Tropical Diseases/Chapter 17
CHAPTER XVII
SPOTTED FEVER OF THE ROCKY MOUNTAINS
Definition.— A specific fever resembling symptomatically typhus exanthematicus, supervening on the bite of a tick— Dermacentor venustus, Banks.
History.— For upwards of thirty years a peculiar disease variously named "spotted fever," "blue disease," " black fever," has been recognized as endemic in limited districts of Montana and Idaho, United States of America. It was first described by Maxey, in 1899, as a distinct disease, and in the spring of 1902 it was investigated by Wilson and Chowning, who attributed it to the presence in the blood of a parasite akin to the babesia of Texas cattle fever. Their results were endorsed by Wesbrook, Cobb and Anderson; but in May, 1904, Wardell Stiles failed to recognize the parasite, either in fresh preparations of the blood or in the preparations of previous investigators. Other observers have been equally unsuccessful; the existence of the so-called Pyrosoma hominis is now discredited, and the germ of Rocky Mountain fever is still unknown.
In 1906 King definitely ascertained that the disease supervened on the bite of" a certain tick, Dermacentor venustus (D. andersoni) (Figs. 64, 65), a discovery subsequently confirmed by Ricketts, who succeeded in conveying the infection to a monkey by means of an infected tick. McClintick in 1911, in researches conducted at the instance of the United States Government, failed to communicate the disease to guineapigs, but unfortunately himself contracted the infection and died.
Geographical distribution.— The disease has been reported for several of the Western States of the American Union Idaho, Montana, Wyoming, Utah, Nevada, Oregon, and Washington State. It is believed to occur also in the Alaska territory. It is found principally in valleys and near the foot-hills of mountains in sharply-defined and limited areas, and is confined to the spring months, the greatest number of cases occurring between March and July. It attacks any age, either sex, and is not directly contagious.
Symptoms.—A short period of malaise is followed by chills, which are repeated with diminishing
Fig. 64.—Dermacentor venustus, ♂. (By courtesy of Prof. Nuttall.)
severity at irregular intervals throughout the attack. By the second day the temperature has risen to 103° or 104° F., and by the fifth day to 105° or 107°. A typhoid-like condition, with low muttering delirium and semi-consciousness, is rapidly developed. If the patient is to recover, the temperature begins to fall about the end of the second week, fever subsiding usually by lysis.
About from the fourth to the seventh day an eruption appears on the wrists, ankles or back, extending rapidly to the trunk, scalp, hands, and feet. At first it consists of minute rose-coloured spots; these soon assume a petechial character and, spreading, tend to become confluent, especially on the more dependent parts of the body and limbs. In other instances the spots remain discrete, brownish or purplish in colour, giving to the surface of the body
Fig. 65.—Dermacentor venustus, ♀. (By courtesy of Prof. Nuttall.)
a speckled appearance. A certain amount of icteric tinting of skin and scleræ is also present. During the third week desquamation sets in, the eruption fading as fever subsides. In some cases the skin of the elbows, fingers, toes, lobes of the ears, etc., becomes gangrenous.
Constipation is usual. The liver is slightly enlarged, the spleen markedly enlarged and tender. The scanty, high-coloured urine may contain albumin and casts. Early, in all severe cases, there is œdema of the face and limbs. Nausea and vomiting set in about the beginning of the second week, and persist in fatal cases. Respiration is rapid. Slight catarrh of the respiratory tract is present throughout; the pulse loses in volume as it increases in frequency. There is but little diminution in the blood count, and only a feeble leucocytosis— 12,000 to 13,000; the hæmoglobin is slightly diminished.
Pathology.— Post-mortem, in addition to the foregoing skin lesions,, there is marked hypostatic congestion of the lungs, subserous petechiæ, softened myocardium, enlarged and softened spleen, fatty degeneration of the hepatic cells, and congestion of the cortex of the kidneys.
Etiology.— The evidence is now conclusive that the germ of Rocky Mountain fever is introduced by the bites of D. venustus*[1] It is only the adult that attacks man. The- Rocky Mountain goat and the domestic sheep also serve as hosts to the adult forms, but the larval and nymph stages develop principally on the ground squirrel, Citellus columbianus, and the woodchuck, Marmota flaviventer. The tick takes two years to develop, hibernating during the winter, feeding but languidly after the beginning of August, and reviving during the first warm days in April. It is possible that the Rocky Mountain goat serves as a natural reservoir of the disease virus.
According to Ricketts, the unrecognised germ is intimately attached to the blood corpuscles, is easily inoculated into man, and can be passed through an indefinite series of monkeys and guineapigs, giving rise in them to the characteristic symptoms, and producing immunitv. The larvæ, nymph, and adult male and female tick are all of them efficient intermediaries Ricketts suggests, seeing that in one place— Montana —the case mortality in man is as high as 90 percent., whereas in another place— Idaho— it is only 5 per cent., that there are two species of tick, in the former D. venustus, in the latter D. maturatus, capable of transmitting the infection. The proportion of infected ticks in natural conditions is small; only 1 in 296 in Ricketts' experience.
In conformity with the seasonal prevalence of the tick, the disease in man is commonest in April, May, and June.*[2]
Treatment and prophylaxis.— In the absence of a specific remedy, treatment must be conducted on general principles, having regard to the natural history and nature of the disease. Attempts at prophylaxis are now being carried out, based on the above-described hypothetical method of transmission of the disease. War is being waged on the ground squirrel and the woodchuck; domestic stock and goats are being systematically dipped to prevent the spread of and, if possible, to exterminate the tick.
Fricks, finding that if D. venustus is placed on the fleece of an unshorn sheep it either dies or remains unimpregnated, and is manifestly on an uncongenial host, has suggested, in addition to the measures just mentioned, turning the badly infected districts into sheep-runs.
- ↑ * D. venustus and D. andersoni are the same species. The differences in the nomenclature of the tick used by various authors have resulted in a good deal of confusion. D. reticulatus and D. accidentalis, apparently distinct species, have at various times been incriminated as carriers of the infection.
- ↑ * Tick paralysis.— According to Hadwen, the tick, D. venustus, as it occurs in the dry district of British Columbia, Keremeos, gives rise to a peculiar form of paraplegia in sheep which, directly or indirectly, may prove fatal. In the same district it affects man and other animals in a similar way. Todd has called attention to this disease, of which he has collected a considerable number of cases, some of them fatal. Nuttall, working in Cambridge, England, has confirmed Hadwen's experiments. He placed one of the ticks received from Hadwen on a healthy dog. Twelve days afterwards the dog became completely paralysed in fore- and hind-legs. Ultimately it gradually recovered. This form of tick disease is manifestly different from Rocky Mountain fever, as it is non-febrile, is unattended with eruption, and is not communicable by inoculation. Possibly it is produced by a poison instilled by the'tick during haustellation. The wound it makes is very painful, is attended with œdema and, on forcible removal of the tick, with free bleeding as if some anticoagulin had been introduced. In sheep the favourite points of attachment of the tick are on the back along the course of the spine; in man, the nape of the neck. A somewhat similar form of paralysis is described by Eaton as following on tick bite in Queensland, Australia, the incriminated tick being Ixodes ricinus. Bancroft reports from the same country a similarly caused form of epileptiform convulsions in cats and dogs.