Find information on thousands of medical conditions and prescription drugs.

St. Anthony's fire

Ergotism is the effect of long-term ergot poisoning, classically due to the ingestion of the alkaloids produced by the Claviceps purpurea fungus which infects rye and other cereals, and more recently by the action of a number of ergoline-based drugs. It is also known as ergotoxicosis or ergot poisoning. more...

Sabinas brittle hair...
Sacral agenesis
Saethre-Chotzen syndrome
Salla disease
Sandhoff disease
Sanfilippo syndrome
Say Meyer syndrome
Scarlet fever
Schamberg disease...
Schmitt Gillenwater Kelly...
Scimitar syndrome
Selective mutism
Sensorineural hearing loss
Septo-optic dysplasia
Serum sickness
Severe acute respiratory...
Severe combined...
Sezary syndrome
Sheehan syndrome
Short bowel syndrome
Short QT syndrome
Shprintzen syndrome
Shulman-Upshaw syndrome
Shwachman syndrome
Shwachman-Diamond syndrome
Shy-Drager syndrome
Sickle-cell disease
Sickle-cell disease
Sickle-cell disease
Silver-Russell dwarfism
Sipple syndrome
Sjogren's syndrome
Sly syndrome
Smith-Magenis Syndrome
Soft tissue sarcoma
Sotos syndrome
Spasmodic dysphonia
Spasmodic torticollis
Spinal cord injury
Spinal muscular atrophy
Spinal shock
Spinal stenosis
Spinocerebellar ataxia
Splenic-flexure syndrome
Squamous cell carcinoma
St. Anthony's fire
Stein-Leventhal syndrome
Stevens-Johnson syndrome
Stickler syndrome
Stiff man syndrome
Still's disease
Stomach cancer
Strep throat
Strumpell-lorrain disease
Sturge-Weber syndrome
Subacute sclerosing...
Sudden infant death syndrome
Sugarman syndrome
Sweet syndrome
Swimmer's ear
Swyer syndrome
Sydenham's chorea
Syndrome X
Synovial osteochondromatosis
Synovial sarcoma
Systemic carnitine...
Systemic lupus erythematosus
Systemic mastocytosis
Systemic sclerosis


The toxic ergoline derivatives are found in ergot-based drugs (such as methylergometrine, ergotamine or, previously, ergotoxine). The deleterious side-effects occur either under high dose or when moderate doses interact with potentiators such as azithromycin.

Classically, eating cereals or cereal-based products contaminated with the fungus Claviceps purpurea also caused ergotism.

Finally, the alkaloids can also pass through lactation from mother to child, causing ergotism in infants.


The symptoms can be roughly divided into convulsive symptoms and gangreneous symptoms.

Convulsive symptoms

Convulsive symptoms include diarrhea, paresthesias, itching, seizures, headaches, nausea and vomiting. Usually the gastrointestinal effects precede CNS effects. As well as seizures there can be hallucinations and mental effects including mania or psychosis. The convulsive symptoms are caused by clavine alkaloids.

Gangrenous symptoms

The dry gangrene is a result of vasoconstriction induced by the ergotamine-ergocristine alkaloids of the fungus. It affects the more poorly vascularized distal structures, such as the fingers and toes. Symptoms include desquamation, weak peripheral pulse, loss of peripheral sensation, edema and ultimately the death and loss of affected tissues.


Epidemics of the disease were identified throughout history, though the references in classical writers are inconclusive. Rye, the main vector for transmitting ergotism, was not grown much around the Mediterranean. When Fuchs separated references to ergotism from erysipelas and other afflictions he found the earliest reference to ergotism in the Annales Xantenses for the year 857: "a Great plague of swollen blisters consumed the people by a loathsome rot, so that their limbs were loosened and fell off before death." In the Middle Ages the gangrenous poisoning was known as ignis sacer ("holy fire") or "Saint Anthony's fire", named for the 4th century hermit of Egypt. The 12th century chronicler Geoffroy du Breuil of Vigeois recorded the mysterious outbreaks in the Limousin region of France, where the gangrenous form of ergotism was associated with the local Saint Martial as much as Saint Anthony. The blight, named from the cock's spur it forms on grasses, was identified and named by Denis Dodart who reported the relation between ergotized rye and bread poisoning in a letter to the French Royal Academy of Sciences in 1676 (John Ray mentioning ergot for the first time in English the next year), but "ergotism" in this modern sense was first recorded in 1853. Research by Linnda Caporael (1976) suggests that many of the people whose accusations resulted in the 1692 Salem witch trials in Massachusetts were genuinely suffering hallucinations and other symptoms of convulsive ergotism. Similar eruptions of ergotism also occurred in Essex and Fairfield counties in Connecticut that damp and cool season, though in Connecticut no one went to the stake. Notable epidemics of ergotism, at first seen as a punishment from God, occurred up into the 19th century. Fewer outbreaks have occurred since then, because in developed countries rye is carefully monitored. When milled the ergot is reduced to a red powder, obvious in lighter grasses but easy to miss in dark rye flour. The last reported outbreak in an industrialized country, which caused more than 200 cases and 4 deaths, occurred in 1951 in Pont St. Esprit, France. In less wealthy countries ergotism still occurs: there was an outbreak in Ethiopia in mid-2001 from contaminated barley. Whenever there is a combination of moist weather, cool temperatures, delayed harvest in lowland crops and rye consumption an outbreak is possible. Russia has been particularly afflicted.


[List your site here Free!]

St. Anthony's fire: diagnosis and management of erysipelas
From American Family Physician, 2/1/95 by Robert L. Bratton

The incidence of erysipelas increased dramatically, for unknown reasons, during the late 1980s.(1) Once referred to as "St. Anthony's Fire," erysipelas can be traced as far back as the Middle Ages. The etiologic agent was once thought to be the ergot alkaloids produced by the fungus Claviceps purpurea, found in contaminated rye. Because patients who had ingested the fungus presented with bright red gangrenous extremities, they were thought to be consumed by the "Holy Fire." It was believed that only the shrine of St. Anthony, an Egyptian monk and healer (251-356 A.D.), could provide relief.(2) An 11th century hospital, the French House of St. Anthony, was devoted to the care of victims of epidemic gangrene and had "fiery red" walls similar to the color of the lesions of erysipelas; hence, the name St. Anthony's Fire.(3)


Erysipelas is a beta-hemolytic streptococcal infection that affects the skin and subcutaneous tissue. Group A streptococci are the most commonly identified causative bacteria. However, groups B, C, D and G streptococci have been isolated from patients with erysipelas. Occasionally, staphylococcal organisms are isolated as well. The infecting organism usually enters the body through nasopharyngeal tissue, trauma sites, insect bites or surgical incisions.

Erysipelas affects persons of all ages, but it is most prevalent among the young and the elderly. The frequency of erysipelas increases during the summer months.(4) Females are more commonly affected than males, and the peak incidence of infection occurs in persons between 60 and 80 years of age.(1) At particular risk are immunocompromised patients, patients taking corticosteroids, patients with acquired immunodeficiency syndrome or diabetes, patients who are alcoholic or patients who are undergoing chemotherapy.

Because erysipelas is an infectious disease, a greater incidence of infection would be expected to occur in settings such as nursing homes, day care centers, military bases and prisons. However, epidemics are rare and isolated cases are the rule.(1)

Clinical Presentation

The clinical presentation of classic erysipelas is distinct. The infection usually has an abrupt onset and a rapid course. The most common presenting symptom is an area of discomfort or paresthesia on the face, usually in the nasal or perinasal region. Occasionally, patients report symptoms of pharyngitis over the days or weeks before the appearance of a facial rash.

An area of erythema forms at the site of discomfort and rapidly enlarges to involve a larger area of the face over the next three to six days (Figure 1). The rash has an irregular leading edge that is distinct, raised and tender to palpation. The advancing erythema is shiny, tense and warm to the touch. Vesicles or bullae may form over the affected area. The eyes and cheeks may become edematous. If the infection spreads to affect most of the face, it may have a "butterfly" distribution and may be mistaken for the facial rash of lupus erythematosus.


As the erythema advances, it may take on a deeper red, ecchymotic appearance, with a bright red leading edge. Within seven to 10 days, the erythematous zones begin to show central clearing, with a gradual return to normal appearance. Areas of skin may exfoliate, and impetiginous lesions or postinflammatory hyperpigmentation may develop in the affected area. During the erythematous stage, patients usually complain of constitutional symptoms, such as fever, chills, arthralgias, fatigue and poor appetite.

Currently, infections involving the face are less common than those affecting the legs.(1) During the early 20th century, 50 to 85 percent of the cases of erysipelas involved the face but, in recent years, the incidence of facial involvement has decreased to about 6 to 19 percent.(5) The relative infrequency of facial erysipelas may be explained by better hygiene.(1) Erysipelas may now more commonly involve an area of the leg used for saphenous vein harvest for coronary artery bypass surgery.(6)


Usually, erysipelas is easily diagnosed on the basis of its clinical manifestations. The characteristic rash, fever and constitutional symptoms typical of infection, including malaise, chills and, occasionally, anorexia or gastrointestinal symptoms, are hallmarks of the disease. The rash is brightly erythematous, well demarcated, indurated, raised and painful to palpation. Also, regional lymph node involvement is often found.

Laboratory findings include moderate leukocytosis with a shift to the left indicative of bacterial infection, an increase in the erythrocyte sedimentation rate, and positive blood cultures in as many as 5 percent of patients. A positive antistreptolysin O titer supports the existence of streptococcal infection. Cultures of the nasopharynx are frequently positive and also support the diagnosis of erysipelas. Cultures of aspirated lymphatic fluid from the leading edge of the rash occasionally grow streptococci, but aspiration of this area is a painful and unnecessary procedure and, therefore, is not recommended.

The differential diagnosis of erysipelas includes contact dermatitis and angioneurotic edema. In these cases, however, fever and tenderness do not usually accompany the rash. Herpes zoster and other forms of cellulitis, such as cellulitis associated with Haemophilus influenzae, should also be considered in the differential diagnosis. H. influenzae cellulitis primarily affects the buccal and periorbital areas and generally occurs in children less than two years of age. It has a rapid course, and bacteremia develops in almost 75 percent of patients. Thus, patients with this form of cellulitis usually have a more toxic appearance than patients with erysipelas.(7)

Erysipeloid is a skin infection caused by the inoculation of Erysipelothrix rhusiopathiae; dead animal products are the source of infection. Erysipeloid can be differentiated from erysipelas by its slow onset, limited spread and lack of constitutional symptoms, and a history of exposure.


Penicillin is the drug of choice for the treatment of erysipelas. If a patient is allergic to penicillin, erythromycin may be substituted. Newer cephalosporins have a broad spectrum of coverage but are often more expensive and are unnecessary unless the infection itself is polymicrobial.(8)

Oral antibiotics are adequate for most cases of erysipelas. Treatment should be continued for 10 to 14 days, or until the rash has completely resolved and the patient is asymptomatic.

Some patients with erysipelas, especially children and debilitated adults, require admission to the hospital and treatment with intravenous or intramuscular antibiotics.(9) The location of lesions and size of the affected area should be considered in the decision to admit a patient. The duration of treatment with intravenous antibiotics should be individualized. In some cases, three to seven days of intravenous treatment are needed. Before treatment with oral antibiotics is initiated in these cases, the erythematous area should be resolving, the patient should be afebrile and leukocytosis should have resolved.

Warm, moist compresses that promote blood flow to the affected area can also be beneficial. A follow-up evaluation in one or two weeks is recommended to ensure that the infection does not recur.


Complications arising from erysipelas are uncommon (13 percent of cases in one study(1)). Patients who have complications often have other underlying disease, such as alcoholism, diabetes, postphlebitic syndrome and AIDS.

The most common complications of erysipelas are abscess formation, gangrene and thrombophlebitis. Septicemia, acute glomerulonephritis and endocarditis are rare (Table 1).(1) Upper airway obstruction and streptococcal toxic shock syndrome have also been reported but are infrequent complications.(10)(11)(12)

TABLE 1 Complications in 529 Cases of Erysipelas

Adapted from Chartier C, Grosshans E. Erysipelas. Int J Dermatol 1990; 29:459-67. Used with permission.

Recurrence of erysipelas is a significant complication and is relatively common in immunocompromised patients. In one study,(13) erysipelas recurred in 29 percent of 149 consecutive patients during a followup period of two to four years. In selected patients with frequent or severe recurrences, prophylactic therapy with oral penicillin may be considered.


(1.)Chartier C, Grosshans E. Erysipelas. Int J Dermatol 1990; 29:459-67.

(2.)Weaver R, Phillips M, Vacek JL. St. Anthony's fire: a medieval disease in modern times: case history. Angiology 1989; 40:929-32.

(3.)Tanner JR. St. Anthony's fire, then and now: a case report and a historical review. Can J Surg 1987; 30:291-3.

(4.)Ronnen M, Suster S, Schewach-Millet M, Modan M. Erysipelas. Changing faces. Int J Dermatol 1985; 24:169-72.

(5.)Ochs MW, Dolwick MF. Facial erysipelas: report of a case and review of the literature. J Oral Maxillofac Surg 1991; 49:1116-20.

(6.)Dan M, Heller K, Shapira I, Vidne B, Shibolet S. Incidence of erysipelas following venectomy for coronary artery bypass surgery. Infection 1987; 15:107-8.

(7.)Waagner DC, McCracken GH Jr. Haemophilus infections. In: Wilson JD, Braunwald E, Isselbacher KJ, Petersdorf RG, Martin JB, Fauci AS, et al., eds. Harrison's Principles of internal medicine. 12th ed. New York: McGraw-Hill, 1991:618.

(8.)Suss SJ, Middleton DB. Cellulitis and related skin infections. Am Fam Physician 1987; 36(3):126-36.

(9.)Jorup-Ronstrom C. Epidemiological, bacteriological and complicating features of erysipelas. Scand J Infect Dis 1986; 18:519-24.

(10.)Bartter T, Dascal A, Carroll K, Curley FJ. 'Toxic strep syndrome.' A manifestation of group A streptococcal infection. Arch Intern Med 1988; 148:1421-4.

(11.)Cone LA, Woodard DR, Schlievert PM, Tomory GS. Clinical and bacteriologic observations of a toxic shock-like syndrome due to Streptococcus pyogenes. N Engl J Med 1987; 317:146-9.

(12.)Guslits B. Upper airway obstruction due to erysipelas. Intensive Care Med 1991; 17:370-1.

(13.)Jorup-Ronstrom C, Britton S. Recurrent erysipelas: predisposing factors and costs of prophylaxis. Infection 1987; 15:105-6.

COPYRIGHT 1995 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group

Return to St. Anthony's fire
Home Contact Resources Exchange Links ebay