Scarlet Fever.


Etiology, Pathology, Symptomology, Diagnosis


Scarlet fever, or scarlatina, is an acute infectious, self-limited disease, characterized in typical cases by sore throat, high temperature, a characteristic rash, desquamation and leucocytosis, one attack of which almost always gives immunity.

As more is known of the predisposing factors than of the exciting cause, predisposition will be first considered.

The most susceptible age is between two and six years, although no age seems to be immune. Cases of congenital scarlatina are reported in which the mother was suffering from the disease during the end of her pregnant period or at the time of her confinement, but cases are comparatively rare before one year of age or after puberty. The season of the year is quite an important factor, the early winter months showing a larger number of cases than other seasons, and it is a notable fact that the mortality is higher among those suffering from the disease in the winter than in the summer.

Individual susceptibility is another factor worthy of mention. Anyone who has come in contact with contagious diseases to any extent has not failed to note the high susceptibility to scarlet fever of some individuals over others.

A child may contract a very virulent form of scarlet fever after one exposure, while the other members of the family may go unscathed after repeated exposures.

The presence of an epidemic of course predisposes, and different epidemics differ in virulence.

Women in childbed are said to be predisposed to the disease.

As to the source of infection, direct contact with the scarlet fever patient is not necessary, for the infection may extend through his personal emanations (nasal and oval excretions, sweat, dermal exfoliations, sputum, urine, feces, and perhaps the breath).

Scarlet fever is communicated to others through all stages of the disease from the incubation period to complete desquamation.

The mode of entrance of the contagion to the body is not very well known, but observation has led us to believe that it is usually through the upper respiratory passages, though it may be through the tonsils, gastro-intestinal tract or recent wounds either surgical or accidental. The period of incubation varies widely in different individuals and in different epidemics. Exceptionally it may be from twenty-four hours to two weeks, but on an average it is from two to six days.

Regarding the exciting cause, nothing definite is known in spite of the almost endless research work that has been done by members of all schools in vain effort to discover the specific germ. One thing, however, is sure, and that is that the streptococcus pyogenes (as shown by the blood agar plate method of Schott, Müller and Rosenow) is almost always present in the throats of scarlet fever patients, and that while it may not be the specific cause, it is beyond doubt responsible for some of the symptoms and most of the complications, but there are objections to the theory of the streptococcus being the causative agent.

Agglutinies are formed in the blood of scarlet fever patients, for the streptococcus pyogenes taken, not only from other patients suffering from scarlet fever, but also patients suffering from such streptococcic infections as erysipelas, cellulitis, etc. Then again blood cultures differ widely in their results. A good culture of streptococci may be grown from the blood of one patient suffering with a mild form of the disease, while absolutely negative results may follow such experiments in a more severe or even fatal case; but still, as a rule, fatal cases show a streptococcaemia.

Another point against the streptococcus being the exciting cause is the fact that while one attack of scarlet fever usually gives immunity from subsequent attacks, an attack of scarlet fever gives no immunity to other streptococcic infection, as erysipelas, etc.

Gaburtitshewsky of Moscow claims to have made a vaccine from dead streptococci which causes an erythema to appear very similar to that of scarlet fever, and also other symptoms such as sore throat, high temperature, etc., running a course very similar to scarlet fever with the exception of there not being any complications, and also that it is not contagious; whether it gives immunity to scarlet fever or not remains yet to be seen.

Laboratory workers state that the opsonic index for the streptococcus pyogenes is much below normal during the incubation period and onset, but that it soon becomes high and remains so until the temperature is normal, when the index drops and fluctuates between normal and slightly above during convalescence.

The general conclusion of authors and men who have done extensive research along this line is that the exciting cause of scarlet fever is a yet unknown specific organism plus a streptococcic infection.

Pathology: There is no distinctive pathology, but the changes revealed by autopsy may be stated briefly as follows:

In cases that die early, the viscera (especially the brain) show deep engorgement. Death at an advanced stage shows the lesions of nephritis, septicopyemia, and occasionally pleuritis, pericarditis, fatty degeneration of the myocardium, endocarditis and meningitis.

Bingel reports eight cases in which the early changes of cirrhosis of the liver were found.

The skin shows an acute hyperemia (dermatitis) with exudation of serum and sound cells in the corium, especially about the blood vessels and hair follicles. The epidermis dies and desquamates. The mucous membranes, particularly of the upper respiratory passage, show inflammation which may be catarrhal, membranous, phlegmonous, or gangrenous. The inflammatory process may travel up the eustachian tube to the middle ear, thence to the mastoid cells, and finally to the lateral sinuses or meninges brain. The liver may show areas of focal necrosis.

Symptoms:—The symptoms differ somewhat but in typical cases the onset is sudden, with nausea and vomiting, sore throat, high temperature (103° to 105°F.) and rapid pulse out of proportion to the temperature. There are quite often convulsions in infants and young children. The tongue is at first coated white but a few days later presents a clean red surface with swollen, elevated papillae, the typical raspberry tongue. Usually within twelve hours after the invasion, the characteristic eruption appears, beginning first in the neck and spreading over the trunk and extremities until the entire body is covered with the exception of the chin and nose and around the mouth, which show a yellowish pallor in striking contradistinction to the bright scarlet color of the eruption.

The eruption may begin on the clavicles, in the axillae or over the groins, or in cases where wounds furnish the portal of entrance, it may begin at the wound and spread from there.

The cervical lymph glands are enlarged and tender. A white blood count shows leucocytosis 12,000 to 20,000 or even higher.

Desquamation usually begins about the 7th or 8th day, proceeding in the order of appearance, and is usually complete by the end of the sixth week, though it occasionally takes seven weeks or even longer for the heels to become entirely clean. Desquamation is in the form of scales, branny on the body, but larger on the hands and feet where the dead epidermis may come off in casts. In some cases the skin can be pulled off in large strips. As desquamation begins the temperature usually falls by lysis, the appetite improves and the child rebels most emphatically against the customary three weeks of liquid diet and four weeks being kept in bed.

In more severe cases, the temperature may go up higher (105 to 107°F.), with marked delirium, and finally in eighteen to thirty-six hours the patient sinks into coma and dies.

The urine is high colored and may show albumin casts and red blood cells.

There is not infrequently cellulitis in the neck.

The nose often shows a purulent discharge, and the tongue, buccal mucous membrane and throat may show large patches of ulceration. Not infrequently a white streptococcic membrane is noted on the tonsils and pharynx at the onset of the disease. In the severer type just mentioned the child presents a picture of positive profound sepsis, and one complication follows another until the patient either dies or gets well after a long and tedious convalescence.

The lymphatic glands, principally the cervical, may break down and suppurate, but I have found that large prophylactic doses of phytolacca will nearly always abort this complication.

Other frequent complications are otitis media and nephritis, but lack of time will not permit going extensively into the complications, so I will pass on to the diagnosis and differential diagnosis.

The cardinal points in the diagnosis of scarlet fever lie in the sudden onset with vomiting (sometimes without nausea), sore throat, high temperature, with rapid pulse out of proportion to the temperature, cervical lymph adenopathy, appearance of the characteristic rash, leucocytosis, and later, the characteristic desquamation, and some observers claim that the finding of the class coccus is a good diagnostic point. My experience has been that this organism is fairly constant in the throats of scarlet fever patients, especially during the initial stages. I found it in about fifty out of a series of seventy-six cases examined.

As to the differential diagnosis the principal difficulty lies in distinguishing this disease from the scarlatinal form of rubeola known under the names of Duke's Disease and Fourth Disease.

In this disease (Duke's) the constitutional symptoms are much the same as in measles, although eruption very closely simulates that of scarlet fever but has more of a rose hue and is less punctate than scarlet fever. Close examination of the body may reveal the maculo-papular eruption of measles and desquamation is not complete as in scarlet fever. A blood count will reveal leucopyemia, or at most no increase in the leucocytes, while scarlet fever shows a more or less marked leucocytosis. It may be necessary to wait for desquamation before an absolute diagnosis can be made.

Ellingwood's Therapeutist, Vol. 2, 1908, was edited by Finley Ellingwood M.D.