In medicine, Aschoff bodies are nodules found in the hearts of individuals with rheumatic fever. They result from inflammation in the heart muscle and are characteristic of rheumatic heart disease. These nodules were discovered independently by Ludwig Aschoff and Paul Rudolf Geipel, and for this reason they are occasionally called Aschoff-Geipel bodies.

Microscopically, Aschoff bodies are areas of inflammation of the connective tissue of the heart, or focal interstitial inflammation. Fully developed Aschoff bodies are granulomatous structures consisting of fibrinoid change, lymphocytic infiltration, occasional plasma cells, and characteristically abnormal macrophages surrounding necrotic centres. Some of these macrophages may fuse to form multinucleated giant cells. Others may become Anitschkow cells or "caterpillar cells", so named because of the appearance of their chromatin.

They are pathognomic foci of fibrinoid necrosis found in many sites, most often the myocardium. Initially they are surrounded by lymphocytes, macrophages, and a few plasma cells, but they are slowly replaced by a fibrous scar. Aschoff bodies are found in all the three layers of the heart, least chance in the pericardium.

In pathology, Anitschkow (or Anichkov) cells are often cells associated with rheumatic heart disease. Anitschkow cells are enlarged macrophages found within granulomas (called Aschoff bodies) associated with the disease.

The cells are also called caterpillar cells, as they have an ovoid nucleus and chromatin that is condensed toward the center of the nucleus in a wavy rod-like pattern that to some resembles a caterpillar. Larger Anitschkow cells may coalesce to form multinucleated Aschoff giant cells. Anitschkow cells were named after the Russian pathologist Nikolai Nikolajewitsch Anitschkow.

Squamous epithelial cells with nuclear changes resembling Anitschkow cells have also been observed in recurrent aphthous stomatitis, iron deficiency anemia, children receiving chemotherapy, as well as in healthy individuals.

Small image of an infected area of the body due to a reaction with an implant

A foreign-body giant cell is a collection of fused macrophages (giant cell) which are generated in response to the presence of a large foreign body. This is particularly evident with implants that cause the body chronic inflammation and foreign body response.

This reaction to the implant causes damages to the infected area, leaving the exterior surface with scars.

The nuclei are arranged in a disorganized manner. The nuclei in this cell are centrally placed and overlap each other. This is in contrast to a Langhans giant cell, where the nuclei are arranged on the border.

Foreign body cells can detect and eliminate

bacteria caught within the body, by sensing the unique sugar coating that are

on the invading prokaryotes. These macrophage cells are one of a few

phagocytic cells, but not the first to come to an injury site, and tend to

linger from anytime between days to weeks. There has been some research done on other variations of

giant calls with different functions.

The foreign body granuloma is a response of biological tissue to any foreign material in the tissue. Tissue-encapsulation of an implant is part of this. An infection around a splinter is part of this, too.

The presence of the implant changes the healing response, and this is called the foreign-body reaction (FBR). FBR consists of: protein adsorption, macrophages, multinucleated foreign body giant cells (macrophage fusion), fibroblasts, and angiogenesis.

It can be caused by beryllium.

Subcutaneous cysts may be surgically opened to remove less mature bots. If more matured, cysts may be opened and "cuterebra" may be removed using mosquito forceps. Covering the pore in petroleum jelly may aide in removal. If larvae are discovered within body tissues, rather than subcutaneously, surgical removal is the only means of treatment. Ivermectin may be administered with corticosteroids to halt larval migration in cats presenting with respiratory cuterebriasis, but this is not approved for use in cats. There is not yet a known cure for cerebrospinal cuterebriasis.

No vaccines are currently available to protect against "S. pyogenes" infection, although research is underway to develop one. Difficulties in developing a vaccine include the wide variety of strains of "S. pyogenes" present in the environment and the large amount of time and people that will be needed for appropriate trials for safety and efficacy of the vaccine.

Rheumatic fever can be prevented by effectively treating strep throat with antibiotics.

In those who have previously had rheumatic fever, antibiotics in a preventative manner are occasionally recommended. As of 2017 the evidence to support long term antibiotics in those with underlying disease; however, is poor.

The American Heart Association suggests that dental health be maintained, and that people with a history of bacterial endocarditis, a heart transplant, artificial heart valves, or "some types of congenital heart defects" may wish to consider long-term antibiotic prophylaxis.

Untreated, the disease has a mortality rate upwards of 90%. Cats treated in the early stages can have a recovery rate of 80–90%. Left untreated, the cats usually die from severe malnutrition or complications from liver failure. Treatment usually involves aggressive feeding through one of several methods.

Cats can have a feeding tube inserted by a veterinarian so that the owner can feed the cat a liquid diet several times a day. They can also be force-fed through the mouth with a syringe. If the cat stops vomiting and regains its appetite, it can be fed in a food dish normally. The key is aggressive feeding so the body stops converting fat in the liver. The cat liver has a high regeneration rate and the disease will eventually reverse assuming that irreparable damage has not been done to the liver.

The best method to combat feline hepatic lipidosis is prevention and early detection. Obesity increases the chances of onset. In addition, if a cat stops eating for 1–2 days, it should be taken to a vet immediately. The longer the disease goes untreated, the higher the mortality rate.

The treatment of choice is penicillin, and the duration of treatment is around 10 days. Antibiotic therapy (using injected penicillin) has been shown to reduce the risk of acute rheumatic fever. In individuals with a penicillin allergy, erythromycin, other macrolides, and cephalosporins have been shown to be effective treatments.

Treatment with ampicillin/sulbactam, amoxicillin/clavulanic acid, or clindamycin is appropriate if deep oropharyngeal abscesses are present, in conjunction with aspiration or drainage. In cases of streptococcal toxic shock syndrome, treatment consists of penicillin and clindamycin, given with intravenous immunoglobulin.

For toxic shock syndrome and necrotizing fasciitis, high-dose penicillin and clindamycin are used. Additionally, for necrotizing fasciitis, surgery is often needed to remove damaged tissue and stop the spread of the infection.

No instance of penicillin resistance has been reported to date, although since 1985, many reports of penicillin tolerance have been made. The reason for the failure of penicillin to treat "S. pyogenes" is most commonly patient noncompliance, but in cases where patients have been compliant with their antibiotic regimen, and treatment failure still occurs, another course of antibiotic treatment with cephalosporins is common.

Definitive diagnosis can only occur with positive identification of the larvae. This involves radiologic imaging (preferably MRI which can reveal larval migration tracks and in some cases the larvae themselves) as well as surgical exploration during which larvae can be removed and examined for identification. Identification of exact species is often impossible as the instars of the various "Cuterebra" and "Trychoderma" spp. exhibit significant resemblance, but identification as a "Cuterebra" bot fly is sufficient for diagnosis as cuterebriasis. Typically, a third larval instar is found and identifiable by its dark, thick, heavily spined body.

"S. pyogenes" infections are best prevented through effective hand hygiene. No vaccines are currently available to protect against "S. pyogenes" infection, although research has been conducted into the development of one. Difficulties in developing a vaccine include the wide variety of strains of "S. pyogenes" present in the environment and the large amount of time and number of people that will be needed for appropriate trials for safety and efficacy of the vaccine.

As many as 90% of Americans and 92% of teenagers use antiperspirants or deodorants. In 2014, the global market for deodorants was estimated at 13.00 billion USD with a compound annual growth rate of 5.62% between 2015 and 2020.

Body odor may be reduced or prevented or even aggravated by using deodorants, antiperspirants, disinfectants, underarm liners, triclosan, special soaps or foams with antiseptic plant extracts such as ribwort and liquorice, chlorophyllin ointments and sprays topically, and chlorophyllin supplements internally. Although body odor is commonly associated with hygiene practices, its presentation can be affected by changes in diet as well as the other factors.

Fungicidal agents such as azadirachtin and phytoallexin have been used against some muscardine pathogens. Silkworm breeders dust their cages with slaked lime to discourage fungal growth. In India a dust of chaff soaked in formalin is applied to the larvae.

The rate of progression varies significantly from person to person.

There is not good data on outcomes; it appears that APBD likely leads to earlier death, but people with APBD can live many years after diagnosis with relatively good quality of life.

Black pigment gallstones can form in Rokitansky–Aschoff sinuses of the gallbladder after the fourth to fifth decades of life in absence of the typical risk factors for bilirubin suprasaturation of bile. Hence, they are associated with gallstones (cholelithiasis). Cases of gall bladder cancer have also been reported to arise from Rokitansky–Aschoff sinuses.

Feline hepatic lipidosis, also known as feline fatty liver syndrome, is one of the most common forms of liver disease of cats. The disease officially has no known cause, though obesity is known to increase the risk. The disease begins when the cat stops eating from a loss of appetite, forcing the liver to convert body fat into usable energy. If this process continues for too long, fat builds up in the cells of the liver, and the disease has officially onset. Prognosis varies depending on the stage of the disease, with both a high recovery and mortality rate at different stages. The disease is reversible through intense feeding. Treatment may involve the insertion of a temporary feeding tube to ensure adequate caloric intake for cats that have stopped eating as a result of this disease.

Rokitansky–Aschoff sinuses, also entrapped epithelial crypts, are pseudodiverticula or pockets in the wall of the gallbladder. They may be microscopic or macroscopic.

Histologically, they are outpouchings of gallbladder mucosa into the gallbladder muscle layer and subserosal tissue as a result of hyperplasia and herniation of epithelial cells through the fibromuscular layer of the gallbladder wall. They are usually referred to as adenomyomatosis.

They are not of themselves considered abnormal, but they can be associated with cholecystitis.

Adenomyomatosis is a benign condition characterized by hyperplastic changes of unknown cause involving the wall of the gallbladder.

One drug in test seemed to prevent the type of muscle loss that occurs in immobile, bedridden patients.

Testing on mice showed that it blocked the activity of a protein present in the muscle that is involved in muscle atrophy. However, the drug's long-term effect on the heart precludes its routine use in humans, and other drugs are being sought.

In alchemy, putrefaction is the same as fermentation, whereby a substance is allowed to rot or decompose undisturbed. In some cases, the commencement of the process is facilitated with a small sample of the desired material to act as a "seed".

Muscardine is a disease of insects. It is caused by many species of entomopathogenic fungus. Many muscardines are known for affecting silkworms. Muscardine may also be called calcino.

While studying muscardine in silkworms in the 19th century, Agostino Bassi found that the causal agent was a fungus. This was the first demonstration of the germ theory of disease, the first time a microorganism was recognized as an animal pathogen.

There are many types of muscardine. They are often named for the color of the conidial layer each fungus leaves on its host.

Certain poisonous substances to the body can delay the process of putrefaction. They include:

- Carbolic acid (Phenol)

- Arsenic and antimony

- Strychnine

- Nux Vomica (Plant)

- Zinc chloride, ZnCl