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 |
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| Trench foot as seen on an unidentified soldier during World War I. | |
| Specialty | Emergency medicine |
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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] |
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| 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 | |
|---|---|
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| 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/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 | |
|---|---|
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| 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]
| Granuloma annulare | |
|---|---|
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| Perforating form of Granuloma annulare on hand | |
| Specialty | Dermatology |
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
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