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.

The blotches are cosmetic damage "unacceptable to consumers" and downgrade fruit from premium fresh-market grade to processing use, i.e. reduce its market value, but leaf and fruit development are not affected.

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.

Yellow-band disease has severely affected reef building corals in the Caribbean. This disease have been associated with lower coral fecundity, altered tissue composition and a lower activites of antixenobiotic and antioxidant enzymes. Compared to the late 1990s, current data suggests that the disease remains a severe epidemic. In one study, 10 meter belt transects were taken at various depths, sampling coral colonies in the Lesser Antilles. At a depth of 5 m, yellow band rings and lesions were found on 79% of the colonies per transect, and only 21% of the colonies in this depth range appeared healthy.

Recent research indicates that yellow-band disease continues to be in an infectious phases in the Caribbean. It has been

found to cause infection in Pacific coral as well.

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.

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.

The newborn`s exposure to the maternal vaginal bacterial flora which contains aerobic and anaerobic bacterial flora can lead to the development of anaerobic bacterial infection. These infections include cellulitis of the site of fetal monitoring (caused by "Bacterodes" spp.), bacteremia, aspiration pneumonia (caused by "Bacterodes" spp.), conjunctivitis (caused by clostridia,) omphalitis (caused by mixed flora), and infant botulism. Clostridial species may play a role in necrotizing enterocolitis. Management of these infection necessitates treating of the underlying condition(s) when present, and administration of proper antimicrobial therapy

Fiddler’s neck does not usually form unless the musician is practicing or playing for more than a few hours each day, and only seems to develop after a few years of serious playing. Thus, when not infected or otherwise problematic, fiddler’s neck may be known as a benign practice mark and may be worn proudly as an indication of long hours of practice. Blum & Ritter (1990) found that 62% of 523 professional violinists and violists in West Germany experienced fiddler’s neck, with the percentage among violists being higher (67%) than among violinists (59%). Viola players are believed to be more predisposed to developing fiddler’s neck than violinists because the viola is larger and heavier, but this has not been empirically confirmed.

The development of fiddler’s neck does not depend on preexisting skin problems, and Blum & Ritter find that only 23% of men and 14% of women in their study reported cutaneous disorders in other parts of the face (mainly acne and eczema) that were independent of playing the violin or viola. Fiddler’s neck may exacerbate existing acne, but acne may also be limited solely to the lesion and not appear elsewhere. Nonetheless, musicians with underlying dermatologic diseases like acne and eczema are more endangered by fiddler’s neck than others. Males may develop folliculitis or boils due to involvement of beard hair.

Podoconiosis is most frequently seen in the highland areas of Africa, India, and Central America. The highest prevalence is seen in Uganda, Tanzania, Kenya, Rwanda, Burundi, Sudan, and Ethiopia. In some areas of Ethiopia, the prevalence is as high as 9%. The incidence of podoconiosis increases with age, likely due to cumulative exposure to irritant soil. It is very rare to see podoconiosis in the 0–5 year old age group, and the incidence rapidly rises from 6 to 20 years of age, with the highest prevalence after 45 years of age. Podoconiosis is most commonly seen in higher altitude areas with volcanic soil, and it is estimated to affect 4 million people worldwide.

Condition predisposing to anaerobic infections include: exposure of a sterile body location to a high inoculum of indigenous bacteria of mucous membrane flora origin, inadequate blood supply and tissue necrosis which lower the oxidation and reduction potential which support the growth of anaerobes. Conditions which can lower the blood supply and can predispose to anaerobic infection are: trauma, foreign body, malignancy, surgery, edema, shock, colitis and vascular disease. Other predisposing conditions include splenectomy, neutropenia, immunosuppression, hypogammaglobinemia, leukemia, collagen vascular disease and cytotoxic drugs and diabetes mellitus. A preexisting infection caused by aerobic or facultative organisms can alter the local tissue conditions and make them more favorable for the growth of anaerobes. Impairment in defense mechanisms due to anaerobic conditions can also favor anaerobic infection. These include production of leukotoxins (by "Fusobacterium" spp.), phagocytosis intracellular killing impairments (often caused by encapsulated anaerobes and by succinic acid ( produced by "Bacteroides" spp.), chemotaxis inhibition (by "Fusobacterium, Prevotella" and "Porphyromonas" spp.), and proteases degradation of serum proteins (by Bacteroides spp.) and production of leukotoxins (by "Fusobacterium" spp.).

The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.

Some infections are more likely to be caused by anaerobic bacteria, and they should be suspected in most instances. These infections include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia and lung abscesses, amnionitis, endometritis, septic abortions, tubo-ovarian abscess, peritonitis and abdominal abscesses following viscus perforation, abscesses in and around the oral and rectal areas, pus-forming necrotizing infections of soft tissue or muscle and postsurgical infections that emerge following procedures on the oral or gastrointestinal tract or female pelvic area. Some solid malignant tumors, ( colonic, uterine and bronchogenic, and head and neck necrotic tumors, are more likely to become secondarily infected with anaerobes. The lack of oxygen within the tumor that are proximal to the endogenous adjacent mucosal flora can predispose such infections.

The cornerstone of prevention and treatment of podoconiosis is avoidance of exposure to irritant soils. Wearing shoes in the presence of irritant soils is the primary method of exposure reduction. In Rwanda, a country of high disease prevalence, the government has banned walking barefoot in public, in order to curtail podoconiosis and other soil-borne diseases.

Once the disease has developed, rigorous foot hygiene including daily washing with soap and water, application of an emollient, and nightly elevation of the affected extremity has been shown to reduce swelling and disability. Compression wrapping and decongestive physiotherapy of the affected extremity has been shown to be effective in other forms of lymphedema, but the benefits of these therapies have not been rigorously studied in podoconiosis. Nodules will not resolve with these conservative measures, although surgical removal of the nodules can be performed.

Also like many other parasite infections, the course of "Echinococcus" infection is complex. The worm has a life cycle that requires definitive hosts and intermediate hosts. Definitive hosts are normally carnivores such as dogs, while intermediate hosts are usually herbivores such as sheep and cattle. Humans function as accidental

hosts, because they are usually a dead end for the parasitic infection cycle.

The proximal causes of fiddler’s neck are friction and pressure, but both repetitive shearing stress and occlusion with consequent trapping of sweat give rise to progressive damage. This damage along with poor hygiene predisposes the area to local infection, and such infection can progress to scarring and other long-term effects. Hot weather is reported to exacerbate fiddler’s neck, as are tiredness, playing emotional music, and playing in smaller groups where individual stress is higher. Type I hypersensitivity reactions may also be involved, particularly to rosewood and ebony in the chinrest and tailpiece, as well as to varnish of the instrument body when chinrests are not used and to rosin deposits on the instrument and on chin cloths. Nickel or other metal allergies are common causes if the chin rest has a metal clip that comes into constant contact with the skin. Rosin exposure in particular may lead to abietic acid dermatitis.

Though heart disease is not exclusive to the poor, there are aspects of a life of poverty that contribute to its development. This category includes coronary heart disease, stroke and heart attack. Heart disease is the leading cause of death worldwide and there are disparities of morbidity between the rich and poor. Studies from around the world link heart disease to poverty. Low neighborhood income and education were associated with higher risk factors. Poor diet, lack of exercise and limited (or no) access to a specialist were all factors related to poverty, though to contribute to heart disease.

Both low income and low education were predictors of coronary heart disease, a subset of cardiovascular disease. Of those admitted to hospital in the United States for heart failure, women and African Americans were more likely to reside in lower income neighborhoods. In the developing world, there is a 10 fold increase in cardiac events in the black and urban populations.

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.

Obstetric fistula or vaginal fistula is a medical condition in which a fistula (hole) develops between either the rectum and vagina (see rectovaginal fistula) or between the bladder and vagina (see vesicovaginal fistula) after severe or failed childbirth, when adequate medical care is not available. It is considered a disease of poverty because of its tendency to occur women in poor countries who do not have health resources comparable to developed nations.

There is most likely a link between children's linear growth and household sanitation practices. The ingestion of high quantities of fecal bacteria by young children through putting soiled fingers or household items in the mouth leads to intestinal infections. This affect children's nutritional status by diminishing appetite, reducing nutrient absorption, and increasing nutrient losses.

The diseases recurrent diarrhoea and intestinal worm infections (helminthiasis) which are both linked to poor sanitation have been shown to contribute to child stunting. The evidence that a condition called environmental enteropathy also stunts children is not conclusively available yet, although the link is plausible and several studies are underway on this topic. Environmental enteropathy is a syndrome causing changes in the small intestine of persons and can be brought on due to lacking basic sanitary facilities and being exposed to faecal contamination on a long-term basis.

Research on a global level has found that the proportion of stunting that could be attributed to five or more episodes of diarrhoea before two years of age was 25%. Since diarrhoea is closely linked with water, sanitation and hygiene (WASH), this is a good indicator for the connection between WASH and stunted growth. To what extent improvements in drinking water safety, toilet use and good handwashing practices contribute to reduce stunting depends on the how bad these practices were prior to interventions.

It has been recorded since the late 19th century and has been reported from most sheep-or goat-raising areas including those in Europe, the Middle East, the United States, Africa, Asia, Alaska, South America, Canada, New Zealand and Australia. Orf is spread by fomites and direct contact. In some environments infection is injected by scratches from thistles of both growing and felled plants. Symptoms include papules and pustules on the lips and muzzle, and less commonly in the mouth of young lambs and on the eyelids, feet, and teats of ewes. The lesions progress to thick crusts which may bleed. Orf in the mouths of lambs may prevent suckling and cause weight loss, and can infect the udder of the mother ewe, thus potentially leading to mastitis. Sheep are prone to reinfection. Occasionally the infection can be extensive and persistent if the animal does not produce an immune response.

A live virus vaccine (ATCvet code: ) is made from scab material and usually given to ewes at the age of two months, but only to lambs when there is an outbreak. The vaccine can cause disease in humans.

In sheep and goats the lesions mostly appear on or near the hairline and elsewhere on the lips and muzzle. In some cases the lesions appear on and in the nostrils, around the eyes, on the thigh, coronet, vulva, udder and axilla. In rare cases, mostly involving young lambs, lesions are found on the tongue, gums, roof of the mouth and the oesophagus. It has also been reported a number of times to cause lesions in the rumen. In one case it was shown that a severe form of orf virus caused an outbreak involving the gastrointestinal tract, lungs, heart, as well as the buccal cavity, cheeks, tongue and lips. Another severe case was reported pharyngitis, genital lesions and infection of the hooves which led to lameness and, in some cases, sloughing of the hoof.

More typically sheep will become free of orf within a week or so as the disease runs its course. Sheep custodians can assist by ensuring infected lambs receive sufficient milk and separating out the infected stock to slow down cross-transmission to healthy animals. It is advisable for those handling infected animals to wear disposable gloves to prevent cross-infection and self-infection. A veterinarian needs to be contacted if there is a risk of misdiagnosis with other, more serious conditions.

Poor maternal nutrition during pregnancy and breastfeeding can lead to stunted growth of their children. Women who are underweight or anemic during pregnancy, are more likely to have stunted children which perpetuates the inter-generational transmission of stunting.

Primarily, orf is a disease of sheep and goats although it has been reported as a natural disease in the following: humans, steenbok and alpacas, chamois and thar, reindeer, musk ox, dog, cat, mountain goat, bighorn sheep, dall sheep, and the red squirrel .

There is no vaccine for SVD. Prevention measures are similar to those for foot-and-mouth disease: controlling animals imported from infected areas, and sanitary disposal of garbage from international aircraft and ships, and thorough cooking of garbage. Infected animals should be placed in strict quarantine. Eradication measures for the disease include quarantining infected areas, depopulation and disposal of infected and contact pigs, and cleaning and disinfecting

contaminated premises.

Cysticercosis is considered as “tools-ready disease” according to WHO. International Task Force for Disease Eradication in 1992 reported that cysticercosis is potentially eradicable. It is feasible because there are no animal reservoirs besides humans and pigs. The only source of "Taenia solium" infection for pigs is from humans, a definite host. Theoretically, breaking the life cycle seems easy by doing intervention strategies from various stages in the life cycle.

For example,

1. Massive chemotherapy of infected individuals, improving sanitation, and educating people are all major ways to discontinue the cycle, in which eggs from human feces are transmitted to other humans and/or pigs.

2. Cooking of pork or freezing it and inspecting meat are effective means to cease the life cycle

3. The management of pigs by treating them or vaccinating them is another possibility to intervene

4. The separation of pigs from human faeces by confining them in enclosed piggeries. In Western European countries post World War 2 the pig industry developed rapidly and most pigs were housed. This was the main reason for pig cysticercosis largely being eliminated from the region. This of course is not a quick answer to the problem in developing countries.

PPE invariably recurs with the resumption of chemotherapy. Long-term chemotherapy may also result in reversible palmoplantar keratoderma. Symptoms resolve 1–2 weeks after cessation of chemotherapy (Apisarnthanarax and Duvic 2003).

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 intervention strategies to eradicate cysticercosis includes surveillance of pigs in foci of transmission and massive chemotherapy treatment of humans. In reality, control of "T. solium" by a single intervention, for instance, by treating only human population will not work because the existing infected pigs can still carry on the cycle. The proposed strategy for eradication is to do multilateral intervention by treating both human and porcine populations. It is feasible because treatment pigs with oxfendazole have been shown to be effective and once treated, they are protected from further infections for at least 3 months.