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.

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.

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.

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

The disease typically develops two to four weeks after a throat infection. Symptoms include: fever, painful joints with those joints affected changing with time, involuntary muscle movements, and occasionally a characteristic non-itchy rash known as erythema marginatum. The heart is involved in about half of cases. Damage to the heart valves usually occurs only after multiple attacks but may occasionally occur after a single case of RF. The damaged valves may result in heart failure and also increase the risk of atrial fibrillation and infection of the valves.

"Rabbits, Hares & Lagomorphs"

Usually there do not appear to be any clinical signs. Subcutaneous cysts, warbles, may present upon larval deposition out of the body at maturation.

"Felines & Canines"

There are three forms in which Cuterebriasis may present:

- Myasis

- Cerebrospinal

- Respiratory

Myasis involves subcutaneous cyst formation due to 3rd larval instar maturation, occurring ~30 days post-entry into the body. Cysts are often found on the face, neck and trunk, but location varies with larval migration within the host. Serous discharge may be observed from these cysts, which are typically 3-5mm in diameter and include a central pore through which the larvae respire. This pore also serves as a means of exit for the larvae, which occurs anywhere between 3 and 8 weeks post-entry.

Cerebrospinal cuterebriasis results from larval migration to the brain. This is seen in cats, and is the proposed cause for feline ischemic encephalopathy and a suggestive causative agent of feline idiopathic vestibular disease. Symptoms of this type of presentation include lethargy, seizures, blindness, abnormal vocalization or gait, circling, and abnormal or no reflex responses. When affecting the central nervous system, cats are known to exhibit violent sneezing attacks that can onset weeks prior to manifestation of other clinical signs.

Respiratory disease results when larval migration occurs through the trachea, pharynx, diaphragm, or lungs. Cuterebriasis has been increasingly noted as a cause for dyspnea in felines.

They form as a result of increased pressure in the gallbladder and recurrent damage to the wall of the gallbladder.

Cuterebriasis is a parasitic disease affecting rodents, lagomorphs (hares, rabbits, pikas), felines and canines. The etiologic agent is the larval development of bot flies within the "Cuterebra" or "Trypoderma" genera, which occurs obligatorily in rodents and lagomorphs, respectively. Felines and canines serve as accidental hosts, but research suggests only by "Trypoderma" spp. Entrance into the body by first instar larva occurs via mucous membranes of natural orifices or open wounds as opposed to direct dermic penetration.

Rheumatic fever (RF) is an inflammatory disease that can involve the heart, joints, skin, and brain. The disease typically develops two to four weeks after a streptococcal throat infection. Signs and symptoms include fever, multiple painful joints, involuntary muscle movements, and occasionally a characteristic non-itchy rash known as erythema marginatum. The heart is involved in about half of cases. Damage to the heart valves, known as rheumatic heart disease (RHD), usually occurs after repeated attacks but can sometimes occur after one. The damaged valves may result in heart failure, atrial fibrillation and infection of the valves.

Rheumatic fever may occur following an infection of the throat by the bacterium "Streptococcus pyogenes". If the infection is untreated rheumatic fever can occur in up to three percent of people. The underlying mechanism is believed to involve the production of antibodies against a person's own tissues. Due to their genetics, some people are more likely to get the disease when exposed to the bacteria than others. Other risk factors include malnutrition and poverty. Diagnosis of RF is often based on the presence of signs and symptoms in combination with evidence of a recent streptococcal infection.

Treating people who have strep throat with antibiotics, such as penicillin, decreases the risk of developing rheumatic fever. In order to avoid antibiotic misuse this often involves testing people with sore throats for the infection, which may not be available in the developing world. Other preventive measures include improved sanitation. In those with rheumatic fever and rheumatic heart disease, prolonged periods of antibiotics are sometimes recommended. Gradual return to normal activities may occur following an attack. Once RHD develops, treatment is more difficult. Occasionally valve replacement surgery or valve repair is required. Otherwise complications are treated as per normal.

Rheumatic fever occurs in about 325,000 children each year and about 33.4 million people currently have rheumatic heart disease. Those who develop RF are most often between the ages of 5 and 14, with 20% of first-time attacks occurring in adults. The disease is most common in the developing world and among indigenous peoples in the developed world. In 2015 it resulted in 319,400 deaths down from 374,000 deaths in 1990. Most deaths occur in the developing world where as many as 12.5% of people affected may die each year. Descriptions of the condition are believed to date back to at least the 5th century BCE in the writings of Hippocrates. The disease is so named because its symptoms are similar to those of some rheumatic disorders.

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.

Acute rheumatic fever (ARF) is a complication of respiratory infections caused by GAS. The M-protein generates antibodies that cross-react with autoantigens on interstitial connective tissue, in particular of the endocardium and synovium, that can lead to significant clinical illness.

Although common in developing countries, ARF is rare in the United States, possibly secondary to improved antibiotic treatment, with small isolated outbreaks reported only occasionally. It is most common among children between 5 and 15 years old and occurs 1–3 weeks after an untreated GAS pharyngitis.

ARF is often clinically diagnosed based on Jones Criteria, which include: pancarditis, migratory polyarthritis of large joints, subcutaneous nodules, erythema marginatum, and sydenham chorea (involuntary, purposeless movement). The most common clinical finding is a migratory arthritis involving multiple joints.

Other indicators of GAS infection such as a DNAase or ASO serology test must confirm the GAS infection. Other minor Jones Criteria are fever, elevated ESR and arthralgia. One of the most serious complications is pancarditis, or inflammation of all three heart tissues. A fibrinous pericarditis can develop with a classic friction rub that can be auscultated. This will give increasing pain upon reclining.

Further endocarditis can develop with aseptic vegetations along the valve closure lines, in particular the mitral valve. Chronic rheumatic heart disease mostly affects the mitral valve, which can become thickened with calcification of the leaflets, often causing fusion of the commissures and chordae tendineae.

Other findings of ARF include erythema marginatum (usually over the spine or other bony areas) and a red expanding rash on the trunk and extremities that recurs over weeks to months. Because of the different ways ARF presents itself, the disease may be difficult to diagnose.

A neurological disorder, Sydenham chorea, can occur months after an initial attack, causing jerky involuntary movements, muscle weakness, slurred speech, and personality changes. Initial episodes of ARF as well as recurrences can be prevented by treatment with appropriate antibiotics.

It is important to distinguish ARF from rheumatic heart disease. ARF is an acute inflammatory reaction with pathognomonic Aschoff bodies histologically and RHD is a non-inflammatory sequela of ARF.

One of the reasons a cat may stop eating is separation anxiety and the emotional stress that results. Moving, gaining or losing housemates or pets, going on vacation, or prolonged boarding are all common situations that pet owners report just prior to the onset of the disease, but it may develop without these conditions existing. Obesity is known to increase the risk of hepatic lipidosis; however, there is no known "official" cause of the disease. Severe anorexia usually precedes the onset of the disease. When the cat has no energy from eating, the liver must metabolize fat deposits in the body into usable energy to sustain life. The cat liver, however, is poor at metabolizing fat, causing a buildup of fat in the cells of the liver, leading to fatty liver. At this point the disease can be diagnosed; however, it will often not be diagnosed, and many animals are euthanized due to improper or no diagnosis.

Feline hepatic lipidosis shares similar symptoms to other problems, including liver disease, renal failure, feline leukemia, Feline infectious peritonitis and some cancers. Diagnosis requires tests that target the liver to make an accurate diagnosis. Jaundice is highly indicative of the disease. Blood tests and a liver biopsy will confirm the presence of the disease.

Post-streptococcal glomerulonephritis (PSGN) is an uncommon complication of either a strep throat or a streptococcal skin infection. It is classified as a type III hypersensitivity reaction. Symptoms of PSGN develop within 10 days following a strep throat or 3 weeks following a GAS skin infection. PSGN involves inflammation of the kidney. Symptoms include pale skin, lethargy, loss of appetite, headache, and dull back pain. Clinical findings may include dark-colored urine, swelling of different parts of the body (edema), and high blood pressure. Treatment of PSGN consists of supportive care.

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

Body odor (American English) or body odour (British English; see spelling differences) is present in animals and humans, and its intensity can be influenced by many factors (behavioral patterns, survival strategies). Body odor has a strong genetic basis both in animals and humans, but it can be also strongly influenced by various diseases and physiological conditions. Body odor is generally considered to be an unpleasant odor among many human cultures.

Adenomyomatosis is caused by an overgrowth of the mucosa, thickening of the muscular wall, and formation of intramural diverticula or sinus tracts termed Rokitansky-Aschoff sinuses.

Most polyps do not cause noticeable symptoms. Gallbladder polyps are usually found incidentally when examining the abdomen by ultrasound for other conditions, usually abdominal pain.

Specific types of additional body parts include:

- Accessory breast – one or more additional breasts

- Accessory spleen – one or more additional spleens

- Cervical rib – an additional rib

- Diphallia - Having two penes/penises.

- Hermaphroditism – having both sexes' sex organs

- Hyperdontia – additional teeth

- Pelvic digit – a bony growth in the soft tissue of the pelvic region

- Polycephaly – an extra head

- Polydactyly – additional fingers or toes

- Polymelia — an extra arm or leg.

- Polyorchidism – having three or more testicles

- Supernumerary bones – these additional bones are fairly common, particularly in the feet, and are frequently mistaken for fractures on x-rays.

- Supernumerary kidney – a third kidney

- Supernumerary nipples – an additional nipple

- Supernumerary phantom limbs – where the brain acts as though a limb were there, but it is not.

- Syndactyly – webbing between the fingers or toes

- Uterus didelphys – two vaginal canals and/or uteri

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.

Ectopia cordis (Greek: ""away / out of place"" + Latin: ""heart"") is a congenital malformation in which the heart is abnormally located either partially or totally outside of the thorax. The ectopic heart can be found along a spectrum of anatomical locations, including the neck, chest, or abdomen. In most cases, the heart protrudes outside the chest through a split sternum.

Supernumerary body parts are most commonly a congenital disorder involving the growth of an additional part of the body and a deviation from the body plan. Body parts may be easily visible or hidden away, such as internal organs.

Many additional body parts form by the same process as conjoined twins: the zygote begins to split but fails to completely separate. This condition may also be a symptom of repeated occurrences of continuous inbreeding in a genetic line.

Examples of atrophy as part of normal development include shrinking and the involution of the thymus in early childhood, and the tonsils in adolescence. In old age, effects include, but are not limited to, loss of teeth, hair, thinning of skin that creates wrinkles, weakening of muscles, loss of weight in organs and sluggish mental activity.