Sooty blotch and flyspeck is a descriptive term for a condition of darkly pigmented blemishes and smudges caused by a number of different fungi affecting fruit including apples, pear, persimmon, banana, papaya, and several other cultivated tree and vine crops. The greenish black coating resembling soot or flyspeck-like dots grow into irregular stains and blotches during the summer or growing season. They can grow into each other and may cover the entire fruit surface. Frequently blotches run down in a track resembling tears (German: "Regenfleckenkrankheit"). The blotches can be removed by vigorous rubbing or be scratched off revealing a normal peel. Symptoms can be seen particularly well when apples are light or green colored. Late varieties are more susceptible, because the disease builds over a longer growing period.

Sooty blotch and flyspeck (SBFS) or apple summer disease is a plant disease caused by a complex of saprophytic fungi which colonize the epicuticular wax layer of apple ("Malus" x "domestica" Borkh.). It is found worldwide in regions with moist growing seasons.

Yellow-band disease (similar to Yellow Blotch disease) is a coral disease that attacks colonies of coral at a time when coral is already under stress from pollution, overfishing, and climate change. It is characterized by large blotches or patches of bleached, yellowed tissue on Caribbean scleractinian corals.

Yellow-band disease is a bacterial infection that spreads over coral, causing the discolored bands of pale-yellow or white lesions along the surface of an infected coral colony. The lesions are the locations where the bacteria have killed the coral’s symbiotic photosynthetic algae, called zooxanthellae which are a major energy source for the coral. This cellular damage and the loss of its major energy source cause the coral to starve, and usually cause coral death. There is evidence that climate change could be worsening the disease.

Coral has a symbiotic relationship with zooxanthellae that provide the coral glucose, glycerol, and amino acids. Under certain water conditions, like fluctuating temperatures and increased nitrogenous waste, corals will appear stressed. Also, these conditions allow for bacteria to grow inside the coral and compete with zooxanthellae. The bacteria produces the characteristic pale yellow lesions and eventually kills the zooxanthellae by impairing its mitosis and its ability to carry out photosynthesis. Yellow-band disease is found on coral reefs in the Caribbean.

On post-mortem examination (necropsy), the most obvious gross lesion is subcutaneous oedema in the submandibular and pectoral (brisket) regions. Petechial haemorrhages are found subcutaneously and in the thoracic cavity. In addition, congestion and various degrees of consolidation of the lung may occur. Animals that die within 24–36 hours, have only few petechial haemorrhages on the heart and generalised congestion of the lung, while in animals that die after 72 hours, petechial and ecchymotic haemorrhages were more evident and lung consolidation are more extensive.

In the human manifestation of the disease, "E. granulosus", "E. multilocularis", "E. oligarthrus" and "E. vogeli" are localized in the liver (in 75% of cases), the lungs (in 5–15% of cases) and other organs in the body such as the spleen, brain, heart, and kidneys (in 10–20% of cases). In the patients who are infected with "E. granulosus" and therefore have cystic echinococcosis, the disease develops as a slow-growing mass in the body. These slow-growing masses, often called cysts, are also found in patients that are infected with alveolar and polycystic echinococcosis. The cysts found in those with cystic echinococcosis are usually filled with a clear fluid called hydatid fluid, are spherical, and typically consist of one compartment and are usually only found in one area of the body. While the cysts found in those with alveolar and polycystic echinococcosis are similar to those found in those with cystic echinococcosis, the alveolar and polycystic echinococcosis cysts usually have multiple compartments and have infiltrative as opposed to expansive growth.

Depending on the location of the cyst in the body, the patient could be asymptomatic even though the cysts have grown to be very large, or be symptomatic even if the cysts are absolutely tiny. If the patient is symptomatic, the symptoms will depend largely on where the cysts are located. For instance, if the patient has cysts in the lungs and is symptomatic, they will have a cough, shortness of breath and/or pain in the chest. On the other hand, if the patient has cysts in the liver and is symptomatic, they will suffer from abdominal pain, abnormal abdominal tenderness, hepatomegaly with an abdominal mass, jaundice, fever and/or anaphylactic reaction. In addition, if the cysts were to rupture while in the body, whether during surgical extraction of the cysts or by trauma to the body, the patient would most likely go into anaphylactic shock and suffer from high fever, pruritus (itching), edema (swelling) of the lips and eyelids, dyspnea, stridor and rhinorrhea.

Unlike intermediate hosts, definitive hosts are usually not hurt very much by the infection. Sometimes, a lack of certain vitamins and minerals can be caused in the host by the very high demand of the parasite.

The incubation period for all species of "Echinococcus" can be months to years, or even decades. It largely depends on the location of the cyst in the body and how fast the cyst is growing.

The primary symptom of podoconiosis is swelling and disfigurement of the lower extremities. The swelling can either be soft and fluid or hard and fibrotic. Multiple firm nodules may develop over time, as well as hyperkeratotic papillomata that resemble moss, which has led to the disease's alternate name of Mossy Foot. The edema of podoconiosis is usually bilateral and asymmetric. Prior to the development of lymphatic failure and frank lymphedema, a prodrome consisting of itching, burning, hyperkeratosis, plantar edema, and rigid digits may occur. As with other forms of tropical lymphedema, chronic disease can lead to fusion of the toes, ulceration, and bacterial superinfection. The disease has an acute component, and sufferers may experience recurrent episodes of lower extremity warmth, firmness, and pain.

A wide variety of clinical signs have been described for HS in cattle and buffaloes. The incubation periods (the time between exposure and observable disease) for buffalo calves 4–10 months of age varies according to the route of infection. The incubation period is 12–14 hours, approximately 30 hours and 46–80 hours for subcutaneous infection, oral infection and natural exposure, respectively.

There is variability in the duration of the clinical course of the disease. In the case of experimental subcutaneous infection, the clinical course lasted only a few hours, while it persisted for 2–5 days following oral infection and in buffaloes and cattle that had been exposed to naturally-infected animals. It has also been recorded from field observations that the clinical courses of per-acute and acute cases were 4–12 hours and 2–3 days, respectively.

Generally, progression of the disease in buffaloes and cattle is divided into three phases. Phase one is characterised by fever, with a rectal temperature of , loss of appetite and depression. Phase two is typified by increased respiration rate (40–50/minute), laboured breathing, clear nasal discharge (turns opaque and mucopurulent as the disease progresses), salivation and submandibular oedema spreading to the pectoral (brisket) region and even to the forelegs. Finally, in phase three, there is typically recumbency, continued acute respiratory distress and terminal septicaemia. The three phases overlap when the disease course is short. In general, buffaloes have a more acute onset of disease than cattle, with a shorter duration.

The most common form found in humans is cystic echinococcosis (also known as unilocular echinococcosis), which is caused by "Echinococcus granulosus sensu lato". The second most common form is alveolar echinococcosis (also known as alveolar colloid of the liver, alveolar hydatid disease, alveolococcosis, multilocular echinococcosis, "small fox tapeworm"), which is caused by "Echinococcus multilocularis" and the third is polycystic echinococcosis (also known as human polycystic hydatid disease, neotropical echinococcosis), which is caused by "Echinococcus vogeli" and very rarely, "Echinococcus oligarthrus". Alveolar and polycystic echinococcosis are rarely diagnosed in humans and are not as widespread as cystic echinococcosis, but polycystic echinococcosis is relatively new on the medical scene and is often left out of conversations dealing with echinococcosis, and alveolar echinococcosis is a serious disease that has not only a significantly high fatality rate, but the potential to become an emerging disease in many countries.

The infections that frequently involve anaerobic bacteria include superficial infections, including infected paronychia, infected human or animal bites, cutaneous ulcers, cellulitis, pyoderma, and hidradenitis suppurativa. Secondary infected sites include secondary infected diaper rash, gastrostomy or tracheostomy site wounds, scabies or kerion infections, eczema, psoriasis, poison ivy, atopic dermatitis, eczema herpeticum, infected subcutaneous sebaceous or inclusion cysts, and postsurgical wound infection.

Skin involvement in subcutaneous tissue infections includes: cutaneous and subcutaneous abscesses, breast abscess, decubitus ulcers, infected pilonidal cyst or sinus, Meleney's ulcer infected diabetic (vascular or trophic) ulcers, bite wound, anaerobic cellulitis and gas gangrene, bacterial synergistic gangrene, and burn wound infection. Deeper anaerobic soft-tissue infections are necrotizing fasciitis, necrotizing synergistic cellulitis, gas gangrene and crepitus cellulitis. These can involve the fascia as well as the muscle surrounded by the fascia, and may also induce myositis and myonecrosis.

The isolates found in soft-tissue infections can vary depending on the type of infection. The infection's location and the circumstances causing the infection can also influence the nature of the microorganisms recovered. Bacteria that are members of the 'normal flora' of the region of the infection are often also isolated from lesions involving anaerobic bacteria.

Specimens obtained from wounds and subcutaneous tissue infections and abscesses in the rectal area (perirectal abscess, decubitus ulcer) or that are of gut flora origin(i.e. diabetic foot infection) often to yield colonic flora organisms. These are generally "B. fragilis" group, "Clostridium" spp., Enterobacteriaceae and "Enterococcus" spp. On the other hand, infections in and around the oropharynx, or infections that originate from that location, frequently contain oral flora organisms (i.e. paronychia, bites, breast abscess). These bacteria include pigmented "Prevotella" and "Porphyromonas, Fusobacterium" and Peptostreptococcus spp. Skin flora organisms such as "S. aureus" and "Streptococcus" spp., or nosocomially acquired microorganisms can be recovered at all body locations. Human bite infections often contain "Eikenella" spp. and animal bites harbor "Pasteurella multocida" in addition to oral flora,

Anaerobes infections are often polymicrobial in nature, and sometimes (i.e. decubitus ulcers, diabetic foot ulcer) they are complicated by bacteremia and or osteomyelitis . Infections which are in the deep tissues ( necrotizing cellulitis, fasciitis and myositis) often include "Clostridium" spp., "S. pyogenes" or polymicrobic combinations of both aerobic and anaerobic bacteria. Gas in the tissues and putrid-like pus with a gray thin quality are often found in these infections, and they are frequently associated with a bacteremia and high mortality rate.

Treatment of deep-seated soft-tissue infections includes: vigorous surgical management that includes surgical debridement and drainage. Even though there are no controlle studies that support this approach improvement of the involved tissues oxygenation by enhancement of blood supply and administration of hyperbaric oxygen, especially in clostridial infection, may be helpful.

Anaerobes have been found in infections throughout the human body. The frequency of their recovery depends on the employment of proper methods of collection of specimen, their transportation to the microbiology laboratory and cultivation. The recovery of organisms depends on the site of infection and is related to the adjacent mucous membranes microbial flora.

Podoconiosis, also known as nonfilarial elephantiasis, is a disease of the lymph vessels of the lower extremities that is caused by chronic exposure to irritant soils. It is the second most common cause of tropical lymphedema after filariasis, and it is characterized by prominent swelling of the lower extremities, which leads to disfigurement and disability.

Fiddler’s neck usually involves highly localized lichenification, mild hyperpigmentation, and erythema where the chin rest or instrument body presses against the skin of the neck. Other signs and symptoms include scale buildup, cyst and scar formation, papules and pustules related to local infection, and focal edema. In Blum & Ritter’s study in West Germany (1990), they found that 27% of their population had only minor issues, 72% had a palpable mass at the site, and 23% reported pain and other signs of inflammation such as hyperthermia, pulsation, and cystic, pustular, or papular lesions. Size of masses were an average of 2 cm in diameter ranging up to 4 cm, some being associated with purulent drainage, continuous discharge, and crusting. Dystrophic calcinosis cutis has also been reported. Other serious sequelae include sialolithiasis of the submandibular gland and adenolymphoma of the parotid gland.

The histopathology of fiddler’s neck frequently shows hyperkeratosis and acanthosis, along with plugging of follicles. Histiocytic infiltration with granulomas to foreign body and follicular cysts are also common. Foreign body granulomas are thought to derive from abrasion of the wooden surface of the chin rest and its absorption into the superficial dermis. The location and complex mechanism of causation for fiddler’s neck give rise to a wider spectrum of skin changes when compared to contact dermatitis from more common irritants. Fiddler’s neck can be differentiated from rosacea and sarcoid reaction with granulomas.

Fiddler's neck, sometimes referred to as a "violin hickey," or a "viola love bite" is an occupational disease that affects violin and viola players.

It is a cutaneous condition usually characterized by redness, thickening, and inflammation on the left side of the neck below the angle of the jaw where the instrument is held. Acne-like lesions and cysts may form at the site due to foreign body reactions, and infections may also occur due to poor hygiene. The primary causes of fiddler's neck are constant friction and local pressure. It is well known among professional orchestra musicians but is "not well recognized by dermatologists", and a red mark on the left side of the neck under the jaw "functions as an identifying sign" of a violinist or violist "in public without seeing the instrument""."

Although the presence of fiddler's neck is sometimes used as an indicator of a violinist's skill, or 'battle scars' from constant practice, many violinists never develop fiddler's neck, due to differences in skin sensitivity, playing habits, and the materials used in the construction of the instrument. An accomplished professional player could practice hard their whole life and never develop fiddler's neck.

After an incubation period of up to seven days, the signs associated with swine vesicular disease occur. The first sign is a transient mild fever. Other signs include:

- Vesicles in the mouth and on the snout and feet

- Lameness and an unsteady gait, shivering and jerking–type leg movements

- Ruptured vesicles can cause ulcers on limbs and feet, and foot pads may be loosened.

Young animals are more severely affected. Recovery often occurs within a week. There is no mortality.

Swine vesicular disease has the same clinical signs as foot-and-mouth disease, and can only be diagnosed by laboratory testing.

The term neurocysticercosis is generally accepted to refer to cysts in the parenchyma of the brain. It presents with seizures and, less commonly, headaches. Cysticerca in brain parenchyma are usually 5–20 mm in diameter. In subarachnoid space and fissures, lesions may be as large as 6 cm in diameter and lobulated. They may be numerous and life-threatening.

Cysts located within the ventricles of the brain can block the outflow of cerebrospinal fluid and present with symptoms of increased intracranial pressure.

Racemose neurocysticercosis refers to cysts in the subarachnoid space. These can occasionally grow into large lobulated masses causing pressure on surrounding structures.

Neurocysticercosis involving the spinal cord, most commonly presenting as back pain and radiculopathy.

Cysticerci can develop in any voluntary muscles in humans. Invasion of muscle by cysticerci can cause myositis, with fever, eosinophilia, and muscular pseudohypertrophy, which initiates with muscle swelling and later progress to atrophy and fibrosis. In most cases, it is asymptomatic since the cysticerci die and become calcified.

Orf is an exanthemous disease caused by a parapox virus and occurring primarily in sheep and goats. It is also known as contagious pustular dermatitis, infectious labial dermatitis, ecthyma contagiosum, thistle disease and scabby mouth. "Orf virus" is zoonotic—it can also infect humans.

Orf is a zoonotic disease, meaning humans can contract this disorder through direct contact with infected sheep and goats or with fomites carrying the orf virus. It causes a purulent-appearing papule locally and generally no systemic symptoms. Infected locations can include the finger, hand, arm, face and even the penis (caused by infection either from the hand during urination or from bestiality). Consequently, it is important to observe good personal hygiene and to wear gloves when treating infected animals. The papule may persist for 7 to 10 weeks and spontaneously resolves. It is an uncommon condition and may be difficult to diagnose.

While orf is usually a benign self-limiting illness, it can be very progressive and even life-threatening in the immune-compromised host. One percent topical cidofovir has been successfully used in a few patients with progressive disease. Serious damage may be inflicted on the eye if it is infected by orf, even among healthy individuals. The virus can survive in the soil for at least six months.

Swine vesicular disease is most commonly brought into a herd by the introduction of a subclinically infected pig.

The disease can be transmitted in feed containing infected meat scraps, or by direct contact with infected feces (such as in an improperly cleaned truck).

The symptoms can occur anywhere between days to months after administration of the offending medication, depending on the dose and speed of administration (Baack and Burgdorf, 1991; Demirçay, 1997). The patient first experiences tingling and/or numbness of the palms and soles that evolves into painful, symmetric, and well-demarcated swelling and red plaques. This is followed by peeling of the skin and resolution of the symptoms (Apisarnthanarax and Duvic 2003).

Chemotherapy-induced acral erythema (also known as palmar-plantar erythrodysesthesia, palmoplantar erythrodysesthesia, or hand-foot syndrome) is reddening, swelling, numbness and desquamation (skin sloughing or peeling) on palms of the hands and soles of the feet (and, occasionally, on the knees, elbows, and elsewhere) that can occur after chemotherapy in patients with cancer. Hand-foot syndrome is also rarely seen in sickle-cell disease. These skin changes usually are well demarcated. Acral erythema typically disappears within a few weeks after discontinuation of the offending drug.

Acute inhalation injury may result from frequent and widespread use of household cleaning agents and industrial gases (including chlorine and ammonia). The airways and lungs receive continuous first-pass exposure to non-toxic and irritant or toxic gases via inhalation. Irritant gases are those that, on inhalation, dissolve in the water of the respiratory tract mucosa and provoke an inflammatory response, usually from the release of acidic or alkaline radicals. Smoke, chlorine, phosgene, sulfur dioxide, hydrogen chloride, hydrogen sulfide, nitrogen dioxide, ozone, and ammonia are common irritants.

Depending on the type and amount of irritant gas inhaled, victims can experience symptoms ranging from minor respiratory discomfort to acute airway and lung injury and even death. A common response cascade to a variety of irritant gases includes inflammation, edema and epithelial sloughing, which if left untreated can result in scar formation and pulmonary and airway remodeling. Currently, mechanical ventilation remains the therapeutic mainstay for pulmonary dysfunction following acute inhalation injury.

Stunted growth, also known as stunting and nutritional stunting, is a reduced growth rate in human development. It is a primary manifestation of malnutrition (or more precisely undernutrition) and recurrent infections, such as diarrhea and helminthiasis, in early childhood and even before birth, due to malnutrition during fetal development brought on by a malnourished mother. The definition of stunting according to the World Health Organisation (WHO) is for the "height for age" value to be less than two standard deviations of the WHO Child Growth Standards median.

As of 2012 an estimated 162 million children under 5 years of age, or 25%, were stunted in 2012. More than 90% of the world's stunted children live in Africa and Asia, where respectively 36% and 56% of children are affected. Once established, stunting and its effects typically become permanent. Stunted children may never regain the height lost as a result of stunting, and most children will never gain the corresponding body weight. Living in an environment where many people defecate in the open due to lack of sanitation, is an important cause of stunted growth in children, for example in India.

Most conditions of STH have a light worm burden and usually have no discernible symptoms. Heavy infections however cause a range of health problems, including abdominal pain, diarrhoea, blood and protein loss, rectal prolapse, and physical and mental retardation.

Severe ascariasis is typically a pneumonia, as the larvae invades lungs, producing fever, cough and dyspnoea during early stage of infection.

Hookworm infections insinuate a skin reaction (dermatitis), increased white blood cells (eosinophils), a pulmonary reaction (pneumonitis), and skin rash (urticarial).

Iron deficiency anaemia due to blood loss is a common symptom.