Human-to-human transmission of diphtheria typically occurs through the air when an infected individual coughs or sneezes. Breathing in particles released from the infected individual leads to infection Contact with any lesions on the skin can also lead to transmission of diphtheria, but this is uncommon. Indirect infections can occur, as well. If an infected individual touches a surface or object, the bacteria can be left behind and remain viable. Also, some evidence indicates diphtheria has the potential to be zoonotic, but this has yet to be confirmed. "Corynebacterium ulcerans" has been found in some animals, which would suggest zoonotic potential

Diphtheria is fatal in between 5% and 10% of cases. In children under five years and adults over 40 years, the fatality rate may be as much as 20%. In 2013, it resulted in 3,300 deaths, down from 8,000 deaths in 1990.

The number of cases has changed over the course of the last 2 decades, specifically throughout developing countries. Better standards of living, mass immunization, improved diagnosis, prompt treatment, and more effective health care have led to the decrease in cases worldwide. However, although outbreaks are rare, they still occur worldwide, especially in developed nations such as Germany among unvaccinated children, and Canada. After the breakup of the former Soviet Union in the early 1990s, vaccination rates in its constituent countries fell so low that an explosion of diphtheria cases occurred. In 1991, 2,000 cases of diphtheria occurred in the USSR. Because of this outbreak, since 1992, many of the cases reported throughout other parts of Europe have been linked to the NIS epidemic. Belgium (3/3) and Finland (10/10) come in first, stating that 100% of cases are connected to this epidemic. However, locations such as Poland and Germany have had a larger number of people diagnosed with Diphtheria overall, but claim that a smaller percentage have been linked directly to the NIS. By 1998 as many as 200,000 cases in the Commonwealth of Independent States were reported, with 5,000 deaths.

Many cases of croup have been prevented by immunization for influenza and diphtheria. At one time, croup referred to a diphtherial disease, but with vaccination, diphtheria is now rare in the developed world.

Croup affects about 15% of children, and usually presents between the ages of 6 months and 5–6 years. It accounts for about 5% of hospital admissions in this population. In rare cases, it may occur in children as young as 3 months and as old as 15 years. Males are affected 50% more frequently than are females, and there is an increased prevalence in autumn.

The most common cause is viral infection and includes adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus. It can also be caused by Epstein-Barr virus, herpes simplex virus, cytomegalovirus, or HIV. The second most common cause is bacterial infection of which the predominant is Group A β-hemolytic streptococcus (GABHS), which causes strep throat. Less common bacterial causes include: "Staphylococcus aureus" (including methicillin resistant Staphylococcus aureus or MRSA ),"Streptococcus pneumoniae", "Mycoplasma pneumoniae", "Chlamydia pneumoniae", "Bordetella pertussis", "Fusobacterium" sp., "Corynebacterium diphtheriae", "Treponema pallidum", and "Neisseria gonorrhoeae".

Anaerobic bacteria have been implicated in tonsillitis and a possible role in the acute inflammatory process is supported by several clinical and scientific observations.

Under normal circumstances, as viruses and bacteria enter the body through the nose and mouth, they are filtered in the tonsils. Within the tonsils, white blood cells of the immune system destroy the viruses or bacteria by producing inflammatory cytokines like phospholipase A2, which also lead to fever. The infection may also be present in the throat and surrounding areas, causing inflammation of the pharynx.

Sometimes, tonsillitis is caused by an infection of spirochaeta and treponema, in this case called Vincent's angina or Plaut-Vincent angina.

Some cases of pharyngitis are caused by fungal infection such as Candida albicans causing oral thrush.

Pharyngitis may also be caused by mechanical, chemical or thermal irritation, for example cold air or acid reflux. Some medications may produce pharyngitis such as pramipexole and antipsychotics.

Since the advent of penicillin in the 1940s, a major preoccupation in the treatment of streptococcal tonsillitis has been the prevention of rheumatic fever, and its major effects on the nervous system (Sydenham's chorea) and heart. Recent evidence would suggest that the rheumatogenic strains of group A beta hemolytic strep have become markedly less prevalent and are now only present in small pockets such as in Salt Lake City, USA. This brings into question the rationale for treating tonsillitis as a means of preventing rheumatic fever.

Complications may rarely include dehydration and kidney failure due to difficulty swallowing, blocked airways due to inflammation, and pharyngitis due to the spread of infection.

An abscess may develop lateral to the tonsil during an infection, typically several days after the onset of tonsillitis. This is termed a peritonsillar abscess (or quinsy).

Rarely, the infection may spread beyond the tonsil resulting in inflammation and infection of the internal jugular vein giving rise to a spreading septicaemia infection (Lemierre's syndrome).

In chronic/recurrent cases (generally defined as seven episodes of tonsillitis in the preceding year, five episodes in each of the preceding two years or three episodes in each of the preceding three years), or in acute cases where the palatine tonsils become so swollen that swallowing is impaired, a tonsillectomy can be performed to remove the tonsils. Patients whose tonsils have been removed are still protected from infection by the rest of their immune system.

In strep throat, very rarely diseases like rheumatic fever or glomerulonephritis can occur. These complications are extremely rare in developed nations but remain a significant problem in poorer nations. Tonsillitis associated with strep throat, if untreated, is hypothesized to lead to pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS).

In 2004, an estimated 350 million individuals were infected worldwide. National and regional prevalences range from over 10% in Asia to under 0.5% in the United States and Northern Europe.

Routes of infection include vertical transmission (such as through childbirth), early life horizontal transmission (bites, lesions, and sanitary habits), and adult horizontal transmission (sexual contact, intravenous drug use).

The primary method of transmission reflects the prevalence of chronic HBV infection in a given area. In low prevalence areas such as the continental United States and Western Europe, injection drug abuse and unprotected sex are the primary methods, although other factors may also be important. In moderate prevalence areas, which include Eastern Europe, Russia, and Japan, where 2–7% of the population is chronically infected, the disease is predominantly spread among children. In high-prevalence areas such as China and South East Asia, transmission during childbirth is most common, although in other areas of high endemicity such as Africa, transmission during childhood is a significant factor. The prevalence of chronic HBV infection in areas of high endemicity is at least 8% with 10–15% prevalence in Africa/Far East. As of 2010, China has 120 million infected people, followed by India and Indonesia with 40 million and 12 million, respectively. According to World Health Organization (WHO), an estimated 600,000 people die every year related to the infection.

In the United States about 19,000 new cases occurred in 2011 down nearly 90% from 1990.

virus DNA persists in the body after infection, and in some people the disease recurs. Although rare, reactivation is seen most often following alcohol or drug use, or in people with impaired immunity. HBV goes through cycles of replication and non-replication. Approximately 50% of overt carriers experience acute reactivation. Males with baseline ALT of 200 UL/L are three times more likely to develop a reactivation than people with lower levels. Although reactivation can occur spontaneously, people who undergo chemotherapy have a higher risk. Immunosuppressive drugs favor increased HBV replication while inhibiting cytotoxic T cell function in the liver. The risk of reactivation varies depending on the serological profile; those with detectable HBsAg in their blood are at the greatest risk, but those with only antibodies to the core antigen are also at risk. The presence of antibodies to the surface antigen, which are considered to be a marker of immunity, does not preclude reactivation. Treatment with prophylactic antiviral drugs can prevent the serious morbidity associated with HBV disease reactivation.

Treatment is usually supportive only, as the disease is self-limiting and usually runs its course in less than a week.

Typically spreads via the fecal-oral route or via respiratory droplets.

Diphtheritic stomatitis is a recently discovered disease and has thus far been reported only in Yellow-eyed penguins ("Megadyptes antipodes"). Its symptoms are similar to human diphtheria and is characterized by infecteous lesions in the mouth area that impede swallowing and cause respiratory troubles. The infection is caused by "Corynebacterium amycolatum", an aerobic Gram-positive bacterium and mainly affects very young chicks. However, it seems likely that a triggering agent (e.g. a virus) might be involved in which renders the corynebacterium a secondary pathogen.

The disease has been a serious cause of mortality in the 2002 and 2004 Yellow-eyed penguin breeding seasons. It seems that only the New Zealand South Island and Stewart Island/Rakiura were affected.

During the latest outbreak of the disease (2004), several treatment methods were tested. Main treatment involved the administration of antibiotics, in some cases glucose solution or dietary mixtures were additionally supplemented. Outcome of the different treatment methods varied greatly. Especially the success of antibiotic treatment and a widespread use on wild animals remains a matter of debate.

The prognosis of eosinophilic myocarditis is anywhere from rapidly fatal to extremely chronic or non-fatal. Progression at a moderate rate over many months to years is the most common prognosis. In addition to the speed of inflammation-based heart muscle injury, the prognosis of eosinophilc myocarditis may be dominated by that of its underlying cause. For example, an underlying malignant cause for the eosinophilia may be survival-limiting.

There are many causes of eosinophilia that may underlie eosinophilic myocarditis. These causes are classified as primary (i.e. a defect intrinsic to the eosinophil cell line), secondary (induced by an underlying disorder that stimulates the proliferation and activation of eosinophils), or idiopathic (i.e. unknown cause). Non-idiopathic causes of the disorder are sub-classified into various forms of allergic, autoimmune, infectious, or malignant diseases and hypersensitivity reactions to drugs, vaccines, or transplanted hearts. While virtually any cause for the elevation and activation of blood eosinophils must be considered as a potential cause for eosinophilic myocarditis, the follow list gives the principal types of eosinophilia known or thought to underlie the disorder.

Primary conditions that may lead to eosinophilic myocarditis are:

- Clonal hypereosinophilia.

- Chronic eosinophilic leukemia.

- The idiopathic hypereosinophilic syndrome.

Secondary conditions that may lead to eosinophilic myocarditis are:

- Infections agents:

- Parasitic worms: various "Ascaris, Strongyloides, Schistosoma, filaria, Trematoda", and "Nematode" species. Parasitic infestations often cause significant heart valve disease along with myocarditis and the disorder in this setting is sometimes termed Tropical endomyocardial fibrosis. While commonly considered to be due to the cited parasites, this particular form of eosinophilic myocarditis may more often develop in individuals with other disorders, e.g. malnutrition, dietary toxins, and genetic predisposition, in addition to or place of round worm infestation.

- Infections by protozoa: various "Toxoplasma gondii, Trypanosoma cruzi, trichinella spiralis, Entamoeba", and "Echinococcus" species.

- Viruses: While some viral infections (e.g. HIV) have been considered causes of eosinophilic endocarditis, a study of 20 patients concluded that viral myocarditis lacks the characteristic of eosinophil-induced damage in hearts taken during cardiac transplantation.

- Allergic and autoimmune diseases such as severe asthma, rhinitis, or urticarial, chronic sinusitis, aspirin-induced asthma, allergic bronchopulmonary aspergillosis, chronic eosinophilic pneumonia, Kimura's disease, polyarteritis nodosa, eosinophilic granulomatosis with polyangiitis (i.e. Churg-Strauss syndrome), and rejection of transplanted hearts.

- Malignancies and/or premalignant hematologic conditions not due to a primary disorder in eosinophils such as Gleich's syndrome, Lymphocyte-variant hypereosinophilia Hodgkin disease, certain T-cell lymphomas, acute myeloid leukemia, the myelodysplastic syndromes, systemic mastocytosis, chronic myeloid leukemia, polycythemia vera, essential thrombocythemia, myelofibrosis, chronic myelomonocytic leukemia, and T-lymphoblastic leukemia/lymphoma-associated or myelodysplastic–myeloproliferative syndrome-associated eosinophilias; IgG4-related disease and Angiolymphoid hyperplasia with eosinophilia as well as non-hematologic cancers such as solid tumors of the lung, gastrointestinal tract, and genitourinary tract.

- Hypersensitivity reactions to agents include:

- Antibiotics/anti-viral agents: various penicillins (e.g. penicillin, ampicillin), cephalosporins (e.g. cephalosporin), tetracyclins (e.g. tetracycline), sulfonamides (e.g. sulfadiazine, sulfafurazole), sulfonylureas, antituburcular drugs (e.g. isoniazid, 4-aminosalicylic acid), linezolid, amphotericin B, chloramphenicol, streptomycin, dapsone, nitrofurantoin, metronidazole, nevirapine, efavirenz, abacavir, nevirapine.

- Anticonvulsants/Antipsychotics/antidepressants: phenindione, phenytoin, phenobarbital, lamotrigine, lamotrigine, clozapine, valproic acid, carbamazepine, desipramine, fluoxetine, amitriptyline, olanzapine.

- Anti-inflammatory agents: ibuprofen, indomethacin, phenylbutazone, oxyphenbutazone, acetazolamide, piroxicam, diclofenac.

- Diuretics: hydrochlorothiazide, spironolactone, chlortalidone.

- ACE inhibitors: captopril, enalapril.

- Other drugs: digoxin, ranitidine, lenalidomide, methyldopa, interleukin 2, dobutamine, acetazolamide.

- Contaminants: Unidentified contaminants inrapeseed oil cause the toxic oil syndrome and in commercial batches of the amino acid, L-tryptophan, cause the eosinophilia–myalgia syndrome.

- Vaccinations: Tetanus toxoid, smallpox, and diphtheria/pertussis/tetanus vaccinations.

Dental infections account for approximately 80% of cases of Ludwig's angina. Mixed infections, due to both aerobes and anaerobes, are of the cellulitis associated with Ludwig's angina. Typically, these include alpha-hemolytic streptococci, staphylococci and bacteroides groups.

The route of infection in most cases is from infected lower molars or from pericoronitis, which is an infection of the gums surrounding the partially erupted lower (usually third) molars. Although the widespread involvement seen in Ludwig's usually develops in immunocompromised persons, it can also develop in otherwise healthy individuals. Thus, it is very important to obtain dental consultation for lower-third molars at the first sign of any pain, bleeding from the gums, sensitivity to heat/cold or swelling at the angle of the jaw.

There has been a single case reported where Ludwig's angina was thought to be caused by a recent Tongue piercing. In addition, Filipino boxer Pancho Villa (1901–1925) died after contracting Ludwig's Angina following a bout with Jimmy McLarnin.

Ludwig's angina, otherwise known as angina ludovici, is a serious, potentially life-threatening cellulitis, or connective tissue infection, of the floor of the mouth, usually occurring in adults with concomitant dental infections and if left untreated, may obstruct the airways, necessitating tracheostomy. It is named after the German physician Wilhelm Friedrich von Ludwig who first described this condition in 1836. Other names include "angina Maligna" and "Morbus Strangularis".

Ludwig's angina should not be confused with "angina pectoris", which is also otherwise commonly known as ""angina"". The word ""angina"" comes from the Greek word ἀγχόνη "ankʰónē", meaning "strangling". In this case, Ludwig's angina refers to the feeling of strangling, not the feeling of chest pain, though there may be chest pain in Ludwig's angina if the infection spreads into the retrosternal space.

The life-threatening nature of this condition generally necessitates surgical management with involvement of critical care physicians such as those found in an intensive care unit.

The condition may be a sign of various disease states, including but not exclusive to the following:

- Cancers

- Lymphoma

- Leukemia

- Infections

- HIV/AIDS

- Tuberculosis

- Mycobacterium avium-intracellulare infection

- Infectious mononucleosis

- Fungal infections (histoplasmosis, coccidioidomycosis)

- Lung abscess

- Infective endocarditis

- Brucellosis

- Pneumocystis pneumonia (most often - in immunocompromised individuals)

- Endocrine disorders

- Menopause

- Premature ovarian failure

- Hyperthyroidism

- Diabetes mellitus (nocturnal hypoglycemia)

- Endocrine tumors (pheochromocytoma, carcinoid)

- Orchiectomy

- Rheumatic disorders

- Takayasu's arteritis

- Temporal arteritis

- Other

- Obstructive sleep apnea

- Gastroesophageal reflux disease

- Chronic fatigue syndrome

- Fibromyalgia

- Granulomatous disease

- Chronic eosinophilic pneumonia

- Lymphoid hyperplasia

- Diabetes insipidus

- Prinzmetal's angina

- Anxiety

- Pregnancy

- Drugs

- Antipyretics (salicylates, acetaminophen)

- Antihypertensives

- Dinitrophenol - a common side effect

- Phenothiazines

- Drug withdrawal: ethanol, benzodiazepines, heroin (and other opiates),

- Over-bundling

- Autonomic over-activity

- IBD (inflammatory bowel disease) - Crohn's disease/ulcerative colitis

Coronary artery disease has a number of well determined risk factors. These include high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, depression, family history, and excessive alcohol. About half of cases are linked to genetics. Smoking and obesity are associated with about 36% and 20% of cases, respectively. Lack of exercise has been linked to 7–12% of cases. Exposure to the herbicide Agent orange may increase risk. Both rheumatoid arthritis and systemic lupus erythematosus are independent risk factors as well.

Job stress appears to play a minor role accounting for about 3% of cases.

In one study, women who were free of stress from work life saw an increase in the diameter of their blood vessels, leading to decreased progression of atherosclerosis. In contrast, women who had high levels of work-related stress experienced a decrease in the diameter of their blood vessels and significantly increased disease progression. Having a type A behavior pattern, a group of personality characteristics including time urgency, competitiveness, hostility, and impatience is linked to an increased risk of coronary disease.

Untreated, the infection may lead to rapid destruction of the periodontium and can spread, as necrotizing stomatitis or noma, into neighbouring tissues in the cheeks, lips or the bones of the jaw. As stated, the condition can occur and be especially dangerous in people with weakened immune systems. This progression to noma is possible in malnourished susceptible individuals, with severe disfigurement possible.

In developed countries, this disease occurs mostly in young adults. In developing countries, NUG may occur in children of low socioeconomic status, usually occurring with malnutrition (especially inadequate protein intake) and shortly after the onset of viral infections (e.g. measles).

Predisposing factors include smoking, viral respiratory infections and immune defects, such as in HIV/AIDS. Uncommon, except in lower socioeconomic classes, this typically affects adolescents and young adults, especially in institutions, armed forces, etc., or people with HIV/AIDS. The disease has occurred in epidemic-like patterns, but it is not contagious.

While the true causes of Tietze's syndrome are not well understood, it often results from a physical strain or minor injury, such as repeated coughing, sneezing, vomiting, or impacts to the chest. It has even been known to occur after hearty bouts of laughter. It can occur by over exerting or by an injury in the chest and breast.

Psychological stress can exacerbate Tietze's syndrome, but there is no evidence to suggest that it is a direct cause.

Patients who have had radiation therapy to the chest/breast will often experience this syndrome which can occur shortly after therapy or years later.

It is found more often in teens than adults.

Dietary cholesterol does not appear to have a significant effect on blood cholesterol and thus recommendations about its consumption may not be needed. Saturated fat is still a concern.

A study showed that those who quit smoking reduced their risk of being hospitalized over the next two years.

Smoking increases blood pressure, as well as increases the risk of high cholesterol. Quitting can lower blood pressure, and triglyceride levels.

Secondhand smoke is also bad for the heart health.