Chapter XXXVIII: Spotted Fever of the Rocky Mountains

DEFINITION AND SYNONYMS

=Definition.=—The disease is chiefly reported from certain sections of the states of Montana and Idaho. The virus is not filterable and is probably bacterial in nature and is transmitted solely by the tick, _Dermacentor andersoni_, which arthropod host gets its infection from certain rodents of the section serving as virus reservoirs.

Maxey described the disease as follows: “An acute endemic,
noncontagious, but probably infectious febrile disease,
characterized clinically by a continuous moderately high fever,
severe arthritic and muscular pains and a profuse, petechial
eruption in the skin, appearing first on the ankles, wrists and
forehead but rapidly spreading to all parts of the body.”

=Synonyms.=—Rocky Mountain fever. Tick fever of the Rocky Mountains. Black fever. Blue disease.

HISTORY AND GEOGRAPHICAL DISTRIBUTION

=History.=—The disease was first noted in the Snake River Valley
of Idaho, about 1893, and in the Bitter Root Valley of Montana,
about 1890. There is some evidence that the disease may have
existed among the Indians prior to the advent of white settlers in
the Bitter Root Valley. The disease was first described by Doctor
M. W. Wood, U. S. A., in 1896. It is interesting to note that the
first white settlers of the Bitter Root Valley suffered from what
was considered a very fatal form of “black measles.”

In 1902 Wilson and Chowning reported that the disease was due to a
piroplasm of the squirrel and that it was transmitted to man by the
bite of a tick (_Dermacentor venustus_). Later Ashburn and others,
while accepting the tick transmission, failed to corroborate the
piroplasm etiology.

It is chiefly to Ricketts that we owe much of our detailed
knowledge of the epidemiology of the disease.

The work of McClintic and Frick along lines of prophylaxis has
given us practical measures for the control of the disease.

The views of Ricketts, Wolbach and Frick as to etiology are
discussed under that heading.

=Geographical Distribution.=—The two best known regions of
prevalence of the disease are the Bitter Root Valley of Montana and
the Snake River Valley of Idaho. It is also reported from limited
sections of Washington, Oregon and California, as also from Nevada
and Utah.

In Wyoming it is rather widely distributed.

ETIOLOGY AND EPIDEMIOLOGY

=Etiology.=—Wolbach states that he has noted certain bacterial forms in the endothelial cells of the blood vessels of guinea pigs infected with the virus, as well as a very general distribution in infected ticks.

There are two morphological types—one, a chromatic-staining
lanceolate diplococcoid organism, found in the circulating blood as
well as in the endothelial cells, the other type—a blue-staining
rod-shaped form.

Ricketts noted certain chromatin-staining bacteria, in man and
in eggs of infected ticks, which were about 1 micron long by ⅓
micron broad, showed chromatin staining, were about the size of
_B. influenzae_, and appeared as two lanceolate-shaped bodies.
These bodies are now considered as belonging to the _Rickettsia_
group of organisms. Wolbach has named the organism of spotted fever
of the Rocky Mountains _Dermacentroxenus rickettsi_. In infected
guinea pigs Wolbach found these bodies particularly abundant in the
endothelial cells.

Frick has also found bodies within the red cells of human cases
and infected guinea pigs, as well as extracellularly, which showed
chromatin-staining characteristics, there often being an elongated
reddish body joined on to a larger blue-staining protoplasm.

In 1902 Wilson and Chowning reported the finding of piroplasm-like
bodies in the blood of human cases of Rocky Mountain Spotted
Fever. Ricketts proved that the virus was not filterable. A tick,
_Dermacentor andersoni_ transmits the disease.

=Epidemiology.=—The transmitting tick, _D. andersoni_ (_D. venustus_) lives on the domesticated animals of the region of geographical distribution of the disease. Ricketts showed that the reservoir of the virus was to be found in ground squirrels, chipmunks, mountain rats, etc., and that ticks feeding on these rodents become infected and transmit the disease to man. The guinea pig, white rat and monkey are also susceptible.

The virus can be propagated indefinitely in guinea pigs without
loss of virulence by weekly blood inoculations in another animal.
The virus seems to be transmitted by the salivary secretion of the
tick and a tick once infected remains infective for the remainder
of life.

Frick succeeded in obtaining anaerobic cultures from infected blood
of a bacillus, somewhat resembling the _B. typhi exanthematici_ of
Plotz. These bacteria, however, did not show complement fixation
with immune serum and were nonpathogenic to guinea pigs.

Spotted fever is a disease of rural districts and tends to give
only one case to a house, thus indicating the negative rôle
of bedbugs, lice, etc. It is at the time when ticks are most
abundant, in the months of the spring, that the disease makes its
appearance. The virus is in the blood during the entire febrile
course.

PATHOLOGY

The cadaver shows marked jaundice with petechial spots on extremities and trunk.

There is marked venous engorgement and the blood is very dark and fluid.

In the blood vessels we have proliferation of the endothelial cells
leading to thrombosis.

Ricketts noted enlargement of the lymph glands. The spleen is three
or four times the normal size and is quite firm. Microscopically
it shows extensive endothelial cell proliferation. The kidneys are
enlarged and congested. Gangrene of the prepuce and scrotum are
often noted.

SYMPTOMATOLOGY

The period of incubation is from five to ten days when the disease sets in with considerable abruptness, with more or less marked rigors, headache, malaise and severe pains of the larger joints, but without inflammatory changes.

Some cases present a prodromal period lasting a day or so with
malaise and chilly sensations followed by the symptoms noted above.
Hyperaesthesia and photophobia are apt to be present during the
course of the disease.

The eruption first appears from the second to the fifth day as
macules about the wrists and ankles, thence spreading over the
extremities and extending to the trunk. These macules tend to
become petechial.

_The Pulse._—The pulse is not very rapid (90-110) and the fever
steadily rises day by day from the initial 102°F to reach a maximum
of about 105°F. by the end of a week or so. A toxaemic condition
appears early.

A stuporous state is fairly common but in many cases the mind is
clear throughout the course.

The spleen is palpable early in the disease and is quite firm, not soft like the spleen of typhoid fever.

The kidney involvement shows itself early as an albuminuria.

Constipation is rather a constant feature.

Icterus and vomiting tend to come on later in severe cases.

_Gangrene._—Gangrene of the tonsils, scrotum and prepuce are more
common in the milder type of the disease, as seen in Idaho, than in
the more severe one of Montana.

There is leucocytosis early in the disease, falling to about 10,000
after a few days. There is an increase in the large mononuclears.
The eosinophiles are decreased in percentage.

DIAGNOSIS

The association of a tick bite and proper geographical distribution is of prime importance. The more sudden onset, joint pains and negative Widal differentiate it from typhoid fever.

Typhus fever shows more marked abruptness of onset and decline
of fever than does Rocky Mountain fever. The guinea pig, while
susceptible to both infections, is more easily infected with this
disease than with typhus fever.

As a matter of fact there are marked clinical resemblances between
typhus fever and Rocky Mountain fever. Tsutsugamushi and trench
fever also have points of resemblance.

PROGNOSIS

It is very remarkable that the disease should rather constantly
give a mortality approximating 75 to 90% in western Montana and
only about 5% for Idaho.

Where the nervous manifestations are marked the prognosis is more
unfavorable. Death tends to occur in the second week and patients
living through this week have a good chance for recovery. The death
rate is greatest in old people and least in young children.

PROPHYLAXIS AND TREATMENT

=Prophylaxis.=—_Dermacentor andersoni_ requires a long time to
become attached and feed on the human host—at least one or more
hours—hence inspection of one’s person for ticks after returning
from exposure and removing those found would tend to prevent
infection.

When these ticks attach themselves to the wool of grazing sheep,
87% seem to die, possibly from the effect of the fat in the wool.

Again such sheep can be dipped for further destruction of the ticks.

=Treatment.=—Just as with typhus fever the most important point
in the care of the patient is good nursing. The room should be
darkened and quiet maintained. Cool sponging lowers the temperature
and is a tonic for the nervous disorders. An ice cap is good for
the headache. The diet should be liquid and water should be given
freely on account of the tendency to renal involvement.

There is a tendency to heart failure so that the recumbent position
is demanded and cardiac stimulants indicated.

Michie and Parsons found sodium citrate of greatest benefit in
treating infected guinea pigs and recommended it for human cases.
It is to be used intravenously and about 60 cc. of a 5% solution
given twice daily. Immune sera were tried out by Ricketts, but
without result.