09-02-2021-2056 - 2371/2-3,4
Friday, September 3, 2021
09-02-2021-2055 - Arsenic As 33
Arsenic is a chemical element with the symbol As and atomic number 33. Arsenic occurs in many minerals, usually in combination with sulfur and metals, but also as a pure elemental crystal. Arsenic is a metalloid. It has various allotropes, but only the gray form, which has a metallic appearance, is important to industry.
The primary use of arsenic is in alloys of lead (for example, in car batteries and ammunition). Arsenic is a common n-type dopant in semiconductor electronic devices. It is also a component of the III-V compound semiconductor gallium arsenide. Arsenic and its compounds, especially the trioxide, are used in the production of pesticides, treated wood products, herbicides, and insecticides. These applications are declining with the increasing recognition of the toxicity of arsenic and its compounds.[8]
A few species of bacteria are able to use arsenic compounds as respiratory metabolites. Trace quantities of arsenic are an essential dietary element in rats, hamsters, goats, chickens, and presumably other species. A role in human metabolism is not known.[9][10][11] However, arsenic poisoning occurs in multicellular life if quantities are larger than needed. Arsenic contamination of groundwater is a problem that affects millions of people across the world.
The United States' Environmental Protection Agency states that all forms of arsenic are a serious risk to human health.[12] The United States' Agency for Toxic Substances and Disease Registry ranked arsenic as number 1 in its 2001 Priority List of Hazardous Substances at Superfund sites.[13] Arsenic is classified as a Group-A carcinogen.[12]
 | |
| Arsenic |
|---|
https://en.wikipedia.org/wiki/Arsenic
09-02-2021-2053 - African trypanosomiasis, also known as African sleeping sickness or simply sleeping sickness, Trypanosoma brucei. Trypanosoma brucei rhodesiense Trypanosoma brucei gambiense insect borne parasitic infection insect transmission vector flys malaria blood cell parasite tsetse fly trypano soma animal trypanosomiasis. tropics tropical disease
African trypanosomiasis, also known as African sleeping sickness or simply sleeping sickness, is an insect-borne parasitic infection of humans and other animals.[3] It is caused by the species Trypanosoma brucei.[3] Humans are infected by two types, Trypanosoma brucei gambiense (TbG) and Trypanosoma brucei rhodesiense (TbR).[3] TbG causes over 98% of reported cases.[1] Both are usually transmitted by the bite of an infected tsetse fly and are most common in rural areas.[3]
Initially, the first stage of the disease is characterized by fevers, headaches, itchiness, and joint pains, beginning one to three weeks after the bite.[1][2] Weeks to months later, the second stage begins with confusion, poor coordination, numbness, and trouble sleeping.[2] Diagnosis is by finding the parasite in a blood smear or in the fluid of a lymph node.[2] A lumbar puncture is often needed to tell the difference between first- and second-stage disease.[2]
Prevention of severe disease involves screening the population at risk with blood tests for TbG.[3]Treatment is easier when the disease is detected early and before neurological symptoms occur.[3]Treatment of the first stage has been with the medications pentamidine or suramin.[3] Treatment of the second stage has involved eflornithine or a combination of nifurtimox and eflornithine for TbG.[2][3]Fexinidazole is a more recent treatment that can be taken by mouth, for either stages of TbG.[3] While melarsoprol works for both types, it is typically only used for TbR, due to serious side effects.[3] Without treatment sleeping sickness typically results in death.[3]
The disease occurs regularly in some regions of sub-Saharan Africa with the population at risk being about 70 million in 36 countries.[5] An estimated 11,000 people are currently infected with 2,800 new infections in 2015.[6][1] In 2018 there were 977 new cases.[3] In 2015 it caused around 3,500 deaths, down from 34,000 in 1990.[4][7] More than 80% of these cases are in the Democratic Republic of the Congo.[1] Three major outbreaks have occurred in recent history: one from 1896 to 1906 primarily in Uganda and the Congo Basin and two in 1920 and 1970 in several African countries.[1] It is classified as a neglected tropical disease.[8] Other animals, such as cows, may carry the disease and become infected in which case it is known as Nagana or animal trypanosomiasis.[1]
| African trypanosomiasis | |
|---|---|
| Other names | Sleeping sickness, African sleeping sickness |
 | |
| Trypanosoma forms in a blood smear | |
| Specialty | Infectious disease |
| Symptoms | Stage 1: Fevers, headaches, itchiness, joint pains[1] Stage 2: Trouble sleeping, confusion, poor coordination[2][1] |
| Usual onset | 1–3 weeks post exposure[2] |
| Types | Trypanosoma brucei gambiense (TbG), Trypanosoma brucei rhodesiense (TbR)[3] |
| Causes | Trypanosoma brucei spread by tsetse flies[3] |
| Diagnostic method | Blood smear, lumbar puncture[2] |
| Medication | Fexinidazole, pentamidine, suramin, eflornithine, nifurtimox[3] |
| Prognosis | Fatal without treatment[3] |
| Frequency | 977 (2018)[3] |
| Deaths | 3,500 (2015)[4] |
Tryptophol is a chemical compound produced by the trypanosomal parasite in sleeping sickness which induces sleep in humans.[24]
The causative agent and vector were identified in 1903 by David Bruce, and the subspecies of the protozoa were differentiated in 1910. Bruce had earlier shown that T. brucei was the cause of a similar disease in horses and cattle that was transmitted by the tse-tse fly (Glossina morsitans).[42]
The first effective treatment, atoxyl, an arsenic-based drug developed by Paul Ehrlich and Kiyoshi Shiga, was introduced in 1910, but blindness was a serious side effect.
Pentamidine, a highly effective drug for the first stage of the disease, has been used since 1937.[48] During the 1950s, it was widely used as a prophylacticagent in western Africa, leading to a sharp decline in infection rates. At the time, eradication of the disease was thought to be at hand.[citation needed][49]
Est. 1800 st.
In 1903, David Bruce recognized the tsetse fly as the arthropod vector.
https://en.wikipedia.org/wiki/African_trypanosomiasis
09-02-2021-2051 - Arsphenamine 606 66 syphilis and African trypanosomiasis 1910 organoarsenic arsenic phorphor dimer azobenzene VIV
Arsphenamine, also known as Salvarsan or compound 606, is a drug that was introduced at the beginning of the 1910s as the first effective treatment for syphilis and African trypanosomiasis.[2] This organoarsenic compound was the first modern antimicrobial agent.[3]
The structure of Arsphenamine has been proposed to be akin to the dimer azobenzene (A), but mass spectral studies published in 2005 suggest[1] it is actually a mixture of the trimer (B) and the pentamer (C).
Salvarsan treatment kit for syphilis, Germany, 1909-1912[4]
Arsphenamine was first synthesized in 1907 in Paul Ehrlich's lab by Alfred Bertheim.[3] The antisyphilitic activity of this compound was discovered by Sahachiro Hata in 1909, during a survey of hundreds of newly synthesized organic arsenical compounds. Ehrlich had theorized that by screening many compounds, a drug could be discovered that would have anti-microbial activity but not kill the human patient. Ehrlich's team began their search for such a "magic bullet" among chemical derivatives of the dangerously toxic drug atoxyl. This project was the first organized team effort to optimize the biological activity of a lead compound through systematic chemical modifications, the basis for nearly all modern pharmaceutical research.[citation needed]
Arsphenamine was used to treat the disease syphilis because it is toxic to the bacterium Treponema pallidum, a spirochete that causes syphilis.[citation needed]
Arsphenamine was originally called "606" because it was the sixth in the sixth group of compounds synthesized for testing; it was marketed by Hoechst AG under the trade name "Salvarsan" in 1910.[5][6] Salvarsan was the first organic antisyphilitic, and a great improvement over the inorganic mercury compounds that had been used previously. It was distributed as a yellow, crystalline, hygroscopic powder that was highly unstable in air.[7] This significantly complicated administration, as the drug had to be dissolved in several hundred milliliters of distilled, sterile water with minimal exposure to air to produce a solution suitable for injection. Some of the side effects attributed to Salvarsan, including rashes, liver damage, and risks of life and limb, were thought to be caused by improper handling and administration.[8] This caused Ehrlich, who worked assiduously to standardize practices, to observe, "the step from the laboratory to the patient's bedside ... is extraordinarily arduous and fraught with danger."[5]
Ehrlich's laboratory developed a more soluble (but slightly less effective) arsenical compound, Neosalvarsan(neoarsphenamine), which was easier to prepare, and it became available in 1912. Less severe side-effects such as nausea and vomiting were still common. An additional problem was that both Salvarsan and Neosalvarsan had to be stored in sealed vials under a nitrogen atmosphere to prevent oxidation. These arsenical compounds were supplanted as treatments for syphilis in the 1940s by penicillin.[9]
https://en.wikipedia.org/wiki/Arsphenamine
09-02-2021-2011 - Immersion foot syndromes Trench foot Tropical ulcer Jungle Rot mycobacteria mycosis sepsis bone
Immersion foot syndromes are a class of foot injury caused by water absorption in the outer layer of skin.[1][2] There are different subclass names for this condition based on the temperature of the water to which the foot is exposed. These include trench foot, tropical immersion foot, and warm water immersion foot.[3]:26–7 In one 3-day military study, it was found that submersion in water allowing for a higher skin temperature resulted in worse skin maceration and pain.[4]
https://en.wikipedia.org/wiki/Immersion_foot_syndromes
Trench foot is a type of foot damage due to moisture.[1] Initial symptoms often include tingling or itching which can progress to numbness.[1][2] The feet may become red or bluish in color.[1] As the condition worsens the feet can start to swell and smell of decay.[1] Complications may include skin breakdown or infection.[1]
Trench foot occurs due to prolonged exposure of the feet to cold, damp, and often unsanitary conditions.[1] Unlike frostbite, trench foot usually occurs at temperatures above freezing.[1] Onset can be as rapid as 10 hours.[1] Risk factors include overly tight boots and not moving.[3] The underlying mechanism is believed to involve constriction of blood vessels resulting in insufficient blood flow to the feet.[1] Diagnosis is based on symptoms and examination.[1]
Prevention involves keeping the feet warm, dry, and clean.[1] After the condition has occurred, pain medications may be required during the gradual rewarming process.[1] Pain may persist for months following treatment.[3] Surgery to remove damaged tissue or amputation may be necessary.[1]
Those in the military are most commonly affected, though cases may also occur in the homeless.[1] The condition was first described during Napoleon Bonaparte's retreat from Russia in the winter of 1812.[1]The word trench in the name is a reference to trench warfare, mainly associated with World War I.[1]
| Trench foot | |
|---|---|
| Other names | immersion foot |
.jpg) | |
| Trench foot as seen on an unidentified soldier during World War I. | |
| Specialty | Emergency medicine |
| Symptoms |
|
| Complications |
|
| Causes |
|
| Treatment |
|
https://en.wikipedia.org/wiki/Trench_foot
Tropical ulcer, more commonly known as jungle rot, is a chronic ulcerative skin lesion thought to be caused by polymicrobial infection with a variety of microorganisms, including mycobacteria. It is common in tropical climates.[2]
Ulcers occur on exposed parts of the body, primarily on anterolateral aspect of the lower limbs and may erode muscles and tendons, and sometimes, the bones.[3] These lesions may frequently develop on preexisting abrasions or sores sometimes beginning from a mere scratch.[1]
| Tropical ulcer | |
|---|---|
| Other names | Aden ulcer, Jungle rot, Malabar ulcer, Tropical phagedena[1] |
 | |
| The left foot of a person with acute tropical ulcer upon his admission to Toborra Goroka Hospital, in Goroka, Papua New Guinea. | |
| Specialty | Dermatology |
https://en.wikipedia.org/wiki/Tropical_ulcer
Pus is an exudate, typically white-yellow, yellow, or yellow-brown, formed at the site of inflammationduring bacterial or fungal infection.[1][2] An accumulation of pus in an enclosed tissue space is known as an abscess, whereas a visible collection of pus within or beneath the epidermis is known as a pustule, pimple or spot.
| Pus | |
|---|---|
 | |
| Eye with conjunctivitis exuding pus | |
| Specialty | Infectious disease |
https://en.wikipedia.org/wiki/Pus
Herou Purease, Tank You. Left Amcan; Right AziV. - SSF
Right Viet-Canco-Phili-Nor-Fin-Attempt (Slav/switz) w/ Left Hook GL deper-neandre. middle East (hair), latino high, brows. Liver failure, lipodystrophy, bone malacia, ricketts, small channular parasite viral loading fung arsenic responsive, thymal disease degen early, neural sloughig-plaquening-malacia (channular/interspaces). 1990, 1930SLV peripheral nervy decars. Oncogenic Virus. FLV. HFV. Avian Synctal Chick Virus Derivative Hum. Cancer Bone Cancer. Fibrotic Cystular Fibrotic. Genetic Deletion/Decay, DEcay signature of asian gene and chromosomal deletion occurance or syndrome USA. Yellow-Browning. Moles-Warts-Tumors dark brown. ARtheriocalssification calcs liques necrots. bubulants. HEP HER HIV PEST. Migrans As, Arthropod-Worm, extremophile. Schitz outcome trend-trad. bone cavitation. mole bone. F-Gan Bubules Dissem Gran Dissem Can. HFM, Hemorrhagia @ GRN, BRN, Purp, [Black] Bluds cryst excissions. ascitic-mito-met. rad-K/Rad-I. WHKAZIVLAYNG
- Diffuse epidermolytic palmoplantar keratoderma (also known as "Palmoplantar keratoderma cum degeneratione granulosa Vörner," "Vörner's epidermolytic palmoplantar keratoderma", and "Vörner keratoderma"[4]) is one of the most common patterns of palmoplantar keratoderma, an autosomal dominant condition that presents within the first few months of life, characterized by a well-demarcated, symmetric thickening of palms and soles, often with a "dirty" snakeskin appearance due to underlying epidermolysis.[1]:506
- Aquagenic keratoderma, also known as acquired aquagenic palmoplantar keratoderma,[4]:788 transient reactive papulotranslucent acrokeratoderma,[4]aquagenic syringeal acrokeratoderma,[4] and aquagenic wrinkling of the palms,[2] is a skin condition characterized by the development of white papuleson the palms after water exposure.[2]:215 The condition causes irritation of the palms when touching certain materials after being wet, e.g., paper, cloth. An association with cystic fibrosis has been suggested.[21] The association with cystic fibrosis suggests an increased salt content in the skin.[22]
Left Cancotic Papulation Neck Rubules. 1945. Mixed Wallace-Smith-Petersen-STDGerm. Infectious Cancer. Zoonit dis, Cancer Bone Cancer. Sarcotic Fibrotic. Lipodystrophy, Redding. Specklularation light brown or red. swelling inflammation clogulation. purulants. HER HIV POX. hole bone. overvaccination. eczema hypersensitivity immunsuppression immune dysfunction degeneratio cancer bone cancer disseminative metastatic type. wee walish weattey. pus blood, chol plam.
| Progressive vaccinia | |
|---|---|
| Other names | Vaccinia gangrenosum, Vaccinia necrosum or disseminated vaccinia |
 | |
| The patient required a skin graft on her upper left arm in order to correct the necrotic vaccination site, due to the onset of progressive vaccinia, formerly known as vaccinia gangrenosum. | |
Necrobiosis lipoidica is a necrotising skin condition that usually occurs in patients with diabetes mellitus but can also be associated with rheumatoid arthritis.[1] In the former case it may be called necrobiosis lipoidica diabeticorum (NLD).[2] NLD occurs in approximately 0.3% of the diabetic population, with the majority of sufferers being women (approximately 3:1 females to males affected).
The severity or control of diabetes in an individual does not affect who will or will not get NLD.[3] Better maintenance of diabetes after being diagnosed with NLD will not change how quickly the NLD will resolve.
| Necrobiosis lipoidica | |
|---|---|
 | |
| Specialty | Dermatology |
https://en.wikipedia.org/wiki/Necrobiosis_lipoidica
---------------------------------------------------------------------------------------------
https://en.wikipedia.org/wiki/Endogenous_retrovirus
https://en.wikipedia.org/wiki/NF-κB
https://en.wikipedia.org/wiki/Calciphylaxis
https://en.wikipedia.org/wiki/Dystrophic_calcification
https://en.wikipedia.org/wiki/Pasteurella
https://en.wikipedia.org/wiki/Palmoplantar_keratoderma
https://en.wikipedia.org/wiki/Vaccinia
https://en.wikipedia.org/wiki/Generalized_vaccinia
https://microbewiki.kenyon.edu/index.php/Granulosis_Virus
https://en.wikipedia.org/wiki/Methotrexate
https://en.wikipedia.org/wiki/Myxococcus
https://seer.cancer.gov/seertools/hemelymph/532b32a0e4b0626b1926e990/
https://seer.cancer.gov/seertools/hemelymph/51f6cf57e3e27c3994bd5363/?q=cytoid#
https://en.wikipedia.org/wiki/Treponema_pallidum
https://en.wikipedia.org/wiki/Simian_immunodeficiency_virus
https://en.wikipedia.org/wiki/Human_T-lymphotropic_virus
https://en.wikipedia.org/wiki/Bacillus_thuringiensis
https://en.wikipedia.org/wiki/Visna-maedi_virus
https://en.wikipedia.org/wiki/Jaagsiekte_sheep_retrovirus
https://en.wikipedia.org/wiki/Caprine_arthritis_encephalitis_virus
https://en.wikipedia.org/wiki/Rhabdomyolysis
https://en.wikipedia.org/wiki/Tumor_necrosis_factor
https://en.wikipedia.org/wiki/Tumor_lysis_syndrome
https://en.wikipedia.org/wiki/Tuberculosis
Dr. F
| Palmoplantar keratoderma | |
|---|---|
 | |
| Patient with severe plantar keratosis. | |
| Specialty | Dermatology |
Palmoplantar keratodermas are a heterogeneous group of disorders characterized by abnormal thickening of the stratum corneum of the palms and soles.
Autosomal recessive, dominant, X-linked, and acquired forms have all been described.[1]:505[2]:211[3]
- Diffuse epidermolytic palmoplantar keratoderma (also known as "Palmoplantar keratoderma cum degeneratione granulosa Vörner," "Vörner's epidermolytic palmoplantar keratoderma", and "Vörner keratoderma"[4]) is one of the most common patterns of palmoplantar keratoderma, an autosomal dominant condition that presents within the first few months of life, characterized by a well-demarcated, symmetric thickening of palms and soles, often with a "dirty" snakeskin appearance due to underlying epidermolysis.[1]:506
- Scleroatrophic syndrome of Huriez (also known as "Huriez syndrome," "Palmoplantar keratoderma with scleroatrophy,"[4] "Palmoplantar keratoderma with sclerodactyly," "Scleroatrophic and keratotic dermatosis of the limbs," and "Sclerotylosis") is an autosomal dominant keratoderma with sclerodactylypresent at birth with a diffuse symmetric keratoderma of the palms and soles.[1]:513[2]:576 An association with 4q23 has been described.[14] It was characterized in 1968.[15]
- Vohwinkel syndrome (also known as "Keratoderma hereditaria mutilans,"[4] "Keratoma hereditaria mutilans,"[4] "Mutilating keratoderma of Vohwinkel",[2]:213 "Mutilating palmoplantar keratoderma"[4]) is a diffuse autosomal dominant keratoderma with onset in early infancy characterized by a honeycombed keratoderma involving the palmoplantar surfaces.[1]:512 Mild to moderate sensorineural hearing loss is often associated.[1] It has been associated with GJB2.[16] It was characterized in 1929.[17]
- Olmsted syndrome (also known as "Mutilating palmoplantar keratoderma with periorificial keratotic plaques," "Mutilating palmoplantar keratoderma with periorificial plaques"[4] and "Polykeratosis of Touraine") is a keratoderma of the palms and soles, with flexion deformity of the digits, that begins in infancy.[1]:510[2]:214[4][18] Treatment with retinoids has been described.[19] It has been associated with mutations in TRPV3.[20]
https://en.wikipedia.org/wiki/Palmoplantar_keratoderma
Granuloma annulare (GA) is a common, sometimes chronic skin condition which presents as reddish bumps on the skin arranged in a circle or ring.[1] It can initially occur at any age, though two-thirds of patients are under 30 years old, and it is seen most often in children and young adults. Females are two times as likely to have it than males.[2]
| Granuloma annulare | |
|---|---|
 | |
| Perforating form of Granuloma annulare on hand | |
| Specialty | Dermatology |
https://en.wikipedia.org/wiki/Granuloma_annulare
Trench fever (also known as "five-day fever", "quintan fever" (Latin: febris quintana), and "urban trench fever"[1]) is a moderately serious disease transmitted by body lice. It infected armies in Flanders, France, Poland, Galicia, Italy, Salonika, Macedonia, Mesopotamia, Russia and Egypt in World War I.[2][3] Three noted sufferers during WWI were the authors J. R. R. Tolkien,[4] A. A. Milne,[5] and C. S. Lewis.[6] From 1915 to 1918 between one-fifth and one-third of all British troops reported ill had trench fever while about one-fifth of ill German and Austrian troops had the disease.[2] The disease persists among the homeless.[7] Outbreaks have been documented, for example, in Seattle[8] and Baltimore in the United States among injection drug users[9]and in Marseille, France,[8] and Burundi.[10]
Trench fever is also called Wolhynia fever, shin bone fever, Meuse fever, His disease and His–Werner disease or Werner-His disease (after Wilhelm His Jr. and Heinrich Werner).
The disease is caused by the bacterium Bartonella quintana (older names: Rochalimea quintana, Rickettsia quintana), found in the stomach walls of the body louse.[3] Bartonella quintana is closely related to Bartonella henselae, the agent of cat scratch fever and bacillary angiomatosis.
https://en.wikipedia.org/wiki/Trench_fever
Serological testing is typically used to obtain a definitive diagnosis. Most serological tests would succeed only after a certain period of time past the symptom onset (usually a week). The differential diagnosis list includes typhus, ehrlichiosis, leptospirosis, Lyme disease, and virus-caused exanthema (measles or rubella).[citation needed]
https://en.wikipedia.org/wiki/Trench_fever
Bacillary angiomatosis (BA) is a form of angiomatosis associated with bacteria of the genus Bartonella.[1]
| Bacillary angiomatosis | |
|---|---|
 | |
| Bartonella (bacterial species which causes this condition) | |
| Specialty | Infectious disease |
https://en.wikipedia.org/wiki/Bacillary_angiomatosis
Bartonella henselae, formerly Rochalimæa, is a proteobacterium that is the causative agent of cat-scratch disease[1] (bartonellosis).
B. henselae is a member of the genus Bartonella, one of the most common types of bacteria in the world. It is a facultative intracellular microbe that targets red blood cells. One study showed it invaded the mature blood cells of humans.[2] It infects the host cell by sticking to it using trimeric autotransporter adhesins.[3] In the United States, about 22,000 people are diagnosed, most under the age of 20. Most often, it is transmitted from kittens.[4]
https://en.wikipedia.org/wiki/Bartonella_henselae
African trypanosomiasis, also known as African sleeping sickness or simply sleeping sickness, is an insect-borne parasitic infection of humans and other animals.[3] It is caused by the species Trypanosoma brucei.[3] Humans are infected by two types, Trypanosoma brucei gambiense (TbG) and Trypanosoma brucei rhodesiense (TbR).[3] TbG causes over 98% of reported cases.[1] Both are usually transmitted by the bite of an infected tsetse fly and are most common in rural areas.[3]
Initially, the first stage of the disease is characterized by fevers, headaches, itchiness, and joint pains, beginning one to three weeks after the bite.[1][2] Weeks to months later, the second stage begins with confusion, poor coordination, numbness, and trouble sleeping.[2] Diagnosis is by finding the parasite in a blood smear or in the fluid of a lymph node.[2] A lumbar puncture is often needed to tell the difference between first- and second-stage disease.[2]
https://en.wikipedia.org/wiki/African_trypanosomiasis
Arsphenamine, also known as Salvarsan or compound 606, is a drug that was introduced at the beginning of the 1910s as the first effective treatment for syphilis and African trypanosomiasis.[2] This organoarsenic compound was the first modern antimicrobial agent.[3]
https://en.wikipedia.org/wiki/Arsphenamine
https://en.wikipedia.org/wiki/Trench_foot
Office of War Information - WW2
Subscribe to:
Posts (Atom)