Necrotising hepatopancreatitis (NHP), is also known as Texas necrotizing hepatopancreatitis (TNHP), Texas Pond Mortality Syndrome (TPMS) and Peru necrotizing hepatopancreatitis (PNHP), is a lethal epizootic disease of farmed shrimp. It is not very well researched yet, but generally assumed to be caused by a bacterial infection.

NHP mainly affects the farmed shrimp species "Litopenaeus vannamei" (Pacific white shrimp) and "Litopenaeus stylirostris" (Western blue shrimp), but has also been reported in three other American species, namely "Farfantepenaeus aztecus", "Farfantepenaeus californiensis", and "Litopenaeus setiferus". The highest mortality rates occur in "L. vannamei", which is one of the two most frequently farmed species of shrimp. Untreated, the disease causes mortality rates of up to 90 percent within 30 days. A first outbreak of NHP had been reported in Texas in 1985; the disease then spread to shrimp aquacultures in South America, in 2009 to China and subsequently Southeast Asia, followed by massive outbreaks in that region in 2012-2013.

NHP is associated with a small, gram-negative, and highly pleomorphic "Rickettsia"-like bacterium that belongs to its own, new genus in the alpha proteobacteria. However, in early-2013 a novel strain of "Vibrio parahaemolyticus" was identified as a more likely causative agent, though involvement of a virus cannot be definitely ruled out yet.

The aetiological agent is the pathogenic agent Candidatus "Hepatobacter penaei", an obligate intracellular bacterium of the Order α-Proteobacteria.

Infected shrimps show gross signs including soft shells and flaccid bodies, black or darkened gills, dark edges of the pleopods, and uropods, and an atrophied hepatopancreas that is whitish instead of orange or tan as is usual.

Whichever of the two bacteria associated with NHP actually causes it, the pathogen seems to prefer high water temperatures (above ) and elevated levels of salinity (more than 20–38 ppt). Avoiding such conditions in shrimp ponds is thus an important disease control measure.

People usually complain of intense pain that may seem excessive given the external appearance of the skin. People initially have signs of inflammation, fever and a fast heart rate. With progression of the disease, often within hours, tissue becomes progressively swollen, the skin becomes discolored and develops blisters. Crepitus may be present and there may be a discharge of fluid, said to resemble "dish-water". Diarrhea and vomiting are also common symptoms.

In the early stages, signs of inflammation may not be apparent if the bacteria are deep within the tissue. If they are "not" deep, signs of inflammation, such as redness and swollen or hot skin, develop very quickly. Skin color may progress to violet, and blisters may form, with subsequent necrosis (death) of the subcutaneous tissues.

Furthermore, people with necrotizing fasciitis typically have a fever and appear sick. Mortality rates are as high as 73% if left untreated. Without surgery and medical assistance, such as antibiotics, the infection will rapidly progress and will eventually lead to death.

When it affects the groin it is known as Fournier gangrene.

Necrotizing fasciitis (NF), commonly known as flesh-eating disease, is an infection that results in the death of the body's soft tissue. It is a severe disease of sudden onset that spreads rapidly. Symptoms include red or purple skin in the affected area, severe pain, fever, and vomiting. The most commonly affected areas are the limbs and perineum.

Typically the infection enters the body through a break in the skin such as a cut or burn. Risk factors include poor immune function such as from diabetes or cancer, obesity, alcoholism, intravenous drug use, and peripheral vascular disease. It is not typically spread between people. The disease is classified into four types, depending on the infecting organism. Between 55% and 80% of cases involve more than one type of bacteria. Methicillin-resistant "Staphylococcus aureus" (MRSA) is involved in up to a third of cases. Medical imaging is helpful to confirm the diagnosis.

Prevention is by good wound care and handwashing. It is usually treated with surgery to remove the infected tissue and intravenous antibiotics. Often a combination of antibiotics are used such as penicillin G, clindamycin, vancomycin, and gentamicin. Delays in surgery are associated with a higher risk of death. Despite high quality treatment the risk of death is between 25% and 35%.

Necrotizing fasciitis affects 0.4 to 1 person per 100,000 per year. Both sexes are affected equally. It becomes more common among older people and is very rare in children. Necrotizing fasciitis has been described at least since the time of Hippocrates. The term "necrotising fasciitis" first came into use in 1952.

Toxic shock syndrome (TSS) is a condition caused by bacterial toxins. Symptoms may include fever, rash, skin peeling, and low blood pressure. There may also be symptoms related to the specific underlying infection such as mastitis, osteomyelitis, necrotising fasciitis, or pneumonia.

TSS is caused by bacteria of either the "Streptococcus pyogenes" or "Staphylococcus aureus" type. Streptococcal toxic shock syndrome (STSS) is sometimes referred to as toxic shock-like syndrome (TSLS). The underlying mechanism involves the production of superantigens during an invasive streptococcus infection or a localized staphylococcus infection. Risk factors for the staphylococcal type include the use of very absorbent tampons and skin lesions in young children. Diagnosis is typically based on symptoms.

Treatment includes antibiotics, incision and drainage of any abscesses, and possibly intravenous immunoglobulin. The need for rapid removal of infected tissue via surgery in those with a streptococcal cause while commonly recommended is poorly supported by the evidence. Some recommend delaying surgical debridement. The overall risk of death in streptococcal disease is about 50% while in staphylococcal disease it is around 5%. Death may occur within 2 days.

In the United States streptococcal TSS occurs in about 3 per 100,000 per year while staphylococcal TSS occurs in about 0.5 per 100,000 per year. The condition is more common in the developing world. It was first described in 1927. Due to the association with very absorbent tampons, these products were removed from sale.

Symptoms of toxic shock syndrome vary depending on the underlying cause. TSS resulting from infection with the bacterium "Staphylococcus aureus" typically manifests in otherwise healthy individuals via signs and symptoms including high fever, accompanied by low blood pressure, malaise and confusion, which can rapidly progress to stupor, coma, and multiple organ failure. The characteristic rash, often seen early in the course of illness, resembles a sunburn, and can involve any region of the body including the lips, mouth, eyes, palms and soles. In patients who survive the initial phase of the infection, the rash desquamates, or peels off, after 10–14 days.

In contrast, TSS caused by the bacterium "Streptococcus pyogenes", or TSLS, typically presents in people with pre-existing skin infections with the bacteria. These individuals often experience severe pain at the site of the skin infection, followed by rapid progression of symptoms as described above for TSS. In contrast to TSS caused by "Staphylococcus", streptococcal TSS less often involves a sunburn-like rash.

Noma is a rapidly progressive, polymicrobial, often gangrenous infection of the mouth or genitals.

The infection in most instances presents as a painless lump just under the skin. In southern Australia, the presentation is more often as a pimple in the skin (dermis) rather than under it. The infection is mostly in the limbs, most often in exposed areas, but not on the hands or feet. In children, all areas may be involved, including the face or abdomen. A more severe form of infection produces diffuse swelling of a limb, which, unlike the papule or nodule, can be painful and accompanied by fever. Infection may frequently follow physical trauma, often minor trauma such as a small scratch.

Abscesses may occur in any kind of solid tissue but most frequently on skin surface (where they may be superficial pustules (boils) or deep skin abscesses), in the lungs, brain, teeth, kidneys, and tonsils. Major complications are spreading of the abscess material to adjacent or remote tissues, and extensive regional tissue death (gangrene).

The main symptoms and signs of a skin abscess are redness, heat, swelling, pain, and loss of function. There may also be high temperature (fever) and chills.

An internal abscess is more difficult to identify, but signs include pain in the affected area, a high temperature, and generally feeling unwell.

Internal abscesses rarely heal themselves, so prompt medical attention is indicated if such an abscess is suspected.

An abscess could potentially be fatal (although this is rare) if it compresses vital structures such as the trachea in the context of a deep neck abscess.

If superficial, abscesses may be fluctuant when palpated. This is a wave-like motion that is caused by movement of the pus inside the abscess.

The mucous membranes of the mouth develop ulcers, and rapid, painless tissue degeneration ensues, which can degrade tissues of the bones in the face.

In a condition sometimes called noma pudendi, noma can also cause tissue damage to the genitals.

Intestinal failure is decreased intestinal function such that nutrients, water, and electrolytes are not sufficiently absorbed. Short bowel syndrome is when there is less than of working bowel and is the most common cause of intestinal failure.

This condition is characterized by:

- a diffuse infiltration of all the skin which never transforms into nodule

- a complete alopecia of eyebrows and eyelashes and body hair

- an anhydrotic and dysesthesic zones of the skin

- a peculiar type of lepra reaction named Lucio's phenomenon or necrotic erythema

Lucio's phenomenon consists of well-shaped erythematous spots which later become necrotic with scabs, ulcerations and scars. These lesion usually on the lower extremities and may be extensive They are frequently painful. Rarely it may be fatal.

Surgery of the anal fistula to drain an abscess treats the fistula and reduces likelihood of its recurrence and the need for repeated surgery. There is no evidence that fecal incontinence is a consequence of this surgery for abscess drainage.

Perianal abscesses can be seen in patients with for example inflammatory bowel disease (such as Crohn's disease) or diabetes. Often the abscess will start as an internal wound caused by ulceration, hard stool or penetrative objects with insufficient lubrication. This wound typically becomes infected as a result of the normal presence of feces in the rectal area, and then develops into an abscess. This often presents itself as a lump of tissue near the anus which grows larger and more painful with time. Like other abscesses, perianal abscesses may require prompt medical treatment, such as an incision and debridement or lancing.

Buruli ulcer is an infectious disease caused by "Mycobacterium ulcerans". The early stage of the infection is characterised by a painless nodule or area of swelling. This nodule can turn into an ulcer. The ulcer may be larger inside than at the surface of the skin, and can be surrounded by swelling. As the disease worsens, bone can be infected. Buruli ulcers most commonly affect the arms or legs; fever is uncommon.

"M. ulcerans" releases a toxin known as mycolactone, which decreases immune system function and results in tissue death. Bacteria from the same family also cause tuberculosis and leprosy ("M. tuberculosis" and "M. leprae", respectively). How the disease is spread is not known. Sources of water may be involved in the spread. As of 2013 there is no effective vaccine.

If people are treated early, antibiotics for eight weeks are effective in 80%. The treatment often includes the medications rifampicin and streptomycin. Clarithromycin or moxifloxacin are sometimes used instead of streptomycin. Other treatments may include cutting out the ulcer. After the infection heals, the area typically has a scar.

In 2015 about 2,000 cases were reported. Buruli ulcers occur most commonly in rural sub-Saharan Africa especially Cote d'Ivoire, but can also occur in Asia, the Western Pacific and the Americas. Children are most commonly infected. Cases have occurred in more than 32 countries. The disease also occurs in a number of animals other than humans. Albert Ruskin Cook was the first to describe buruli ulcers in 1897. It is classified as a neglected tropical disease.

The symptoms of short bowel syndrome can include:

- Abdominal pain

- Diarrhea and steatorrhea (oily, bulky stool, which can be malodorous)

- Fluid depletion

- Weight loss and malnutrition

- Fatigue

Persons with short bowel syndrome may have complications caused by malabsorption of vitamins and minerals, such as deficiencies in vitamins A, D, E, K, B (folic acid), and B, calcium, magnesium, iron, and zinc. These may appear as anemia, hyperkeratosis (scaling of the skin), easy bruising, muscle spasms, poor blood clotting, and bone pain.

NL/NLD most frequently appears on the patient's shins, often on both legs, although it may also occur on forearms, hands, trunk, and, rarely, nipple, penis, and surgical sites. The lesions are often asymptomatic but may become tender and ulcerate when injured. The first symptom of NL is often a "bruised" appearance (erythema) that is not necessarily associated with a known injury. The extent to which NL is inherited is unknown.

NLD appears as a hardened, raised area of the skin. The center of the affected area usually has a yellowish tint while the area surrounding it is a dark pink. It is possible for the affected area to spread or turn into an open sore. When this happens the patient is at greater risk of developing ulcers. If an injury to the skin occurs on the affected area, it may not heal properly or it will leave a dark scar.

Necrobiosis lipoidica is a necrotising skin condition that usually occurs in patients with diabetes mellitus but can also be associated with rheumatoid arthritis. In the former case it may be called necrobiosis lipoidica diabeticorum (NLD). 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. Better maintenance of diabetes after being diagnosed with NLD will not change how quickly the NLD will resolve.

The main pathological features of this disease are a vasculitis affecting all cutaneous vessels.

There are by five characteristic features:

- colonisation of endothelial cells by acid-fast bacilli

- endothelial proliferation and marked thickening of vessel walls to the point of obliteration

- angiogenesis

- vascular ectasia

- thrombosis of the superficial and mid-dermal blood vessels

The likely pathogenesis is endothelial cell injury due to colonization/invasion followed by proliferation, angiogensis, thrombosis and vessel ectasia.

Wet beriberi affects the heart and circulatory system. It is sometimes fatal, as it causes a combination of heart failure and weakening of the capillary walls, which causes the peripheral tissues to become edematous. Wet beriberi is characterized by:

- Increased heart rate

- Vasodilation leading to decreased systemic vascular resistance, and high output cardiac failure

- Elevated jugular venous pressure

- Dyspnea (shortness of breath) on exertion

- Paroxysmal nocturnal dyspnea

- Peripheral edema (swelling of lower legs)

Symptoms of beriberi include weight loss, emotional disturbances, impaired sensory perception, weakness and pain in the limbs, and periods of irregular heart rate. Edema (swelling of bodily tissues) is common. It may increase the amount of lactic acid and pyruvic acid within the blood. In advanced cases, the disease may cause high-output cardiac failure and death.

Symptoms may occur concurrently with those of Wernicke's encephalopathy, a primarily neurological thiamine-deficiency related condition.

Beriberi is divided into four categories as follows. The first three are historical and the fourth, gastrointestinal beriberi, was recognized in 2004:

- "Dry beriberi" specially affects the peripheral nervous system

- "Wet beriberi" specially affects the cardiovascular system and other bodily systems

- "Infantile beriberi" affects the babies of malnourished mothers

- "Gastrointestinal beriberi" affects the digestive system and other bodily systems

Symptoms of scleritis include:

- Redness of the sclera and conjunctiva, sometimes changing to a purple hue

- Severe ocular pain, which may radiate to the temple or jaw. The pain is often described as deep or boring.

- Photophobia and tearing

- Decrease in visual acuity, possibly leading to blindness

The pain of episcleritis is less severe than in scleritis. In hyperemia, there is a visible increase in the blood flow to the sclera (hyperaemia), which accounts for the redness of the eye. Unlike in conjunctivitis, this redness will not move with gentle pressure to the conjunctiva.

Scleritis is a serious inflammatory disease that affects the white outer coating of the eye, known as the sclera. The disease is often contracted through association with other diseases of the body, such as granulomatosis with polyangiitis or rheumatoid arthritis. There are three types of scleritis: diffuse scleritis (the most common), nodular scleritis, and necrotizing scleritis (the most severe). Scleritis may be the first symptom of onset of connective tissue disease.

Episcleritis is inflammation of the episclera, a less serious condition that seldom develops into scleritis.

May have no signs and symptoms or they may include:

- cough, but not prominent;

- chest pain (not common);

- breathing difficulty (fast and shallow);

- low oxygen saturation;

- pleural effusion (transudate type);

- cyanosis (late sign);

- increased heart rate.

It is a common misconception that atelectasis causes fever. A study of 100 post-op patients followed with serial chest X-rays and temperature measurements showed that the incidence of fever decreased as the incidence of atelectasis increased. A recent review article summarizing the available published evidence on the association between atelectasis and post-op fever concluded that there is no clinical evidence supporting this doctrine.

In rounded atelectasis (Folded lung or Blesovsky syndrome), an outer portion of the lung slowly collapses as a result of scarring and shrinkage of the membrane layers covering the lungs (pleura), which would show as visceral pleural thickening and entrapment of lung tissue. This produces a rounded appearance on x-ray that doctors may mistake for a tumor. Rounded atelectasis is usually a complication of asbestos-induced disease of the pleura, but it may also result from other types of chronic scarring and thickening of the pleura.

Barotrauma can affect the external, middle, or inner ear. Middle ear barotrauma (MEBT) is the most common being experienced by between 10% and 30% of divers and is due to insufficient equilibration of the middle ear. External ear barotrauma may occur on ascent if high pressure air is trapped in the external auditory canal either by tight fitting diving equipment or ear wax. Inner ear barotrauma (IEBT), though much less common than MEBT, shares a similar mechanism. Mechanical trauma to the inner ear can lead to varying degrees of conductive and sensorineural hearing loss as well as vertigo. It is also common for conditions affecting the inner ear to result in auditory hypersensitivity.

Patients with acquired non-inflammatory myopathy typically experience weakness, cramping, stiffness, and tetany, most commonly in skeletal muscle surrounding the limbs and upper shoulder girdle.

The most commonly reported symptoms are:

- Muscle fatigue

- Pain

- Muscle spasms and cramps

- Tingling

- Numbness

- Tetany

- Loss of coordination and balance

- Lack of fine and gross motor control

- Muscular wasting and atrophy