this parasite.[3]
During sporulation, many Bt strains produce crystal proteins (proteinaceous inclusions), called delta endotoxins, that have insecticidal action. This has led to their use as insecticides, and more recently to genetically modified crops using Bt genes, such as Bt corn.[4] Many crystal-producing Bt strains, though, do not have insecticidal properties.[5] The subspecies israelensis is commonly used for control of mosquitoes[6] and of fungus gnats.[7]
As a toxic mechanism, cry proteins bind to specific receptors on the membranes of mid-gut (epithelial) cells of the targeted pests, resulting in their rupture. Other organisms (including humans, other animals and non-targeted insects) that lack the appropriate receptors in their gut cannot be affected by the cry protein, and therefore are not affected by Bt.[8][9]
https://en.wikipedia.org/wiki/Bacillus_thuringiensis
betaretrovirus, FeLV, HTLV-1, TLS, SIV, human T-cell leukemia-lymphoma virus (HTLV), VISNA LENTIVIRI, CAPRINE-OVINE, Equine infectious anemia virus) and transmitted by insects EIAV. Methroxetrate.
bacillus thurig GRam positive
+ssDNA, +sDNA +sRNA +ssRNA +xyz *** -DNA ---DNA --RNA
Viri Genome
Bone decay
100Centillion folding exponential per scale unit yoct expo etc.
zero setters fold
time ben scal non-time
no quartz to measure; no middle east copper to carry; no powder to kill
disease transform time strain self shed
force and intermolecular fraction by hole, or ripture
yocto field; nano field
Hole for Gangrene sulfur and phosphorous acid tolerant enth/heat/temp/entro/etc. Earth-Univ Cond any manner of approach-presentation; growth trained/shaped/etc.
Matrix netting, biofilming of cellular composition of human body (wet matrix tissufication of human previou so)
Junction expansion; Particle incorporation deprecation adherance reduction force typing
Helpless innocent hostage bacteria/life/existence (known, unknown)/etc. Want to Kill USA, amcan, methroxetrate, earth, etc..
Tuesday, August 24, 2021
08-24-2021-0839 - Evolutionary Grade
In alpha taxonomy, a grade is a taxon united by a level of morphological or physiologicalcomplexity. The term was coined by British biologist Julian Huxley, to contrast with clade, a strictly phylogenetic unit.[1]
An evolutionary grade is a group of species united by morphological or physiological traits, that has given rise to another group that has major differences from the ancestral condition, and is thus not considered part of the ancestral group, while still having enough similarities that we can group them under the same clade. The ancestral group will not be phylogenetically complete (i.e. will not form a clade), so will represent a paraphyletic taxon.
In order to fully understand evolutionary grades, one must first get a better understanding of Phylogenetics, defined as "In biology, is the study of the evolutionary history and relationships among individuals or groups of organisms (e.g. species, or populations). These relationships are discovered through phylogenetic inference methods that evaluate observed heritable traits, such as DNA sequences or morphology under a model of evolution of these traits"
The most commonly cited example is that of reptiles. In the early 19th century, the French naturalist Latreille was the first to divide tetrapods into the four familiar classes of amphibians, reptiles, birds, and mammals.[2] In this system, reptiles are characterized by traits such as laying membranous or shelled eggs, having skin covered in scales or scutes, and having a 'cold-blooded' metabolism. However, the ancestors of mammals and birds also had these traits and so birds and mammals can be said to "have evolved from reptiles", making the reptiles, when defined by these traits, a grade rather than a clade.[3] In microbiology, taxa that are thus seen as excluded from their evolutionary grade parent group are called taxa in disguise.[4]
Paraphyletic taxa will often, but not always, represent evolutionary grades. In some cases paraphyletic taxa are united simply by not being part of any other groups, and give rise to so-called wastebasket taxa which may even be polyphyletic.
Grades in systematics[edit]
The traditional Linnaean way of defining taxa is through the use of anatomical traits. When the actual phylogenetic relationship is unknown, well defined groups sometimes turn out to be defined by traits that are primitive rather than derived. In Linnaean systematics, evolutionary grades are accepted in higher taxonomic ranks, though generally avoided at family level and below. In phylogenetic nomenclature evolutionary grades (or any other form of paraphyly) are not accepted.[5]
Where information about phylogenetic relationships is available, organisms are preferentially grouped into clades. Where data is lacking, or groups of uncertain relationship are to be compared, the cladistic method is limited and grade provides a useful tool for comparing organisms. This is particularly common in palaeontology, where fossilsare often fragmentary and difficult to interpret. Thus, traditional palaeontological works are often using evolutionary grades as formal or informal taxa, including examples such as labyrinthodonts, anapsids, synapsids, dinosaurs, ammonites, eurypterids, lobopodians and many of the more well known taxa of human evolution. Organizing organisms into grades rather than strict clades can also be very useful to understand the evolutionary sequence behind major diversification of both animals[6] and plants.[7]
Evolutionary grades, being united by gross morphological traits, are often eminently recognizable in the field. While taxonomy seeks to eliminate paraphyletic taxa, such grades are sometimes kept as formal or informal groups on the basis of their usefulness for laymen and field researchers.[5] In bacteriology, the renaming of species or groups that turn out to be evolutionary grades is kept to a minimum to avoid misunderstanding, which in the case of pathogens could have fatal consequences. When referring to a group of organisms, the term "grade" is usually enclosed in quotation marks to denote its status as a paraphyletic term.
Grades and phylogenetic nomenclature[edit]
With the rise of phylogenetic nomenclature, the use of evolutionary grades as formal taxa has come under debate. Under a strict phylogenetic approach, only monophyletic taxa are recognized.[8] This differs from the more traditional approach of evolutionary taxonomy.[9] The difference in approach has led to a vigorous debate between proponents of the two approaches to taxonomy, particularly in well established fields like vertebrate palaeontology and botany.[10] The difference between the statement "B is part of A" (phylogenetic approach) and "B has evolved from A" (evolutionary approach) is, however, one of semantics rather than of phylogeny. Both express the same phylogeny, but the former emphasizes the phylogenetic continuum while the latter emphasizes a distinct shift in anatomy or ecology in B relative to A.
Examples[edit]
- Fish represent a grade, inasmuch as they have given rise to the land vertebrates. In turn, the three traditional classes of fish (Agnatha, Chondrichthyesand Osteichthyes) all represent evolutionary grades.[11]
- Amphibians in the biological sense (including the extinct Labyrinthodonts) represent a grade, since they are also the ancestors of the amniotes.[11]
- Reptiles represent a grade composed of the cold-blooded amniotes; this excludes birds and mammals.[3]
- Dinosaurs were proposed to be the ancestors of birds as early as the 1860s.[12] Yet the term sees popular use as an evolutionary grade excluding birds, though most scientists use a monophyletic Dinosauria.
- Lizards represent an evolutionary grade, defined by their retention of limbs relative to snakes and amphisbaenians.[13] However, defining lizards by the presence of limbs is incorrect, as there are many species of legless lizards, which are considered true lizards.
- Green algae represent a grade, since they are the ancestors of land plants.
- Prokaryotes, which include cellular organisms lacking a nucleus, represent a grade, since they are the ancestors of eukaryotes, which includes animals, plants, fungi, and protists; and the last of these four groups also represents a grade, since it excludes the previous three groups.
- Crustaceans represent a grade, since they are the ancestors of hexapods, which includes insects and related taxa.
- Monkeys represent a grade, since they include the ancestors of apes (including humans).
- Likewise, apes represent a grade in common usage, but are a clade if humans are included.
https://en.wikipedia.org/wiki/Evolutionary_grade
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