Decay Matter induction
FPoisidon
Alkylation, Nuclearization, Nuc Tag, Intercalation, Modification of STD biochem.
Leukemiaes, RAdiation induction, Immunosuppression, Cell Signal dysf ind env, dysregs, fungies.
Env - fungies murcomycotics mycobacteriaes bacteriophagulants
Viridaes - Fungal gene encode, carry sustain fragment to build
Bacteriaes - viridae encombants, helping make stuff from/etc. virus
fungal leukemiaes
murcomycotics mycotics fpo hydropo envstddissem air-sporeluant/viridae friendly
viridaes - SIVA, SIV, HEVA, HIVS, HIV, HI-R-us
Autoimmune prolif syndrom; acute myeloblasia lukes
fungal leukemiaes (blood parasite threads and fungees where decay matters)
Carbonaceous Chondrites eaters
props hydrags for dis emr and emf
As nitric acid was added to a column containing an ion-exchange resin and americium, the chemicals exploded, blowing out "pieces of glass and plastic" (plexiglass[4]) from the glove box.[2] Harold McCluskey was exposed to at least 37 MBq of americium-241 and nitric acid.[5]He was hit on the right side by a mixture of nitric acid, broken glass, americium and ion exchange resin.[6]
https://en.wikipedia.org/wiki/Harold_McCluskey
08-05-2021-1057 - TLS et EMR
08-05-2021-1054 - Radiation
08-05-2021-1051 - DNA parasite w effect macro w ap...
08-05-2021-1042 - Acute lymphoblastic leukemia
1. Coovules
2. Aerosol/Aeronautics/Air-med/gas-stb-org/etc. (hydaulics, space, excision of std env stp etc.)
3. Bone-cellular-genetic-etc. dysfunction induction wh dissemination whether or not identifiable outcome
4. Tumor Lysis Syndrome, ALBL; Bone degen, bone decay, cog depre, etc.
5. Ancestors-et-f. Rabys Poolio viridae of bone-blood-nerve systinis. Zoonotics. Neander Disease (europe, norway, germany, etc.). Torture disease. Derived from torted hums. Recommend do no injury/release contemp/violence/etc. of ancient gem/treasure infectious disease.
6. Radiation environment (EMR, Wireless, Rad K, Nuc Med CL1 2021, etc.)
7. Alkylation agent, intercalations, particle, chemical, resistant; all env conditions resistant (subbuild).
8. Hydric Acid, Resination-Glassification of Air due chemical compo isolated/suspended/etc. to gas pha or sol-gel dep on cond etc., Ion collection, channel formations/matricings, etc. rads. radioak potas nitrog helium hydrides hyd trit hydrogen chunking oxygen warping plane warps etc.
9. DNA parasite v. etc.
10. Fungization - ful-gan, hepashityls, mycotics, thrasis/thratix, fungal leukemiaes et murcomycotix/ffs/fungiesvar et -/|HIV-Americanium.
11. Decayin gMatter
12. prog cycles TLS ABL AIPS rapid cyc
13. G pro VIR ev
08-11-2021-0521 - Lipopolysaccharides ENDOTOXINS
Lipopolysaccharides (LPS), also known as endotoxins, are large molecules consisting of a lipid and a polysaccharide composed of O-antigen, outer core and inner core joined by a covalent bond; they are found in the outer membrane of Gram-negative bacteria. The term lipooligosaccharide ("LOS") is used to refer to a low-molecular-weight form of bacterial lipopolysaccharides.
Today, the term endotoxin is mostly used synonymously with LPS,[1] although there are a few endotoxins that are not related to LPS, such as the so-called delta endotoxin proteins secreted by Bacillus thuringiensis.https://en.wikipedia.org/wiki/Lipopolysaccharide
Note 2. Solution 2.
Note 3. Biofilm, plaque, tartar, calculus, calcification/mineralization, liequefacation/liquificaton/etc.
Note 4. USA NAC DOM Volatile org chemicals, infiltration/irritation, inflammation, inflammatory response cascade/cycling/layers/etc., wound healing/healing, granulation, keloid scarring/scarring/subst matrix/time variance/etc., biofilm deposition, plaquening (embeddement hairing), signal interference, mineralization, etc..
Note 5. Delta.
Wednesday, August 11, 2021
08-11-2021-0051 - Fungal Leukeamiaes - sp - fungus, fungal derivatives et priming by alkylation agents rads radk immunosups overvac genotox-viral gene transplant-activation of tumor gene-cell signal dysfunction/decay matter/fungai susecept/etc..
Pagetoid reticulosis (also known as "acral mycoses fungoides",[1] "localized epidermotropic reticulosis",[1] "mycosis fungoides palmaris et plantaris",[1] "unilesional mycosis fungoides",[2] and "Woringer–Kolopp disease"[1]) is a cutaneous condition, an uncommon lymphoproliferative disorder, sometimes considered a form of mycosis fungoides.[1]:734
https://en.wikipedia.org/wiki/Pagetoid_reticulosis
Mycosis fungoides, also known as Alibert-Bazin syndrome or granuloma fungoides,[1] is the most common form of cutaneous T-cell lymphoma. It generally affects the skin, but may progress internally over time. Symptoms include rash, tumors, skin lesions, and itchy skin.
While the cause remains unclear, most cases are not hereditary. Most cases are in people over 20 years of age, and it is more common in men than women. Treatment options include sunlight exposure, ultraviolet light, topical corticosteroids, chemotherapy, and radiotherapy.
sp - fungus, fungal derivatives et priming by alkylation agents rads radk immunosups overvac genotox-viral gene transplant-activation of tumor gene-cell signal dysfunction/decay matter/fungai susecept/etc..
https://en.wikipedia.org/wiki/Mycosis_fungoides
While uncommon in solid tumors, chromosomal translocations are a common cause of these diseases. This commonly leads to a different approach in diagnosis and treatment of haematological malignancies.
A subgroup of them are more severe and are known as haematological malignancies (British English)/hematological malignancies (American English) or blood cancer. They may also be referred to as liquid tumors.[3][4]
Tumors of the hematopoietic and lymphoid tissues (American English) or tumours of the haematopoietic and lymphoid malignancies (British English) are tumors that affect the blood, bone marrow, lymph, and lymphatic system.[1][2]Because these tissues are all intimately connected through both the circulatory system and the immune system, a disease affecting one will often affect the others as well, making myeloproliferation and lymphoproliferation (and thus the leukemiasand the lymphomas) closely related and often overlapping problems.
Hematological malignancies may derive from either of the two major blood cell lineages: myeloid and lymphoid cell lines. The myeloid cell line normally produces granulocytes, erythrocytes, thrombocytes, macrophages and mast cells; the lymphoid cell line produces B, T, NK and plasma cells. Lymphomas, lymphocytic leukemias, and myeloma are from the lymphoid line, while acute and chronic myelogenous leukemia, myelodysplastic syndromes and myeloproliferative diseases are myeloid in origin.
A subgroup of them are more severe and are known as haematological malignancies (British English)/hematological malignancies (American English) or blood cancer. They may also be referred to as liquid tumors.[3][4]
https://en.wikipedia.org/wiki/Tumors_of_the_hematopoietic_and_lymphoid_tissues
Wednesday, August 11, 2021
08-11-2021-0357 - CD30 TNFRSF87654
Non-mycosis fungoides CD30− cutaneous large T-cell lymphoma is a cutaneous condition that usually presents as solitary or generalized plaques, nodules, or tumors of short duration.[1]:738
https://en.wikipedia.org/wiki/Non-mycosis_fungoides_CD30%E2%88%92_cutaneous_large_T-cell_lymphoma
CD30, also known as TNFRSF8, is a cell membrane protein of the tumor necrosis factor receptor family and tumor marker.
https://en.wikipedia.org/wiki/CD30
By Nikiya Anton Bettey at August 11, 2021
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Some causes of fungal meningitis include Cryptococcus, Histoplasma, Blastomyces, Coccidioides, and Candida.
https://www.cdc.gov/meningitis/fungal.html
Sarcocystis is a genus of protozoan parasites, the majority of species infecting mammals, and some infecting reptiles and birds.
The lifecycle of a typical member of this genus involves two host species, a definitive host and an intermediate host. Often, the definitive host is a predator and the intermediate host is its prey. The parasite reproduces sexually in the gut of the definitive host, is passed with the feces, and ingested by the intermediate host. There, it eventually enters muscle tissue. When the intermediate host is eaten by the definitive host, the cycle is completed. The definitive host usually does not show any symptoms of infection, but the intermediate host does.
About 130 recognized species are in this genus. Revision of the taxonomy of the genus is ongoing, and all the currently recognised species may be a much smaller number of species that can infect multiple hosts.
The name Sarcocystis is dervived from Greek: sarx = flesh and kystis = bladder.
https://en.wikipedia.org/wiki/Sarcocystis
Tularemia, also known as rabbit fever, is an infectious disease caused by the bacteriumFrancisella tularensis.[4] Symptoms may include fever, skin ulcers, and enlarged lymph nodes.[3]Occasionally, a form that results in pneumonia or a throat infection may occur.[3]
The bacterium is typically spread by ticks, deer flies, or contact with infected animals.[4] It may also be spread by drinking contaminated water or breathing in contaminated dust.[4] It does not spread directly between people.[8] Diagnosis is by blood tests or cultures of the infected site.[5][9]
Prevention is by using insect repellent, wearing long pants, rapidly removing ticks, and not disturbing dead animals.[6] Treatment is typically with the antibiotic streptomycin.[9] Gentamicin, doxycycline, or ciprofloxacin may also be used.[5]
Between the 1970s and 2015, around 200 cases were reported in the United States a year.[7] Males are affected more often than females.[7] It occurs most frequently in the young and the middle aged.[7] In the United States, most cases occur in the summer.[7] The disease is named after Tulare County, California, where the disease was discovered in 1911.[10] A number of other animals, such as rabbits, may also be infected.[4]
https://en.wikipedia.org/wiki/Tularemia
Neurocysticercosis /ˈnjʊəroʊˌsɪstiˌsɜːrˈkoʊsɪs/ is a specific form of the infectious parasitic disease cysticercosisthat is caused by the infection with Taenia solium, a tapeworm found in pigs. Neurocysticercosis occurs when cysts formed by the infection take hold within the brain, causing neurologic syndromes such as epileptic seizures. It is a common cause of seizures worldwide. It has been called a "hidden epidemic"[1] and "arguably the most common parasitic disease of the human nervous system".[2] Common symptoms of neurocysticercosis include seizures, headaches, blindness, meningitis and dementia.[3]
https://en.wikipedia.org/wiki/Neurocysticercosis
Naegleria fowleri, colloquially known as a "brain-eating amoeba", is a species of the genus Naegleria, belonging to the phylum Percolozoa, which is technically not classified as true amoeba, but a shapeshifting amoeboflagellate excavate.[1] It is a free-living, bacteria-eating microorganism that can be pathogenic, causing an extremely rare sudden, severe and usually fatal brain infection called naegleriasis or primary amoebic meningoencephalitis (PAM).[2] This microorganism is typically found in bodies of warm freshwater,[3] such as ponds, lakes,[4] rivers, hot springs,[5] warm water discharge from industrial or power plants,[6] geothermal well water,[7] poorly maintained or minimally chlorinated (under 0.5 mg/m3 residual) swimming pools,[8] water heaters,[9] soil, and pipes connected to tap water.[10] It can be seen in either an amoeboid or temporary flagellatestage.[11]
The naegleriasis infection has been documented in Australia in 1965,[12] Czechoslovakia in 1962 to 1965,[13] USA in 2003, 2011, 2013, and 2020, and Pakistan in 2008.[2]
https://en.wikipedia.org/wiki/Naegleria_fowleri
Angomonas deanei is a flagellated trypanosomatid. It is an obligate parasite in the gastrointestinal tract of insects, and is in turn a host to symbiotic bacteria. The bacterial endosymbiont maintains a permanent mutualistic relationship with the protozoan such that it is no longer able to reproduce and survive on its own.[3]The symbiosis is similar to that found in another protist Strigomonas culicis.[4]
The species name was accepted as Crithidia deanei until 2011, when phylogenetic analysis revealed that it belongs to the genus Angomonas, thereby becoming Angomonas deanei. The symbiotic bacterium is a member of the β-proteobacterium that descended from the common ancestor with the genus Bordetella,[2] or more likely, Taylorella.[5] The two organisms have depended on each other so much that the bacterium cannot reproduce and the protozoan can no longer infect insects when they are isolated.[1][6] Thus, this organismal association is a fine model for the evidence of the endosymbiotic theory in nature, which explains the origin of eukaryotic cell organelles such as mitochondria and plastids from individual prokaryotes.[7][8]
https://en.wikipedia.org/wiki/Angomonas_deanei
Procyclins also known as procyclic acidic repetitive proteins or PARP[1] are proteins developed in the surface coating of Trypanosoma brucei parasites while in their tsetse fly vector.[2] The cell surface of the bloodstream form features a dense coat of variable surface glycoproteins (VSGs) which is replaced by an equally dense coat of procyclins when the parasite differentiates into the procylic form in the tsetse fly midgut.
There are six or seven procyclin genes that encode unusual proteins with extensive tandem repeat units of glutamic acid (E) and proline (P), referred to as EP repeats (EP1, EP1-2, EP2, EP2-1, EP3, EP3-2, EP3-4), and two genes that encode proteins with internal pentapeptide GPEET repeats (GPEET2).[3]
EP1 is a 141 amino acids protein and EP2 is a 129 AA protein. Both proteins have their coding genes situated on chromosome 10. GPEET2 is a 114 AA protein and EP3-2 is 123 AA protein with genes situated on chromosome 6.
https://en.wikipedia.org/wiki/Procyclin
Variant surface glycoprotein (VSG) is a ~60kDa protein which densely packs the cell surface of protozoan parasites belonging to the genus Trypanosoma. This genus is notable for their cell surface proteins. They were first isolated from Trypanosoma brucei in 1975 by George Cross.[1] VSG allows the trypanosomatid parasites to evade the mammalian host's immune system by extensive antigenic variation. They form a 12–15 nm surface coat. VSG dimers, ~90% of all cell surface protein. It also makes up ~10% of total cell protein. For this reason, these proteins are highly immunogenic and an immune response raised against a specific VSG coat will rapidly kill trypanosomes expressing this variant. However, with each cell division there is a possibility that the progeny will switch expression to change the VSG that is being expressed. VSG has no prescribed biochemical activity.
https://en.wikipedia.org/wiki/Variant_surface_glycoprotein
Jaenimonas is a genus of trypanosomatid parasite that infects mushroom-feeding Drosophila, similar to Crithidiaparasites of Bumblebees. Jaenimonas drosophilae is the sole representative of this genus.[1] The genus is named in honor of John Jaenike, a prominent ecologist and evolutionary biologist whose work on mushroom-feeding flies laid the foundation for studies on mycophagous Drosophila.[2][3][4] Jaenike was also an early proponent of the Red Queen hypothesis.[5]
https://en.wikipedia.org/wiki/Jaenimonas
Tritrichomonas foetus is a species of single-celled flagellated parasites that is known to be a pathogen of the bovine reproductive tract as well as the intestinal tract of cats. In cattle, the organism is transmitted to the female vagina and uterus from the foreskin of the bull where the parasite is known to reside. It causes infertility, and, at times, has caused spontaneous abortions in the first trimester. In the last ten years, there have been reports of Tritrichomonas foetus in the feces of young cats that have diarrhea[1] and live in households with multiple cats. Tritrichomonas foetus looks similarly to Giardia and is often misdiagnosed for it when viewed under a microscope.[2]
https://en.wikipedia.org/wiki/Tritrichomonas_foetus
Leptomonas is a genus of parasitic flagellate protist belonging to family Trypanosomatidae and subfamily Leishmaniinae sensu Maslov & Lukeš 2012.[1] It is a monoxenous parasite of mainly Hemiptera, Diptera, and Siphonaptera insects.[2]
In addition to Leptomonas, one-host trypanosomatids from insects have been traditionally placed in genera Crithidia, Blastocrithidia, Herpetomonas, Rhynchoidomonas, and Wallaceina.[3][4]
https://en.wikipedia.org/wiki/Leptomonas
Leishmania tropica is a species of flagellate parasites that infects humans and hyraxes, and the cause of the disease Leishmaniasis RecidivansOr bugdadsore, a form of cutaneous leishmaniasis. L. tropica infection results in non-ulcerating disease. Cause Oriental sores<Korean J. Parasitol. 2007 Jun;45(2):103-9.> <Mahmoudzadeh-Niknam H1, Kiaei SS, Iravani D.>
https://en.wikipedia.org/wiki/Leishmania_tropica
Blastocrithidia is a genus of parasitic flagellate protist belonging to the family Trypanosomatidae.[1] It is a monoxenous parasite of heteropteran insects,[3] mainly inhabiting their hindgut and glands.[4]
https://en.wikipedia.org/wiki/Blastocrithidia
Trypanosomatida is a group of kinetoplastid excavates distinguished by having only a single flagellum. The name is derived from the Greek trypano (borer) and soma (body) because of the corkscrew-like motion of some trypanosomatid species. All members are exclusively parasitic, found primarily in insects.[1] A few genera have life-cycles involving a secondary host, which may be a vertebrate, invertebrate or plant. These include several species that cause major diseases in humans.[2] Trypanosomatida are intracellular parasites.
https://en.wikipedia.org/wiki/Trypanosomatida#Morphologies
Wallaceina is a genus of parasitic flagellate protist belonging to the family Trypanosomatidae.[1][2] This generic name is a replacement name for Proteomonas Podlipaev, Frolov et Kolesnikov, 1990 because the latter Proteomonaswas already attributed to a cryptomonad.[1] Wallaceina is a taxonomic patronym honoring the protistologist Franklin G. Wallace, a pioneer in the modern taxonomy of trypanosomatids.
Wallaceina is a monoxenous parasite of insects. Other one-host trypanosomatids from hemipteran and dipteraninsects have been traditionally placed in genera Blastocrithidia, Crithidia, Leptomonas, Herpetomonas, and Rhynchoidomonas.[3][4] Wallaceina is characterized by endomastigote morphological forms, whereas epimastigotes and opisthomastigotes are features of the genera Blastocrithidia and Herpetomonas, respectively.[4]
Comparison and phylogenetic analysis of 18S ribosomal RNA and glycosomal glyceraldehyde-3-phosphatedehydrogenase sequences of trypanosomatid taxa indicate that the genus Wallaceina is polyphyletic. It is therefore suggested to reassign Wallaceina species either to Crithidia brevicula (for Wallaceina brevicula, W. inconstans, W. vicina, and W. podlipaevi) or to the newly proposed genus Wallacemonas (for Wallaceina collosoma, W. rigida, and W. raviniae).[5]
https://en.wikipedia.org/wiki/Wallaceina
Trypanosomatida is a group of kinetoplastid excavates distinguished by having only a single flagellum. The name is derived from the Greek trypano (borer) and soma (body) because of the corkscrew-like motion of some trypanosomatid species. All members are exclusively parasitic, found primarily in insects.[1] A few genera have life-cycles involving a secondary host, which may be a vertebrate, invertebrate or plant. These include several species that cause major diseases in humans.[2] Trypanosomatida are intracellular parasites.
(malaria)
https://en.wikipedia.org/wiki/Trypanosomatida#Morphologies
An exotoxin is a toxin secreted by bacteria.[1] An exotoxin can cause damage to the host by destroying cells or disrupting normal cellular metabolism. They are highly potent and can cause major damage to the host. Exotoxins may be secreted, or, similar to endotoxins, may be released during lysis of the cell. Gram negative pathogens may secrete outer membrane vesicles containing lipopolysaccharide endotoxin and some virulence proteins in the bounding membrane along with some other toxins as intra-vesicular contents, thus adding a previously unforeseen dimension to the well-known eukaryote process of membrane vesicle trafficking, which is quite active at the host-pathogen interface.
https://en.wikipedia.org/wiki/Exotoxin
Ovis is a genus of mammals, part of the Caprinae subfamily of the ruminant family Bovidae.[1] Its seven highly sociable species are known as sheep. Domestic sheep are members of the genus, and are thought to be descended from the wild mouflon of central and southwest Asia.
https://en.wikipedia.org/wiki/Ovis
Four recognised species infect cattle: S. bovifelis, S. bovihominis (S. hominis), S. cruzi (S. bovicanis), and S. hirsuta. S. cruzi is the only species known to be pathogenic in cattle. Several clinical syndromes have been reported in connection with this parasite: eosinophilic myositis; abortions, stillbirths, and deaths in pregnant cows; two cases of necrotic encephalitis in heifers have also been reported. Typical clinical signs of acute bovine sarcocystosis are: anorexia, pyrexia (42°C or more), anemia, cachexia, enlarged palpable lymph nodes, excessive salivation, and loss of hair at the tip of the tail.[12]
Four recognised species infect cattle: S. bovifelis, S. bovihominis (S. hominis), S. cruzi (S. bovicanis), and S. hirsuta. S. cruzi is the only species known to be pathogenic in cattle. Several clinical syndromes have been reported in connection with this parasite: eosinophilic myositis; abortions, stillbirths, and deaths in pregnant cows; two cases of necrotic encephalitis in heifers have also been reported. Typical clinical signs of acute bovine sarcocystosis are: anorexia, pyrexia (42°C or more), anemia, cachexia, enlarged palpable lymph nodes, excessive salivation, and loss of hair at the tip of the tail.[12]
Sheep may be infected by four recognized species of Sarcocystis: S. arieticanis and S. tenella (S. ovicanis) are pathogenic; S. gigantea (S. ovifelis) and S. medusiformis are nonpathogenic. Infection with these parasites is common in the US with over 80% of sheep examined showing evidence of infection.[13] S. arieticanis and S. tenellaboth produce extraintestinal disease. Anemia, anorexia, ataxia, and abortions are the chief clinical signs. Myositis with flaccid paralysis has been reported as a consequence of infection. Ovine protozoan myeloencephalitis is a recognised syndrome that may occur in outbreaks. The usual pathological findings in such cases are multifocal spinal cord white matter oedema and necrosis, glial nodules and mild to moderate nonsuppurative encephalomyelitis. The diagnosis may be established finding protozoan bodies (12.7–23.0 μm) that stain immunocytochemically for Sarcocystis epitopes.
Four recognised species infect pigs: S. medusiformis, S. meischeriana (S. suicanis), S. porcifelis, and S. suihominis. S. porcifelis is pathogenic for pigs causing diarrhea, myositis and lameness.
Five species infect horses: S. asinus, S. bertrami, S. equicanis, S. fayeri, and S. neurona (S. falcatula). All use canids as definitive hosts; transplacental infection has also been reported. S. neurona causes equine protozoal myeloencephalitis. Exposure to this parasite appears to be common in the United States, with serological surveys indicating that 50–60% percent of all horses in the Midwest United States have been exposed to it. Clinical signs include gait abnormalities including ataxia, knuckling, and crossing over. Muscle atrophy, usually unilateral, may occur. The lesions are typically focal. Brain stem involvement is common. Depression, weakness, head tilt, and dysphagia also occur. S. fayeri may cause myositis in horses.
Fatal infection of an alpaca (Lama pacos) with an unnamed species has been reported. Findings included disseminated eosinophilic myositis, abortion, and haemoabdomen. The myositis was associated with hameorrhage, necrosis, and degeneration.[14] Infection by S. tilopodi of muscle tissue in the guanaco has been reported.[15]
S. hemionilatrantis infects mule deer. Death from experimental inoculation has been reported.
These parasites can also infect birds, producing three different clinical forms: an acute pulmonary disease, muscular disease, and neurological disease. Symptoms include lethargy, shortness of breath, tail bobbing, yellow-tinted droppings, and sudden death. The presence of the cysts in the muscle of wild birds is known as "rice breast".
https://en.wikipedia.org/wiki/Sarcocystis
Sarcocystis neurona is primarily a neural parasite of horses and its management is of concern in veterinarian medicine. The protozoan Sarcocystis neurona is a protozoan of single celled character and belongs to the family, Sarcocystidae, a group called coccidia.[1] The protozoan, S. neurona, is a member of the genus Sarcocystis, and is most commonly associated with equine protozoal myeloencephalitis (EPM).[2] The protozoan, S. neurona, can be easily cultivated and genetically manipulated, hence its common use as a model to study numerous aspects of cell biology.[3]
https://en.wikipedia.org/wiki/Sarcocystis_neurona
Equine protozoal myeloencephalitis (EPM), is a disease caused by the apicomplexan parasite Sarcocystis neurona[1] that affects the central nervous system of horses.
https://en.wikipedia.org/wiki/Equine_protozoal_myeloencephalitis
Infectious stages[edit]
A sporozoite (ancient Greek sporos, seed + zōon, animal) is the cell form that infects new hosts. In Plasmodium, for instance, the sporozoites are cells that develop in the mosquito's salivary glands, leave the mosquito during a blood meal, and enter liver cells (hepatocytes), where they multiply. Cells infected with sporozoites eventually burst, releasing merozoites into the bloodstream.[8] Sporozoites are motile and they move by gliding.
A merozoite (G. meros, part [of a series] +zōon, animal) is the result of merogony that takes place within a host cell. During this stage, the parasite infects the host's cells and then replicates its own nucleus and induces cell segmentation in a form of asexual reproduction. In coccidiosis, merozoites form the first phase of the internal life cycle of coccidian. In the case of Plasmodium, merozoites infect red blood cells and then rapidly reproduce asexually. The red blood cell host is destroyed by this process, which releases many new merozoites that go on to find new blood-borne hosts. Merozoites are motile. Before schizogony, the merozoite is also known as the schizozoite.[9]
https://en.wikipedia.org/wiki/Apicomplexan_life_cycle#schizont
A merozoite (G. meros, part [of a series] +zōon, animal) is the result of merogony that takes place within a host cell. During this stage, the parasite infects the host's cells and then replicates its own nucleus and induces cell segmentation in a form of asexual reproduction. In coccidiosis, merozoites form the first phase of the internal life cycle of coccidian. In the case of Plasmodium, merozoites infect red blood cells and then rapidly reproduce asexually. The red blood cell host is destroyed by this process, which releases many new merozoites that go on to find new blood-borne hosts. Merozoites are motile. Before schizogony, the merozoite is also known as the schizozoite.[9]
A gametocyte (G. gametēs, partner + kytos, cell) is a name given to a parasite's gamete-forming cells. A male gametocyte divides to give many flagellated microgametes, whereas the female gametocyte differentiates to a macrogamete.[10]
An ookinete (G. ōon, egg + kinētos, motile) is a fertilised zygote capable of moving spontaneously. It penetrates epithelial cells lining the midgut of mosquitoes to form a thick-walled structure known as an oocyst under the mosquito's outer gut lining.[11] Ookinetes are motile and they move by gliding.
A trophozoite (G. trophē, nourishment + zōon, animal) is the activated, intracellular feeding stage in the apicomplexan life cycle. After gorging itself on its host, the trophozoite undergoes schizogony and develops into a schizont, later releasing merozoites.
A hypnozoite (G. hypnos, sleep + zōon, animal) is a quiescent parasite stage that is best known for its "... probable association with latency and relapse in human malarial infections caused by Plasmodium ovale and P. vivax".[12] Hypnozoites are directly sporozoite-derived.[13]
A bradyzoite (G. bradys, slow + zōon, animal) is a sessile, slow-growing form of zoonotic microorganisms such as Toxoplasma gondii, among others responsible for parasitic infections. In chronic (latent) toxoplasmosis, bradyzoites microscopically present as clusters enclosed by an irregular crescent-shaped wall (cysts) in infected muscle and brain tissues. Also known as a bradyzoic merozoite.[14]
A tachyzoite (G. tachys, fast + zōon, animal), contrasting with a bradyzoite, is a form typified by rapid growth and replication. Tachyzoites are the motile forms of those coccidians which form tissue pseudocysts, such as Toxoplasma and Sarcocystis. Typically infecting cellular vacuoles, tachyzoites divide by endodyogeny and endopolygeny. Also known as a tachyzoic merozoite (same journal reference as for "bradyzoic merozoite", above).
An oocyst (G. ōon, egg + kystis, bladder) is a hardy, thick-walled spore, able to survive for lengthy periods outside a host. The zygote develops within the spore, which acts to protect it during transfer to new hosts. Organisms that create oocysts include Eimeria, Isospora, Cryptosporidium, and Toxoplasma.
https://en.wikipedia.org/wiki/Apicomplexan_life_cycle#merozoite
Apicomplexans, a group of intracellular parasites, have life cycle stages evolved to allow them to survive the wide variety of environments they are exposed to during their complex life cycle.[1] Each stage in the life cycle of an apicomplexan organism is typified by a cellular variety with a distinct morphology and biochemistry.
Not all apicomplexa develop all the following cellular varieties and division methods. This presentation is intended as an outline of a hypothetical generalised apicomplexan organism.
https://en.wikipedia.org/wiki/Apicomplexan_life_cycle#bradyzoite
Gregarina garnhami is a eukaryotic unicellular organism belonging to the Apicomplexa described in 1956 by Canning as a parasite found in several locusts, such as the desert locust, African migratory locust, and Egyptian locust. Especially, the desert locust is the host for this species, as up to 100% of animals can become infected.[1] An estimated thousands of different species of gregarines can be in insects and 99% of these gregarines still need to be described. Each insect is said to host multiple species.[2][3] A remarkable feature of G. garnhami is its auto-fluorescence.
https://en.wikipedia.org/wiki/Gregarina_garnhami
Schizocystidae is a genus of parasitic alveolates in the phylum Apicomplexa.
Species in this family infect insects (Diptera).
https://en.wikipedia.org/wiki/Schizocystis
The human TNF gene was cloned in 1985.[30] It maps to chromosome 6p21.3, spans about 3 kilobases and contains 4 exons. The last exon shares similarity with lymphotoxin alpha (LTA, once named as TNF-β).[31] The three prime untranslated region (3'-UTR) of TNF contains an AU-rich element(ARE).
https://en.wikipedia.org/wiki/Tumor_necrosis_factor
LPS is the major component of the outer membrane of Gram-negative bacteria, contributing greatly to the structural integrity of the bacteria, and protecting the membrane from certain kinds of chemical attack. LPS is the most abundant antigen on the cell surface of most Gram-negative bacteria, contributing up to 80% of the outer membrane of E. coli and Salmonella.[4] LPS increases the negative charge of the cell membrane and helps stabilize the overall membrane structure. It is of crucial importance to many Gram-negative bacteria, which die if it is mutated or removed; however, it appears that LPS is nonessential in at least some Gram-negative bacteria, such as Neisseria meningitidis, Moraxella catarrhalis, and Acinetobacter baumannii.[5]LPS induces a strong response from normal animal immune systems. It has also been implicated in non-pathogenic aspects of bacterial ecology, including surface adhesion, bacteriophage sensitivity, and interactions with predators such as amoebae.
LPS is required for the proper conformation of omptin activity; however, smooth LPS will sterically hinder omptins.
https://en.wikipedia.org/wiki/Lipopolysaccharide
Wednesday, August 11, 2021
08-11-2021-0357 - CD30 TNFRSF87654
Non-mycosis fungoides CD30− cutaneous large T-cell lymphoma is a cutaneous condition that usually presents as solitary or generalized plaques, nodules, or tumors of short duration.[1]:738
https://en.wikipedia.org/wiki/Non-mycosis_fungoides_CD30%E2%88%92_cutaneous_large_T-cell_lymphoma
CD30, also known as TNFRSF8, is a cell membrane protein of the tumor necrosis factor receptor family and tumor marker.
https://en.wikipedia.org/wiki/CD30
By Nikiya Anton Bettey at August 11, 2021
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Wednesday, August 11, 2021
08-11-2021-0051 - Fungal Leukeamiaes - sp - fungus, fungal derivatives et priming by alkylation agents rads radk immunosups overvac genotox-viral gene transplant-activation of tumor gene-cell signal dysfunction/decay matter/fungai susecept/etc..
Pagetoid reticulosis (also known as "acral mycoses fungoides",[1] "localized epidermotropic reticulosis",[1] "mycosis fungoides palmaris et plantaris",[1] "unilesional mycosis fungoides",[2] and "Woringer–Kolopp disease"[1]) is a cutaneous condition, an uncommon lymphoproliferative disorder, sometimes considered a form of mycosis fungoides.[1]:734
https://en.wikipedia.org/wiki/Pagetoid_reticulosis
Mycosis fungoides, also known as Alibert-Bazin syndrome or granuloma fungoides,[1] is the most common form of cutaneous T-cell lymphoma. It generally affects the skin, but may progress internally over time. Symptoms include rash, tumors, skin lesions, and itchy skin.
While the cause remains unclear, most cases are not hereditary. Most cases are in people over 20 years of age, and it is more common in men than women. Treatment options include sunlight exposure, ultraviolet light, topical corticosteroids, chemotherapy, and radiotherapy.
sp - fungus, fungal derivatives et priming by alkylation agents rads radk immunosups overvac genotox-viral gene transplant-activation of tumor gene-cell signal dysfunction/decay matter/fungai susecept/etc..
https://en.wikipedia.org/wiki/Mycosis_fungoides
While uncommon in solid tumors, chromosomal translocations are a common cause of these diseases. This commonly leads to a different approach in diagnosis and treatment of haematological malignancies.
A subgroup of them are more severe and are known as haematological malignancies (British English)/hematological malignancies (American English) or blood cancer. They may also be referred to as liquid tumors.[3][4]
Tumors of the hematopoietic and lymphoid tissues (American English) or tumours of the haematopoietic and lymphoid malignancies (British English) are tumors that affect the blood, bone marrow, lymph, and lymphatic system.[1][2]Because these tissues are all intimately connected through both the circulatory system and the immune system, a disease affecting one will often affect the others as well, making myeloproliferation and lymphoproliferation (and thus the leukemiasand the lymphomas) closely related and often overlapping problems.
Hematological malignancies may derive from either of the two major blood cell lineages: myeloid and lymphoid cell lines. The myeloid cell line normally produces granulocytes, erythrocytes, thrombocytes, macrophages and mast cells; the lymphoid cell line produces B, T, NK and plasma cells. Lymphomas, lymphocytic leukemias, and myeloma are from the lymphoid line, while acute and chronic myelogenous leukemia, myelodysplastic syndromes and myeloproliferative diseases are myeloid in origin.
A subgroup of them are more severe and are known as haematological malignancies (British English)/hematological malignancies (American English) or blood cancer. They may also be referred to as liquid tumors.[3][4]
https://en.wikipedia.org/wiki/Tumors_of_the_hematopoietic_and_lymphoid_tissues
08-11-2021-0521 - Lipopolysaccharides ENDOTOXINS
Lipopolysaccharides (LPS), also known as endotoxins, are large molecules consisting of a lipid and a polysaccharide composed of O-antigen, outer core and inner core joined by a covalent bond; they are found in the outer membrane of Gram-negative bacteria. The term lipooligosaccharide ("LOS") is used to refer to a low-molecular-weight form of bacterial lipopolysaccharides.
Today, the term endotoxin is mostly used synonymously with LPS,[1] although there are a few endotoxins that are not related to LPS, such as the so-called delta endotoxin proteins secreted by Bacillus thuringiensis.https://en.wikipedia.org/wiki/Lipopolysaccharide
Aspergillosis is a fungal infection of usually the lungs,[1] caused by the genus Aspergillus, a common mold that is breathed in frequently from the air around, but does not usually affect most people.[2][3] It generally occurs in people with lung diseases such as asthma, cystic fibrosis or tuberculosis, or those who have had a stem cell or organ transplant, and those who cannot fight infection because of medications they take such as steroids and some cancer treatments.[1][4]Rarely, it can affect skin.[4][5]
Aspergillosis occurs in humans, birds and other animals. Aspergillosis occurs in chronic or acute forms which are clinically very distinct. Most cases of acute aspergillosis occur in people with severely compromised immune systems, e.g. those undergoing bone marrow transplantation.[6]Chronic colonization or infection can cause complications in people with underlying respiratory illnesses, such as asthma,[7] cystic fibrosis,[8] sarcoidosis,[9] tuberculosis, or chronic obstructive pulmonary disease.[10] Most commonly, aspergillosis occurs in the form of chronic pulmonary aspergillosis (CPA), aspergilloma, or allergic bronchopulmonary aspergillosis (ABPA).[11] Some forms are intertwined; for example ABPA and simple aspergilloma can progress to CPA.
Other, noninvasive manifestations include fungal sinusitis (both allergic in nature and with established fungal balls), otomycosis (ear infection), keratitis (eye infection), and onychomycosis(nail infection). In most instances, these are less severe, and curable with effective antifungaltreatment.
Trichophyton is a genus of fungi, which includes the parasitic varieties that cause tinea, including athlete's foot, ringworm, jock itch, and similar infections of the nail, beard, skin and scalp. Trichophyton fungi are moldscharacterized by the development of both smooth-walled macro- and microconidia. Macroconidia are mostly borne laterally directly on the hyphae or on short pedicels, and are thin- or thick-walled, clavate to fusiform, and range from 4 to 8 by 8 to 50 μm in size. Macroconidia are few or absent in many species. Microconidia are spherical, pyriform to clavate or of irregular shape, and range from 2 to 3 by 2 to 4 μm in size.
https://en.wikipedia.org/wiki/Trichophyton#Species_and_their_natural_reservoirs
| Coccidioidomycosis | |
|---|---|
 | |
| Histopathological changes in a case of coccidioidomycosis of the lung showing a large fibrocaseous nodule. | |
| Specialty | Infectious disease |
| Types | Acute, chronic[1] |
| Causes | Coccidioides[2] |
| Treatment | Antifungal medication[1] |
| Medication | Amphotericin B, itraconazole, fluconazole[1] |
Coccidioidomycosis (/kɒkˌsɪdiɔɪdoʊmaɪˈkoʊsɪs/, kok-sid-ee-oy-doh-my-KOH-sis), commonly known as cocci,[3] Valley fever,[3] as well as California fever,[4] desert rheumatism,[4] or San Joaquin Valley fever,[4] is a mammalian fungal disease caused by Coccidioides immitis or Coccidioides posadasii.[5] Coccidioidomycosis is endemic in certain parts of the United States in Arizona, California, Nevada, New Mexico, Texas, Utah, and northern Mexico.[6]
C. immitis is a dimorphic saprophytic fungus that grows as a mycelium in the soil and produces a spherule form in the host organism. It resides in the soil in certain parts of the southwestern United States, most notably in California and Arizona.[3] It is also commonly found in northern Mexico, and parts of Central and South America.[3] C. immitis is dormant during long dry spells, then develops as a mold with long filaments that break off into airborne spores when it rains. The spores, known as arthroconidia, are swept into the air by disruption of the soil, such as during construction, farming, or an earthquake.[7] Windstorms may also cause epidemics far from endemic areas. In December 1977, a windstorm in an endemic area around Arvin, California led to several hundred cases, including deaths, in non-endemic areas hundreds of miles away.[8]
Coccidioidomycosis is a common cause of community-acquired pneumonia in the endemic areas of the United States.[3] Infections usually occur due to inhalation of the arthroconidial spores after soil disruption.[3] The disease is not contagious.[3] In some cases the infection may recur or become chronic.
https://en.wikipedia.org/wiki/Coccidioidomycosis
Histoplasmosis is a disease caused by the fungus Histoplasma capsulatum.[2] Symptoms of this infection vary greatly, but the disease affects primarily the lungs.[3] Occasionally, other organs are affected; called disseminated histoplasmosis, it can be fatal if left untreated.
Histoplasmosis is common among AIDS patients because of their suppressed immunity.[4] In immunocompetent individuals, past infection results in partial protection against ill effects if reinfected.
Histoplasma capsulatum is found in soil, often associated with decaying bat guano or bird droppings. Disruption of soil from excavation or construction can release infectious elements that are inhaled and settle into the lung.
From 1938 to 2013 in the US, 105 outbreaks were reported in 26 states and Puerto Rico. In 1978-1979 during a large urban outbreak in which 100,000 people were exposed to the fungus in Indianapolis,[5] victims had pericarditis, rheumatological syndromes, esophageal and vocal cord ulcers, parotitis, adrenal insufficiency, uveitis, fibrosing mediastinitis, interstitial nephritis, intestinal lymphangiectasia, and epididymitis. Histoplasmosis mimics colds, pneumonia, and the flu, and can be shed by bats in their feces.
https://en.wikipedia.org/wiki/Histoplasmosis
Primary pulmonary coccidioidomycosis is an infection caused by inhalation of Coccidioides immitis.[1]:314 Once pulmonary symptoms subside, about 30% of women and 15% of men will have allergic skin manifestations in the form of erythema nodosum.[1]:314 A coccidioidoma is a benign localized residual granulomatous lesion or scar that can remain in the lung's tissues following primary pulmonary coccidioidomycosis.[2]
https://en.wikipedia.org/wiki/Primary_pulmonary_coccidioidomycosis
Blastomycosis is a fungal infection caused by inhaling Blastomyces dermatitidis spores.[4][5] If it involves only the lungs, it is called pulmonary blastomycosis.[6] Only about half of people with the disease have symptoms, which can include fever, cough, night sweats, muscle pains, weight loss, chest pain, and feeling tired.[7] These symptoms usually develop between three weeks and three months after breathing in the spores.[7] In those with weak immune systems, the disease can spread to other areas of the body, including the skin and bones.[6]
Blastomyces dermatitidis is found in the soil and decaying organic matter like wood or leaves.[3]Participating in outdoor activities like hunting or camping in wooded areas increases the risk of developing blastomycosis.[8] There is no vaccine, but the disease can be prevented by not disturbing the soil.[8] Treatment is with itraconazole for mild or moderate disease and amphotericin B for severe disease.[3] With both, the duration of treatment is 6–12 months.[9] Overall, 4-6% of people who develop blastomycosis die; however, if the central nervous system is involved, this rises to 18%. People with AIDS or on medications that suppress the immune system have the highest risk of death at 25-40%.[10]
Blastomycosis is endemic to the eastern United States, especially the Ohio and Mississippi River valleys, the Great Lakes, and the St. Lawrence River. It is also endemic to some parts of Canada, including Quebec, Ontario, and Manitoba.[3] In these areas, there are about 1 to 2 cases per 100,000 per year.[11] Blastomycosis was first described by Thomas Casper Gilchrist in 1894; because of this, it is sometimes called "Gilchrist's disease".[12]
https://en.wikipedia.org/wiki/Blastomycosis
Paracoccidioidomycosis (PCM) is an acute to chronic fungal infection caused by fungi in the genus Paracoccidioides, including Paracoccidioides brasiliensis and Paracoccidioides lutzii. It is endemic to Central and South America,[8] and is considered to be a neglected endemic mycosis, a type of neglected tropical disease.[9]
https://en.wikipedia.org/wiki/Paracoccidioidomycosis
Talaromyces marneffei, formerly called Penicillium marneffei,[1] was identified in 1956.[2] The organism is endemic to southeast Asia where it is an important cause of opportunistic infections in those with HIV/AIDS-related immunodeficiency. Incidence of T. marneffei infections has increased due to a rise in HIV infection rates in the region.[3][4]
When it was classified as a Penicillium, it was the only known thermally dimorphic species of that genus that caused a lethal systemic infection (talaromycosis), with fever and anaemia similar to disseminatedcryptococcosis. This contrasted with related Penicillium species that are usually regarded as unimportant in terms of causing human disease.[citation needed]
https://en.wikipedia.org/wiki/Talaromyces_marneffei
Aspergillus (/ˌæspərˈdʒɪləs/) is a genus consisting of a few hundred mold species found in various climates worldwide.
Aspergillus was first catalogued in 1729 by the Italian priest and biologist Pier Antonio Micheli. Viewing the fungi under a microscope, Micheli was reminded of the shape of an aspergillum (holy water sprinkler), from Latin spargere (to sprinkle), and named the genus accordingly.[1] Aspergillum is an asexual spore-forming structure common to all Aspergillus species; around one-third of species are also known to have a sexual stage.[2] While some species of Aspergillus are known to cause fungal infections, others are of commercial importance.
https://en.wikipedia.org/wiki/Aspergillus
Cryptococcosis is a potentially fatal fungal infection of mainly the lungs, presenting as a pneumonia, and brain, where it appears as a meningitis.[4][9] Cough, difficulty breathing, chest painand fever are seen when the lungs are infected.[5] When the brain is infected, symptoms include headache, fever, neck pain, nausea and vomiting, light sensitivity and confusion or changes in behaviour.[5] It can also affect other parts of the body including skin, where it may appear as several fluid-filled nodules with dead tissue.[6]
https://en.wikipedia.org/wiki/Cryptococcosis
Trichosporonosis is a systemic disease associated with fungi in the genus Trichosporon.
It can appear in patients who are immunosuppressed.[1]
https://en.wikipedia.org/wiki/Trichosporonosis
Kerion Celsi is the result of the host's response to a fungal ringworm infection of the hair follicles of the scalp (occasionally the beard) that can be accompanied by secondary bacterial infection(s). It usually appears as raised, spongy lesions, and typically occurs in children.[1] This honeycomb is a painful inflammatory reaction with deep suppurative lesions on the scalp. Follicles may be seen discharging pus. There may be sinus formation and rarely mycetoma-like grains are produced. It is usually caused by dermatophytes (fungal infections of the skin affecting humans and animals) such as Trichophyton verrucosum, T. mentagrophytes,[1] and Microsporum canis. Treatment with oral griseofulvin common.[1]
https://en.wikipedia.org/wiki/Kerion
Hyalohyphomycosis is a group of opportunistic mycotic infections[1] caused by nondematiaceous molds, and may be contrasted with phaeohyphomycosis.[2]:329
A hyalohyphomycetes example is Fusarium.[3]
https://en.wikipedia.org/wiki/Hyalohyphomycosis
Phaeohyphomycosis is a diverse group of fungal infections,[6] caused by dematiaceous fungi whose morphologic characteristics in tissue include hyphae, yeast-like cells, or a combination of these.[7]:324 It can be associated an array of melanistic filamentous fungi including Alternaria species,[8] Exophiala jeanselmei,[9] and Rhinocladiella mackenziei.[10]
The term “phaeohyphomycosis” was introduced to determine infections caused by dematiaceous (pigmented) filamentous fungi which contain melanin in their cell walls.[11] Phaeohyphomycosis is an uncommon infection, however the number of case reported has been increasing in recent years. Fungal melanin is thought to be a virulence factor. The outcome of antifungal treatment is poor, and mortality is almost 80%.[12] Phaeohyphomycosis has been attributed to more than 100 species and 60 genera of fungi over the past several decades. The pathogens are considered opportunistic. Almost all cases of widely disseminated infection have occurred in immunosuppressed people.[12]
https://en.wikipedia.org/wiki/Phaeohyphomycosis
- deep subcutaneous plaque/nodular lesion form that occurs in immunosuppressed hosts. Tinea corporis is the name of the subset of this disease that remains restricted to the stratum corneum. Otherwise, the atypical deeper involvement is known as Majocchi's granuloma.[7] Because keratinophilic dermatophytes digest keratin, the introduction of keratin into the dermis may also act as a medium for continued growth of the organism.
Majocchi's granuloma is a skin condition characterized by deep, pustular plaques, and is a form of tinea corporis. It is a localized form of fungal folliculitis. Lesions often have a pink and scaly central component with pustules or folliculocentric papules at the periphery.[1] The name comes from Professor Domenico Majocchi, who discovered the disorder in 1883.[2] Majocchi was a professor of dermatology at the University of Parma and later the University of Bologna.[2] The most common dermatophyte is called Trichophyton rubrum.
https://en.wikipedia.org/wiki/Fungal_folliculitis
Alternariosis is an infection by Alternaria, presenting cutaneously as focal, ulcerated papules and plaques.[1]:330
Treatment with itraconazole has been reported.[2]
https://en.wikipedia.org/wiki/Alternariosis
The common house mouse TNF and human TNF are structurally different.[36] The 17-kilodalton (kDa) TNF protomers (185-amino acid-long) are composed of two antiparallel β-pleated sheets with antiparallel β-strands, forming a 'jelly roll' β-structure, typical for the TNF family, but also found in viral capsid proteins.
https://en.wikipedia.org/wiki/Tumor_necrosis_factor
Toxoplasma gondii (/ˈtɒksoʊplæzmə ˈɡɒndiaɪ/) is an obligate intracellular parasitic protozoan (specifically an apicomplexan) that causes toxoplasmosis.[3] Found worldwide, T. gondii is capable of infecting virtually all warm-blooded animals,[4]:1 but felids, such as domestic cats, are the only known definitive hosts in which the parasite may undergo sexual reproduction.[5][6]
https://en.wikipedia.org/wiki/Toxoplasma_gondii
Following the initial period of infection characterized by tachyzoite proliferation throughout the body, pressure from the host's immune system causes T. gondii tachyzoites to convert into bradyzoites, the semidormant, slowly dividing cellular stage of the parasite.[36] Inside host cells, clusters of these bradyzoites are known as tissue cysts. The cyst wall is formed by the parasitophorous vacuole membrane.[29]:343 Although bradyzoite-containing tissue cysts can form in virtually any organ, tissue cysts predominantly form and persist in the brain, the eyes, and striated muscle (including the heart).[29]:343 However, specific tissue tropisms can vary between intermediate host species; in pigs, the majority of tissue cysts are found in muscle tissue, whereas in mice, the majority of cysts are found in the brain.[29]:41
Cysts usually range in size between five and 50 µm in diameter,[37] (with 50 µm being about two-thirds the width of the average human hair).[38]
Consumption of tissue cysts in meat is one of the primary means of T. gondii infection, both for humans and for meat-eating, warm-blooded animals.[29]:3Humans consume tissue cysts when eating raw or undercooked meat (particularly pork and lamb).[39] Tissue cyst consumption is also the primary means by which cats are infected.[4]:46
An exhibit at the San Diego Natural History Museum states urban runoff with cat feces transports Toxoplasma gondii into the ocean, which can kill sea otters.[40]
Examination of black-footed penguins with toxoplasmosis reveals hepatomegaly, splenomegaly, cranial hemorrhage, and necrotic kidneys (Ploeg, et al., 2011). Alveolar and hepatic tissue presents a high number of immune cells like macrophages containing tachyzoites of T. gondii.[76] Histopathological features in other animals affected with toxoplasmosis had tachyzoites in eye structures like the retina which lead to blindness.[76]
https://en.wikipedia.org/wiki/Toxoplasma_gondii
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