These hard, brittle, irregular grains are caused by various species

of fungi of which the best known is Carter’s black mycetoma

(_Madurella mycetomi_). This species was cultured by Wright and

first shows a grayish growth, later becoming black. Other black

varieties of mycetoma are due to various other fungi. Bouffard’s

black variety is caused by _Aspergillus bouffardi_. DeBeurmann’s

black mycetoma has as cause _Sporotrichum beurmanni_.

Besides the white and black varieties we also have a red variety of

mycetoma. The fungus grains are quite small and reddish in color.

It is not an uncommon infection in certain parts of Africa, as

Senegal. The cause is _Nocardia pelletieri_.

Boyd and Crutchfield have noted an ascomycete in an American case,

with white granules, to which has been given the name _Alleschiria

boydii_.

=Epidemiology.=—We know very little about the occurrence of these

mycetoma fungi, other than in man. It is thought that such fungi lead

a saprophytic existence on thorns or blades of grass or spine-like

grains of various cereals. Thus Nicolle’s case in Tunis started from

a puncture wound by a grain of barley.

As the vast majority of such cases are noted in the feet, and as

such cases are chiefly in those who work barefooted, it seems

reasonable to consider that the fungi are introduced on some

puncturing object and the external wound having healed development

goes on in the deeper structures.

PATHOLOGY

In more than 75% of cases of mycetoma the foot is the only part

infected. More rarely there is involvement of hands, knees and

buttocks.

The affected part shows nodules on the external surface which

connect with the granulomatous lesions of the interior of the foot

by sinuses. In advanced cases there may be a network of sinuses

and cyst-like dilatations which are filled with a viscid fluid

packed with the small fish-roe granules in the white variety or the

gunpowder grains of the black mycetoma. The bony structures of the

foot may undergo disintegration as well as muscular and areolar

tissue so that on cutting into such a foot there is nothing normal

remaining—simply a cheesy mass.

In the early granulomatous areas are found the actinomyces-like

granules surrounded by an area of mononuclear and polymorphonuclear

infiltration. Giant cells are occasionally found. There is an

inflammatory oedema. Externally we have connective tissue cells and

a fibrous wall. The blood vessels show endothelial proliferation

and thrombosis.

SYMPTOMATOLOGY

The disease usually begins in the sole of the foot with the formation

of firm swellings about ½ inch in diameter. The cases are rarely seen

at this stage, the natives waiting before seeking medical advice

until the nodule has softened and begun to discharge the viscid fluid

with the various-colored granules floating in it. As stated before,

the soft, yellowish-white, fish-roe-like granules are most commonly

observed, the more friable, hard, gunpowder-like grains less so. The

nodules continue to form and to break down until the foot has become

greatly enlarged, the under surface bulging out in a convex mass with

the toes and heels appearing as if raised up. The dorsal surface is

also puffed up and studded with broken down nodules, and the sides

well rounded. There is no increase in the length of the foot. This

swollen distorted foot is borne on a thin peg-like leg which makes

the size of the foot more striking. Very rarely cases have been

reported where the hand or thigh have been involved.

If one probes the discharging sinuses bone may or may not be felt

according to the advancement of the degenerative changes. There is

rarely pain or bleeding following the probing.

It is more from the onerous burden of carrying around this fungoid

mass of a foot, 3 or 4 times the normal size, than pain, that the

patient complains of.

[Illustration: FIG. 126.—Mycetoma. (From Greene.)]

Uncomplicated cases do not show fever and the occasional

enlargement of lymphatic glands is probably connected with

bacterial infections.

There are never visceral metastases in mycetoma as is true of the

nearly related actinomycosis.

The process shows no tendency to heal naturally or under treatment

but fortunately does not extend, the process being confined to

a foot or a hand. The joints are rarely if ever invaded. Unless

the sinus-riddled member is amputated the drain on the patient

gradually exhausts him and death ensues in ten or fifteen years.

DIAGNOSIS

The distorted appearance of the foot or hand, riddled with sinuses

discharging a viscid fluid containing the variously colored granules,

which upon microscopical examination are found to be sclerotia of

fungi, is absolutely diagnostic. As regards recognition of the

causative fungus one should culture the discharge or grains on

maltose agar, potato or rather dry blood serum. The recognition of

species of fungi is a very difficult matter, even for an expert.

PROGNOSIS

This is absolutely unfavorable as regards the relief of the condition

but as regards life it is not unfavorable provided the drain on the

system is gotten rid of by amputation of the part.

PROPHYLAXIS AND TREATMENT

=Prophylaxis.=—The wearing of shoes in the fields or forests would

seem to be the best means of protection against small wounds from

thorns, splinters and the like.

Then, too, any such wound which might occur should be treated with

tincture of iodine.

[Illustration: FIG. 127.—Important tropical fungi.]

=Treatment.=—It is usual to try the effects of curetting the lesions

and if taken early enough this may have effect. As a rule the process

goes on but is limited to the member attacked so that amputation of

the diseased part brings about a cure. Iodide of potash is of no

value. X-ray treatment seems to be of value in relieving the pain and

in lessening the discharge from the sinuses but is of questionable

curative effect. It might be of greater value if tried early in the

disease.

CHAPTER XXIX

GRANULOMA VENEREUM

HISTORY AND GEOGRAPHICAL DISTRIBUTION

=History.=—It is generally stated that Daniels first noted the

disease in British Guiana, in 1896, but Daniels regards the disease

previously described by Macleod from India under the designation

“serpiginous ulceration of the genitals,” as referring to granuloma

venereum.

=Geographical Distribution.=—Cases of the disease have been

chiefly reported from British Guiana and the West Indies. It is now

recognized, however, that it occurs in India, China and Northern

Australia as well as in some of the islands of the Pacific. It also

occurs in Northern and Central Africa.

Grindon has reported 3 cases from the United States.

ETIOLOGY

Various spirochaetes have been reported as present in the lesions.

The finding by Wise of spirochaetes resembling _Treponema pallidum_

has not been generally accepted.

Donovan has reported the presence, in scrapings from the

ulcerations, of an oval bacillus (1½ × 2 microns) which was

contained in large phagocytic cells. There were sometimes several

such bodies in a single cell.

Flu has recently reported the presence in plasma cells as well

as occasionally in other cells of a capsulated organism which he

believes related to the Friedlander group. His cultural work has

not been conclusive. It is probable that this capsulated organism

is merely a secondary invader.

There is also a suggestion of the cellular reaction characteristic

of the chlamydozoa.

The disease is rather more common in women than in men and is

rarely seen before the period of puberty. It is thought that it is

transmitted by sexual intercourse.

PATHOLOGY

The pathological process manifests itself as a small round cell

infiltration of the superficial portion of the corium. The growth

is well supplied with blood vessels. Giant cell formation and

caseation have not been noted. There is an abundance of plasma

cells.

There is a marked tendency to the formation of fibrous tissue.

SYMPTOMATOLOGY

The disease usually first shows itself as a papule or vesicle on the

penis or labia minora. The process extends and the thin epidermal

layer rubs off leaving a surface of granulations which bleed easily

and give off a creamy discharge which is frequently very offensive.

[Illustration: FIG. 128.—Venereal granuloma. (After Martini; from

Mense.)]

The process usually extends from the penis to the groins by

continuity and thence down the inner surfaces of the thigh. When

the glans penis is involved there may be a fungating growth

suggestive of epithelioma. In the female the process extends from

the labia minora into the vagina and also to the labia majora and

thence to the perineum and perianal region. Recto-vaginal fistulae

often result. The process extends more rapidly and markedly when

invading mucous membranes.

While the granulomatous process is advancing there is frequently

cicatrization of the areas previously invaded forming a scar tissue

which breaks down easily. There is little pain or itching and the

general health is not impaired.

There is no enlargement of the lymphatic glands. Although the

process extends by continuity yet it may also pass to parts in

contact with the diseased area. While healing of affected skin

tends to occur that of mucous membrane does not.

There is really very little tendency to ulceration.

DIAGNOSIS

It is usual to suspect a syphilitic process but the absence of gland

involvement and secondary manifestations of syphilis negatives this.

It may be suggestive of tuberculous or epitheliomatous processes.

The marked chronicity and tendency to scarring are striking.

TREATMENT

Excision of the entire granulomatous area going well into the normal

skin has been thought by some to be the only cure.

Ordinary antisyphilitic treatment does not seem to have any effect

and the good reports that have been made as to therapeutic success

with salvarsan may have been due to diagnosing a syphilitic process

as granuloma venereum. Radiotherapy has been recommended.

Local treatment with antiseptic or deodorant washes or ointments is

necessary in these cases.

_Antimony Treatment._—Breinl reports success in treatment by using

tartar emetic injections. This treatment is now the standard one

and the drug is given intravenously as described under treatment of

leishmaniasis. It is also recommended to apply locally compresses

soaked with a ½% solution of tartar emetic.

SECTION VI

TROPICAL SKIN DISEASES

CHAPTER XXX

TROPICAL ULCER

GENERAL CONSIDERATIONS

Under the names tropical phagedaena or tropical ulcer various skin

lesions have been described, from all parts of the tropics, which

vary greatly in etiology and symptomatology.

These skin ulcers are most frequently observed on the dorsum of the

foot or front of the leg but may appear on the hands or forearms and

have rarely been reported from other parts of the body.

There is no doubt but that many of the cases reported as tropical

ulcer are really manifestations of tertiary syphilis.

Jeanselme has noted the insignificant manifestations of the

secondary stage of syphilis in natives of Indo-China and the

malignancy of the tertiary ones as regards the skin lesions. In

fact a striking feature of the late stages of syphilis in the

natives of the tropical world is the frequency and severity of skin

lesions and the rarity or absence of involvement of the central

nervous system to produce tabes or general paresis.

Again congenital syphilis is common in most tropical countries

which have been visited by white men for long periods and Jeanselme

has noted the rarity in natives so affected of interstitial

keratitis and Hutchinson’s teeth, signs upon which medical men are

apt to base a diagnosis of such a condition.

Again, Butler, studying the serological side of 27 ulcerations

which clinically could be diagnosed as tropical ulcer, obtained

strongly positive Wassermann tests in 26, or 96 per cent. of the

cases. Shattuck found that about 94% of the chronic ulcerations of

the Philippines could be ascribed to syphilis.

Besides syphilis one must bear in mind the possibility of the ulcers

being a manifestation of tertiary yaws, a condition which also gives

a high percentage of positive Wassermann tests.

In Guam, the natives separate the ulcerations about the lower

extremities from the naso-pharyngeal ones by designating the

former cases llagosos and the latter gangosas. It is probable

that the leg ulcers are manifestations of the same disease as the

naso-pharyngeal ones whether it be syphilis or yaws. These ulcers

of the leg in Guam as well as those studied by Butler in the

Philippines would certainly be classed as tropical ulcers.

There are undoubtedly many cases which can be explained by

infections with ordinary pyogenic organisms of the skin which are

enabled to get a foothold in an abrasion or other minor wound, in a

person whose resistance has been reduced by such cachexia-producing

diseases as malaria, dysentery or ancylostomiasis.

Indeed some authorities attach special importance to the tibial

ulcers found in advanced cases of hookworm disease. Some of the

sores are due to irritating applications used by the natives of

many countries as setons. In many instances the sores are from

neglected wounds.

Vincent has called attention to the association of the fusiform

bacillus and delicate spirillum, better known in connection with

Vincent’s angina, in smears from tropical ulcers.

Such findings have also caused many to consider tropical ulcer as

related to hospital gangrene. There is no doubt but that smears

from the dirty membranous deposit on these ulcers do frequently

show the fusiform bacillus and at times the spirillum, but we also

frequently find various fungi in such smears. Very few hold that

these have anything to do with the production of the ulcer.

Inoculation experiments have as a rule been indefinite in result.

LeDantec has incriminated a very large Gram-negative bacillus which

was noncultivable.

Prowazek believes that he has found the cause in a spirochaete which

possesses fewer turns and these more widely separated than those

of the spirochaete of syphilis. The association with the fusiform

bacillus has also been noted.

Wolbach and Todd note the frequent finding of spirochaetes in

tropical ulcers and attach considerable importance to a spirochaete

with abruptly tapering ends. The name of Spirochaeta schaudinni has

been given to the organism. They also generally found associated

micrococci and bacilli as well as the fusiform bacillus.

Other than the noting of granulation tissue and the presence of

plasma and small round cells there does not seem to be anything

definite in the histopathology of tropical ulcer. This is what

one might expect in view of the lack of definite knowledge of the

condition.

_Veld sore._—Under the name of Veld sore we have a form of tropical

ulcer which is common in various desert regions.

These ulcerations may appear on the face as well as on the dorsal

surfaces of the hands or forearms or on the lower extremities. They

seem to arise from infections of abrasions of the exposed parts.

In the early stages of the lesion the diphtheria bacillus has been

frequently isolated and some of the cases have been followed by

diphtheritic palsies. It would appear that these lesions have at

times been those of cutaneous diphtheria. Such cases were reported

by Craig in cases in the Sinai desert. The simultaneous existence

of cases of ordinary faucial diphtheria should make one suspicious

of the real nature of such ulcerations. Skin diphtheria is more

frequent than is generally considered.

SYMPTOMATOLOGY

These ulcers are most frequently found on the dorsum of the foot,

over the shin and about the external malleolus. More rarely they

involve the dorsum of the hand or back of the wrist.

In the multiplicity of clinical descriptions from various parts of

the tropics we obtain two types of ulceration.

One is that of a rather chronic ulcer, which slowly develops from

a painless swelling, which is not unlike a gummatous process.

Surrounding the swelling there is a circumscribed, reddened, glazed

area of skin. After two or three weeks the swelling begins to soften

and a serous fluid exudes from its summit.

Ulceration, with the frequent formation of a membrane-like deposit,

now sets in and later on we have a more or less punched-out ulcer

showing indurated margins. There may be no impairment in the health

of those with this type of ulcer.

The other type is generally seen in persons who are much debilitated

or suffering from some cachectic state. In the earliest stages

these sores seem to resemble an area which has been excoriated

and inoculated with vaccine virus, there being a rather dry,

angry-looking spot of erythema. This within a few hours may be

surrounded by a circle of vesicles beyond which is an encircling

inflammatory areola.

There is marked subjective pain and tenderness. The serum from

the vesicles fails to show any bacteria and the cellular contents

are made up almost entirely of polymorphonuclear leucocytes.

Within a few hours to one or two days the area within the ring

of vesicles is converted into a dark gray to black pultaceous

diphtheroid membrane which when detached shows underlying fungating

granulations, covered with greenish-yellow pus. This membrane, if

stripped off, tends to reform with great rapidity (twenty-four to

forty-eight hours), and in many respects resembles the membrane of

diphtheria except for its dark color.

These ulcerations extend with great rapidity and even when showing

a tendency to heal may suddenly, from a point along the margin,

proceed to form a new area of ulceration, extending somewhat as

would a ringworm. When the original site of ulceration fails

to heal during a period of several weeks, the edges become

rather indurated but do not show the punched-out or undermined

characteristics of the first type.

These cases last for months and are far more tantalizing than

the former type of ulceration for the reason that from time to

time they show a strong tendency to heal, the process clearing up

almost entirely, when suddenly the former area of the ulceration is

equalled or exceeded.

TREATMENT

Many of these ulcerations yield readily to salvarsan and in such

cases we naturally think of a syphilitic or framboesial etiology.

Castellani has recommended a protargol ointment, 5 to 10%, which is

applied to the ulcer after previous flushing with hydrogen peroxide

or other antiseptic lotion.

At times thorough cauterization with pure carbolic acid followed by

neutralization with alcohol may shorten the process.

Iodide of potash benefits some cases but has no effect on others

and the same is true of mercurial treatment.

An 8% ointment of scarlet red should be tried on these sores when

treatment with ordinary applications fails.

CHAPTER XXXI

TINEA IMBRICATA

GENERAL CONSIDERATIONS

This form of tropical ringworm is chiefly found in the islands of

the South Pacific and in the Malay Archipelago. It is also found in

Southern China and quite recently has extended to Southern India and

Ceylon. Recently it has been reported from Brazil.

On account of the disease having been carried from the Tokelau Group

to Samoa it is often designated _tokelau_.

Manson was the first to recognize the affection as due to a fungus

which he demonstrated microscopically in the scales.

He was also able to transmit the disease by inoculation experiments

and found that after about ten days a raised, brownish spot appeared

at the site of inoculation. This spot increased in size until when

about ¼ inch in diameter its central portion became detached, thus

giving rise to several thin, rosette-like scales, free at the center

but still attached peripherally. The fungus advances peripherally,

leaving a smooth surface within. Again there is a similar process

developing in the original central spot to again form a circle of

scales within the older and more peripheral circle. The process is

repeated until several rings of scales are formed each originating

from the central focus as concentric ripples form on water from the

fall of a pebble.

These scale circles are from ⅛ to ½ inch apart and give a festooned

appearance to the affected skin. It was formerly supposed that the

causative fungus was _Aspergillus concentricus_ but Castellani has

demonstrated that fungi of this genus, when present, are merely

accidental. He has isolated in cultures what he considers the

causative fungus, _Endodermophyton concentricum_. He treated scales

for ten minutes with absolute alcohol and then placed single scales

in a series of tubes of maltose bouillon.

The fungus grows between the rete malpighii and the external

epidermal layers forming a network of mycelial threads, about 3

microns broad.

Another fungus cultured from tinea imbricata scales is

_Endodermophyton indicum._ Inoculation of this organism in pure

culture produced the disease.

The characteristics of the genus _Endodermophyton_ are: The

growth of a mycelial network between the rete malpighii and the

superficial epidermal layers; in cultures only mycelial filaments

are found; there are no conidia-bearing hyphae.

The fungus is also called _Trichophyton concentricum_.

When this skin disease is introduced into a country with high

relative humidity and fairly uniform temperature, between 80° and

90°F. it spreads with great rapidity.

A dry climate or one showing considerable variations in temperature

is not favorable for its spread.

SYMPTOMATOLOGY

[Illustration: FIG. 129.—Tinea imbricata from the South Seas. (After

Kramen; from Mense.)]

The clinical characteristic of this form of ringworm is the

presence of rosette-like lesions of several concentric circles of

shingle-like, papery scales which are fixed peripherally and free

toward the center, thus, from its imbrications, suggesting the name

given it by Manson.

If one passes the finger over the affected surface from without

inward there is no sensation of roughness but if passed from the

center outward the free borders of scales cause a sensation of

roughness.

As these circles extend peripherally they meet the peripheral rings

of other circles so that various curves appear which give the general

appearance of watered silk.

The flaky scales are of tissue paper thinness and are of a dirty,

brownish-gray color.

The general health of the patient is not affected but the itching

is very severe.

There is an entire absence of inflammation about this ringworm thus

differentiating it from the more common tropical ringworms. Again

the axillae and crotch are much more rarely affected than in other

ringworms as is also true of the face, palms of hands and soles of

feet. The scalp is never affected.

Some claim that the fungus never invades the nails but Manson

states that this frequently occurs. The presence of the fungus in

a scale treated with 10% solution of sodium hydrate differentiates

the scales from those of ichthyosis.

Tinea intersecta is somewhat similar to tinea imbricata when

first appearing, showing dark brown patches but it never shows

the concentric rings. The ordinary ringworms present inflammatory

characteristics.

TREATMENT

A thorough preliminary scrubbing with soap and water in order better

to expose the fungus to curative applications is important.

For treatment Manson recommends iodine liniment. This contains 12½%

of iodine as against 7% for the tincture. The liniment has also

3½% of glycerine which is not an ingredient of the tincture. Both

tincture and liniment have 5% of potassium iodide. The application of

the tincture does not seem to be as satisfactory as the liniment, the

stronger preparation being more effective.

Chrysarobin is very effective but very irritant and has to be

used with care. An application of a 5% solution of chrysarobin in

chloroform to the affected area, then painting it over with a 50%

aqueous solution of ichthyol, often gives good results.

Some prefer a 2% to 5% ointment of chrysarobin. Chrysarobin

produces a conjunctivitis if used near the eyes. Again if absorbed

it may act as a renal irritant.

Castellani strongly recommends the use of resorcin in tincture

of benzoin (60 to 120 grains of resorcin in 1 ounce of tincture

of benzoin). Either remedy alone has very little effect, the

combination being necessary. The application is made once or twice

daily. In addition to this treatment the patient should be scrubbed

with sand-soap and hot water twice a week.

As regards prophylaxis the clothing should be boiled. The natives

attach value in preventing the disease to anointing the body with

cocoanut oil.

CHAPTER XXXII

TINEA CRURIS

GENERAL CONSIDERATIONS

Under the name “dhobie itch” this fungus affection is probably better

known to Europeans than any other tropical skin disease. This name

dhobie or washerman’s itch has been given on account of associating

it with the infection of the underclothing while being washed in the

pools or streams along with the garments of those who have this skin

disease. This, like every other widespread view, has probably some

foundation but cannot be verified. It is the eczema marginatum of

Hebra.

This affection is caused by various species of _Epidermophyton_.

This genus differs from _Trichophyton_ in that it never invades the

hair or hair follicles.

The species which have been more frequently reported are

_Epidermophyton cruris_, _E. perneti_ and _E. rubrum_. The mycelium

is about 4 microns broad and the spores about 5 or 6 microns. All

of these fungi can be cultured on Sabouraud’s maltose agar, growth

appearing in about a week, except _E. perneti_, which grows more

rapidly.

SYMPTOMATOLOGY

The favorite site is the crotch although the axillary region is also

frequently involved. The process starts as a papule but these rapidly

develop and give rise to an angry red, swollen patch with sharply

delimited margins. These red, festooned patches are usually limited

to the perineum, scrotum and inner surfaces of the thighs.

The itching is unbearable and many secondary infections or eczematous

lesions result from the fierce scratching of the parts.

If the patient goes to a cooler place the process subsides to

return when he comes back to the hot moist climate where the

infection was originally contracted.

In some cases the fungus invades the region between the toes and

gives rise to intolerable itching and from secondary bacterial

infections to a condition known as “Mango toe.”

It has seemed to me that when one has a coccal infection engrafted

upon the fungus one the condition becomes what might be termed

fulminating, so rapidly does the itch extend.

TREATMENT

When the process is markedly inflammatory mild applications are

indicated, such as calamine lotion (30 grains each of calamine

and zinc oxide with 5 or 10 drops of carbolic acid in 1 ounce of

saturated solution of boric acid).

A 10% to 15% solution of sodium hyposulphite can, however, be used on

the area even when markedly inflammatory.

Iodine applications are too irritating for the region of the scrotum.

An ointment of resorcin, 20 to 30 grains with 1 dram of sulphur

to the ounce, may be tried. If chrysarobin be used it should be

applied with greatest care as noted under tinea imbricata. Many

advocate applications of solutions of salicylic acid in alcohol, 2%

to 5%.

Manson’s dusting powder of equal parts of boric acid, zinc oxide

and starch should be freely used.

CHAPTER XXXIII

PINTA

GENERAL CONSIDERATIONS

This is a parasitic skin affection due to various species of fungi.

It is only found in the tropical portion of the new world, and is

especially prevalent in Colombia, where it has been estimated 4% of

the population have the disease. It is also found in Mexico, Central

America and some of the other countries of South America as well as

Colombia.

Other names for the disease are caraate and mal de los pintos.

At first it was thought that the different colors shown by the

eruption were due to varying depths of the proliferating fungi in

the skin layers but it is now known that the explanation is in a

variety of species in the different types of pinta.

The pure violet pinta is caused by _Aspergillus pictor_ while the

grayish-violet one is due to _Penicillium montoyai_. A species

of _Monilia_ causes the white variety and different species of

_Montoyella_ a black and a red variety respectively. The genus

_Montoyella_ is stated by Castellani to have both slender and thick

mycelial threads, from the thicker of which spring delicate hyphae

terminating in pear-shaped conidia.

Material scraped from the lesions and mounted in liquor

potassae shows the fructification terminations characteristic

of _Aspergillus_ or _Penicillium_ in the violet or gray-violet

varieties while the white, black and red ones only show mycelial

threads and scattered spores. These pinta species of fungi can be

cultivated on Sabouraud’s medium.

Montoya thinks that the pinta fungi lead a saprophytic existence

in the waters of mines or other places with a constant high

temperature, and states that he has obtained pure cultures from

such sources.

SYMPTOMATOLOGY

The spots of the eruption are generally first noted on the hands or

face and are rather rough, dry and only slightly raised. Itching is

quite marked and the scratching probably is largely responsible for

the gradual spread of the affection over the body generally.

The palms of the hands, soles of the feet and nails are never

involved. The course is essentially chronic and shows no tendency to

spontaneous cure.

The red pinta is that most often found in white people, the patches

being of brick-red color.

The white pinta may not only be caused by a species of _Monilia_

but it may represent an area formerly invaded by a species

producing some other color and then dying out leaving a

vitiligo-like area.

The violet pinta is quite common among miners, while the black one

is the type which more often appears in the black population. The

black varieties may show either a pure black or a violet-black

color.

TREATMENT

Local applications of iodine preparations or of chrysarobin seem most

effective. The resorcin sulphur ointment noted under tinea cruris is

best for the face.

CHAPTER XXXIV

MINOR TROPICAL AFFECTIONS OF THE SKIN

DERMATOPHILIASIS

This is a skin infection due to the penetration of the region about

the feet and especially the toes by the female sand flea or chigoe.

It is also sometimes called the jigger. This flea is a member of

the subfamily Sarcopsyllinae which differs from the ordinary flea

subfamily in that the impregnated female becomes fixed in the tissues

of the host instead of developing her eggs in a free state. The

proper name for this flea is _Dermatophilus penetrans_, synonym

_Sarcopsylla penetrans_. It is found abundantly in Central America

and Northern South America as well as in the West Indies. It is also

found in East and West Africa as well as India and is apparently

rapidly spreading over the tropical world.

[Illustration: FIG. 130.—Sandflea female; much enlarged. (From

Mense.)

FIG. 131.—Sandflea male; much enlarged. (From Mense.)]

This flea attacks not only man but many wild and domesticated

animals as well, and in particular the pig. The males and females

live in dry sandy soil and feed on the blood of various mammals.

The importance of the parasite is that upon impregnation the

female ceases to lead a free existence but burrows into the tissues

of man or other host and becomes enormously distended with eggs.

There is some question as to whether these eggs are extruded by the

female or whether they are set free in the ulceration process which

tends to occur around the imbedded flea. The eggs develop into

13-segment larvae, which form a cocoon from which the insect comes

out in about ten days.

[Illustration: FIG. 132.—Sandflea female. Shortly after penetrating

the skin. The anterior part of the abdomen is much more distended

than the posterior; the enlarged part is disk-shaped, not globular.

(From Mense.)]

The female flea tends to burrow into the skin about the sides of

the toe nails, although more rarely boring into other parts of

the body as penis, scrotum, thighs or hands. Finally only the tip

of the abdomen projects. This marks the black spot which is noted

in the tense itching area which is quite white unless bacterial

infection starts up inflammation.

The swelling is about the size of a small pea by the end of five or

six days. Ulceration is the usual termination of the infection if

untreated and such ulcers may be very intractable or form a favorable

soil for infection with the tetanus bacillus. Quiros has estimated

that 250 deaths from tetanus occurred in Costa Rica in 4 years from

infection of nigua (sand flea) ulcerations.

Well-made shoes are most important in prophylaxis and the best

treatment is to enucleate the egg-distended flea with a needle

and then touch the cavity with pure carbolic acid followed by

neutralization with alcohol. It is astonishing how expert the

natives become in dissecting out these insects.

TROPICAL IMPETIGO

Under the designation pemphigus contagiosus Manson describes a very

common skin disease of the tropics. The condition, however, is not

pemphigus. A bacteriological examination shows in the smear great

numbers of pus cells containing phagocytized diplococci. Wherry has

named the organism _Diplococcus pemphigi contagiosi_. As a matter

of fact, culturally, this organism is the common _Staphylococcus

pyogenes aureus_.

It is also a matter of common observation that this organism when

in pus cells of active inflammatory processes shows a diplococcus

morphology rather than a staphylococcal one.

These staphylococcal lesions which do not start in the hair

follicles are often designated as “pyoses.”

The disease is markedly contagious in children and is strikingly

autoinoculable so that unless the first lesion is taken in hand

immediately the eruption may become generalized. A small spot of

erythema first appears which rapidly becomes vesicular, the bleb

covering the entire spot, so that there is practically no surrounding

inflammatory areola.

The diaphanous covering rubs off with the slightest touch and

leaves underneath a raw-looking surface which extends peripherally

to form an angry-looking red patch an inch or more in diameter. In

adults it rarely affects parts other than the axilla or crotch.

The general health of the child is practically unaffected.

The usual treatment is with bichloride lotions followed by a

dusting powder of equal parts of boric acid, starch and zinc oxide.

I have found, however, that an ointment of ammoniated mercury, 2%

to 5% according to age, is the most satisfactory treatment.

_Tropical Boils._—It is interesting that the same organism

responsible for this more fulminating lesion should be the one

responsible for the common cosmopolitan boil and in fact boils are

exceedingly common in the tropics. These boils may be larger and

with a greater tendency to widespread distribution and in some

regions they are so common as to have a regional designation (Nile

boils). The staphylococcus of tropical impetigo seems to have

greater virulence than that of the boils. Autogenous vaccines are

often most successful in the treatment of boils.

PIEDRA

This is a fungus disease of the hairs in which small nodules form

along the shaft. They are about the size of the nits of head lice but

more or less surround the hair instead of projecting off at an angle

as do the ovoid lice nits. These little masses are black in color

and very hard, hence the name piedra—stone. The disease is chiefly

found in Colombia and is thought to be due to the application, by the

women, of a mucilaginous preparation to their hair. If an infected

hair be examined in liquor potassae the nodule will be found to

be made up of faceted bodies matted to the side of or, at times,

encircling the hair. These bodies are the spores of _Trichosporum

giganteum_.

Besides piedra there are also other nodular affections of the

hairs due to species of _Nocardia_. Chalmers has recently reported

several cases of trichonocardiasis where the axillary hairs were

matted together and the skin of the region inflamed. Castellani

called attention to this condition in 1911 and reported a narrow,

bacillus-like fungus as the cause, _Nocardia tenuis_. The nodules

are rather soft and may be yellow, black or red in color.

Microscopical examination shows the fungus.

Chalmers had excellent results by treating the affected hairs with a

2% formalin solution in alcohol. At night a 2% ointment of sulphur

was applied. A 5% alcoholic solution of salicylic acid has also been

recommended.

[Illustration: FIG. 133.—Insects in which the larval stage is

important. (1) _Chrysomyia macellaria_; (2) larva; (3) _Dermatobia

cyaniventris_ larva, early stage (ver macaque); (4) _D. cyaniventris_

larva, later stage (torcel or berne); (5) _D. cyaniventris_; (6)

_Auchmeromyia luteola_; (7) _A. luteola_, larva; (8) _Sarcophaga

magnifica_; (9) _S. magnifica_ larva; (10) _Anthomyia pluvialis_;

(11) _A. pluvialis_ larva.]

CUTANEOUS MYIASES

=Ver Macaque.=—The best known of these myiases is that due to the

larva of a botfly (Oestridae), _Dermatobia cyaniventris_.

The larva is at first club shaped and in this stage is called ver

macaque. Later on it becomes worm shaped and is then called torcel in

Venezuela or berne in Brazil. The natives of most of the countries

where the infection is found have called the larvae “mosquito

worms” or “gusano de zancudo” and they have even incriminated large

mosquitoes belonging to the genus _Psorophora_ as being responsible

for the infections.

Surcouf has noted that these fly larvae have been found cemented to

mosquitoes of the genus _Janthinosoma_ by a glue-like substance.

These mosquitoes are vicious biters and evidently the young larvae

escape from the eggs attached to the mosquito and enter the wound

made by the biting parts of the mosquito. Some have thought that

_D. cyaniventris_ deposits its eggs in a glue-like material on the

leaves of plants and that they stick to mosquitoes flying about

such plants. From the facts that these eggs apparently only become

attached to this particular mosquito, and further in that the eggs

are attached in a constant manner with the hatching end outward, it

would seem that the mother fly must in some way seize the mosquito

and deposit her eggs on it. As the larva grows in the subcutaneous

tissues of man or other animals a tumor-like swelling develops with

a central orifice, toward which the posterior extremity of the

larva points and through which it takes air into its spiracles.

It has been stated that the eggs of _D. cyaniventris_ may be

conveyed by ticks.

The swelling somewhat resembles a blind boil and may be as large as a

pigeon’s egg.

These botfly boils tend to break down and discharge a sero-purulent

fluid and it is supposed that the larva, when mature, escapes as a

result of the disintegration of the tumor.

In Brazil they make tobacco juice applications which cause the

larva to protrude and then squeeze it out. The injection of a

little chloroform into the larva with a hypodermic syringe, prior

to its extraction with a forceps, makes the process less painful.

=The Screw Worm.=—This is the larva of a bluebottle fly, _Chrysomyia

macellaria_, which differs from the common bluebottle fly, _Lucilia_,

by having 3 black lines on scutum. This muscid fly lays 200 to 300

eggs in wounds or orifices having offensive discharges, as from nose,

ears, etc. The larvae burrow into the adjacent tissues and cause

frightful destruction of all soft parts. The mature larvae are a

little more than ⅔ inch long and have circlets of spines around each

of the 12 segments.

This infection is especially common in tropical and subtropical

America and is important in animals as well as man.

In Yount’s 23 cases 18 were of nasal myiasis; the mortality for

the 23 cases was 15% and for the nasal ones 22%. Irrigation with

chloroform water or a 5% carbolic acid or compound cresol solution

gives the best results in treatment. If the larvae reach the

sinuses it may be necessary to open them to get at the parasites.

CREEPING ERUPTION

This is a skin affection which is also called larva migrans

on account of its being due to the burrowing of more or less

undetermined fly larvae in the subcutaneous tissues. In their

advance, which is at the rate of from one to several inches daily,

they leave a raised pinkish line. The burrow is approximately ⅙ inch

in diameter. The disease is most common in Southern Russia but is

also found in Africa, Asia and South America. Looss considers that

hookworm larvae, when penetrating the skin, may produce similar

lesions.

[Illustration: FIG. 134.—Wing venation of Diptera. _A_, first

posterior cell; _B_, discal mid cross-vein; a, auxiliary vein;

_C_, marginal cell; _D_, submarginal cell. In the illustration of

the Chrysops wing, the letter “B,” indicating the discal cell, is

misplaced. It should be in the same relative position as in the

Tabanus wing.]

TUMBU FLY DISEASE

This African myiasis is due to the penetration of thighs or buttocks

by the larvae of _Cordylobia anthropophaga_. The appearance of the

tumefied area is quite similar to that of the tumor of _Dermatobia

cyaniventris_ and the treatment is similar.

CRAW-CRAW

This is a rather chronic papular skin disease which is reported from

the west coast of Africa. These papules may be as large as a small

pea and are quite hard. They are found chiefly on legs and arms. The

proximal lymphatic glands may be enlarged.

[Illustration: FIG. 135.—Markings of breathing slits on posterior

stigmata of various larvae. 1. _Musca domestica_, showing both

stigmata; 2. _Calliphora vomitoria_; 3. _Stomoxys calcitrans_; 4.

_Auchmeromyia luteola_; 5. _Cordylobia anthropophaga_; 6. _Sarcophaga

magnifica_.]

Undoubtedly many of the cases called craw-craw are scabies. In fact

the Africans give the name to a host of different skin affections.

O’Niel thought he had found a filarial larva in one of his cases

and Nielly incriminated a nematode larva of the Anguillulidae

family. The cause is unknown and the disease very intractable to

treatment.

SECTION VII

TROPICAL DISEASES OF DISPUTED NATURE OR MINOR IMPORTANCE

CHAPTER XXXV

VERRUGA PERUVIANA AND OROYA FEVER

It is thought that Oroya fever was the disease which proved so

fatal to Pizarro’s army in the 16th century. In 1870, great

interest was aroused in these diseases on account of their

prevalence in the workmen constructing the railroad from Lima to

Oroya, a town in the Andes. At this time there was much conflict

of opinion as to whether the two diseases were identical. In 1885,

Carrion, a medical student of Lima, inoculated himself with the

blood from a verruga lesion and died from Oroya fever about one

month later. As the result of this it seemed to be established

that infection with verruga material would produce the serious

first-stage fever and many call the fever Carrion’s disease.

Consequently these two diseases have, until recently, been

considered as two stages of the same disease, the usual idea being

that Oroya fever is the first stage, following which, provided

the patient does not die from this very fatal fever, there sets

in an eruption which is the second or verruga stage. In order to

reconcile the observations of the development of the eruptive stage

without a severe, febrile, preliminary one of three or four weeks,

it was considered that the first stage might be exceedingly mild.

Strong and his colleagues, however, inoculated a volunteer with

material from verruga lesions and sixteen days later the eruption

appeared without the preliminary fever and anaemia that are so

characteristic of Oroya fever, and it is now recognized that they are

two distinct entities.

OROYA FEVER

GENERAL CONSIDERATIONS

Oroya fever is an acute, infectious disease, often terminating

fatally, caused by the _Bartonella bacilliformis_, and characterized

by an insidious onset, irregular fever, pains in the bones and a

rapidly developing anaemia of the pernicious anaemia type.

The disease is chiefly found in towns situated in narrow,

wind-protected valleys of the west side of the Andes, at elevations

of from 3000 to 9000 feet. Townsend has suggested that a species of

_Phlebotomus_, _P. verrucarum_, which is very prevalent, may be the

transmitting agent. This investigator believes that verruga and Oroya

fever are the same disease. It may be stated that malaria and enteric

fevers, as well as verruga, are common in the localities where Oroya

fever prevails and much of the confusion in the literature of Oroya

fever is due to failure to differentiate the better known conditions.

Strong noted that Oroya fever was common from January to April,

particularly towards the close of the warm, rainy season. Cases were

rare in April and May and did not occur in the months of June, July

and August. He notes that verruga was not uncommon at the time when

Oroya fever was not occurring. Concomitant infection with Oroya fever

and verruga may occur but this is also true of malaria or malaria and

verruga may exist at the same time.

Barton isolated a paratyphoid bacillus from the blood of a patient,

besides which other bacteria have also been isolated. In 1909,

Barton noted certain rod-like organisms in the red cells of Oroya

fever patients which he considered protozoal in nature.

Strong and his colleagues found in the blood of Oroya fever cases

rod-shaped forms in the red cells, varying from 1 to 2 microns in

length, the red cells containing from 1 to 30 of these elements.

A study of sections of lymphatic glands of severe fatal cases showed

great numbers of these bodies packed in the endothelial cells. These

cells rupture and set free the organisms.

Intravenous inoculation of blood containing these elements

into monkeys and rabbits was negative in result. Strong failed

to cultivate the organism. These organisms were considered as

intermediate between bacteria and protozoa. They are closely

related to _Grahamella_ and the Harvard commission has proposed

the name _Bartonella bacilliformis_. In many ways they resemble

piroplasms, especially _Theileria_.

PATHOLOGY

At autopsy the skin shows the pale yellowish waxy hue of pernicious

anaemia. The lymphatic glands are somewhat enlarged and may be

oedematous. The heart is flabby and ecchymoses may be present in

the pericardium. The spleen is enlarged, shows numerous infarctions

and contains large amounts of pigment in the form of yellowish

masses or granules deposited between the splenic cells and in the

endothelial leucocytes. This pigment is like melanin in not giving

the iron reaction. The liver likewise is enlarged, shows areas of

toxic degeneration and contains moderate amounts of pigment. The

femoral marrow is soft and dark red. Microscopically, the endothelial

cells of the lymphatics distended with the causative organisms were

particularly noted by Strong.

SYMPTOMATOLOGY

The incubation period is about three weeks and the onset of the

disease is marked by malaise and apathy, to be followed by a

rapidly developing anaemia, of the pernicious anaemia type, with an

irregular fever of a remittent character fluctuating between 100°

and 102°F. and only exceptionally going up to 104°F., and pains in

head, joints and bones. The tenderness over the bones is undoubtedly

associated with the marked changes going on in the bone marrow and is

particularly marked over the sternum.

The patient rapidly develops a very severe anaemia and death

results in 20 to 40% of cases in two or three weeks. Delirium is

often noted.

The spleen and the lymphatic glands are somewhat enlarged.

Associated with the profound anaemia there may be oedema of legs

and about joints and functional cardiac murmurs. The kidneys do not

seem to be affected. There may be a diarrhoea in the later stages

of the disease. There is no eruption in uncomplicated cases.

The most important findings in the disease are those in connection

with the blood examination. The rod-shaped organisms, which are

thought to be the cause of the disease, are somewhat difficult to

observe in fresh blood preparations. They show definite motility

within the red cells, particularly after warming the blood slide. The

motion is a rather gliding one. In Romanowsky-stained preparations

the 1 to 2 micron-long rods within the red cells may occur singly or

in numbers of 4 or 5. V-shapes are frequently seen. The rod shows a

bluish staining with a deep purplish-red chromatin-stained granule at

one extremity. Rounded, oval or pear-shaped forms may also be seen.

While the parasites are present in great numbers in severe cases they

may be very scarce in mild forms of the disease.

Very striking is the rapidly developing anaemia which frequently

shows a red cell count of less than a million within a few days.

Normoblasts are quite numerous and fulminating cases show numerous

megaloblasts.

Polychromatophilia and poikilocytosis are noted.

In the red cells we have the picture of a rapidly developing

pernicious anaemia The color index is above 1.

The leucocytes number about 20,000 of which 60 to 70% are

neutrophiles. Immature neutrophiles, as the metamyelocyte, are very

common.

PROPHYLAXIS AND TREATMENT

The transmitting agent not being known we are in the dark as to

prevention. Evidence points to some arthropod biting at night as the

incidence of the disease decreased when those working in the Oroya

fever zone were compelled to leave the valleys before sundown. The

treatment is largely one of nursing although some have reported

favorably from the intravenous administration of salvarsan.

VERRUGA PERUVIANA

GENERAL CONSIDERATIONS

Verruga peruviana is an infectious eruptive disease, caused by an

unidentified virus, lasting two or three months, and characterized by

successive eruptions exhibiting two types of lesion,—the miliary and

the nodular,—both of which show a pronounced tendency to ulceration

and haemorrhage. The eruption of verruga somewhat resembles that of

yaws and it was at one time suggested that verruga was simply yaws

as influenced by high altitude. Strong and his colleagues found

that they could infect rabbits intratesticularly and that lesions

resembling those of man could be produced in dogs and monkeys

by cutaneous and subcutaneous inoculations. The virus has been

transmitted from monkey to monkey. The monkey is not as susceptible

to the virus as man and the rabbit and dog less so. Inoculation of

the monkey is not followed by a generalized eruption. The Wassermann

reaction was negative. In extracts from the granulomatous lesions

they found a very active haemolysin. It will be remembered that

animals are not susceptible to Oroya fever blood inoculations.

From the fact that it is possible to inoculate a person by rubbing

verruga material on a scarified surface it would seem that the

infection might be transmitted by insects.

As regards the pathology of verruga, Cole has noted involvement

of the lymphatic channels, which become obstructed by a cellular

exudate, around which lymphatics are found plasma cells and

fibroblasts. There is marked dilatation of the capillary blood

vessels. The structure of these granulomatous tumors is very

vascular, almost cavernous, hence the tendency to haemorrhage. The

haemolysin may also be operative in the liability to haemorrhage.

Strong and his colleagues found the early lesions to consist of

newly formed blood vessels lying in an oedematous connective

tissue. The endothelial cells lining them may be in more than

one layer. Around these blood vessels we have aggregations of

cells which are considered as angioblasts. These angioblasts show

frequent mitotic figures. There is a resemblance to a fibrosarcoma.

SYMPTOMATOLOGY AND TREATMENT

The period of incubation is about two weeks as shown by experimental

inoculation but may be as long from the standpoint of clinical

observation as forty days. At the onset we have rather severe pains

of joints, especially the knees, ankles and wrists, together with

a fever sometimes reaching 104°F. but usually not above 100°F.

Following the eruption, the temperature usually subsides to normal

in a few days. The eruption shows two types, the one with numerous,

small, wart-like lesions, not exceeding the size of a small pea (2

to 5 mm.)—the miliary type, and the other, with less numerous but

much larger nodular masses—the nodular type. The latter type is more

rarely seen than the former.

[Illustration: FIG. 136.—Verruga Peruviana. (From Ruge and zur

Verth.)]

_The Miliary Type._—The eruption is most abundant on the face

and extensor surfaces of the extremities and less common on the

trunk. In this type a pink macule appears which rapidly takes on a

bright red color and becomes nodular. These nodules may be flat or

somewhat pedunculated and bleed easily. At first smooth and shiny,

it later on shrivels up without leaving a scar. This form of the

eruption may involve the mucous membranes, as of conjunctivae,

nose, pharynx, etc. In children the disease is usually of a mild

type.

_The Nodular Type._—The _nodular eruption_ develops slowly and the

lesions may become as large as a pigeon’s egg. They tend to become

strangulated and then show as ulcerating, fungating masses which

are a source of danger from haemorrhage. The nodular eruption does

not invade mucous membranes and is usually confined to the regions

of joints, as flexures of elbows, knees, etc.

The eruptions tend to come out in crops and the duration of the

disease extends over two or three months.

_Treatment._—The ordinary principles of cleanliness apply to the

care of the lesions to prevent secondary infections. When the large

tumor-like masses begin to ulcerate or become gangrenous they

should be excised. It must be remembered that dangerous bleeding

may occur at unexpected times, for which reason the patients should

be provided with styptics or compresses to prevent serious loss of

blood.

CHAPTER XXXVI

DENGUE AND DENGUE-LIKE FEVERS

DEFINITION AND SYNONYMS

=Definition.=—Dengue is an epidemic disease due to an

ultramicroscopic, filterable virus which has been stated to be

transmitted by _Culex fatigans_. More recent work points to

_Stegomyia_.

It is characterized by an initial three or four-day febrile paroxysm

of very sudden onset, a remission, which comes on about the fourth

day and a terminal rise of temperature for two or three days—_the

saddle-back temperature course_.

Backache and pains about the muscular attachments at the joints and

especially a marked postorbital soreness are important features.

An eruption appears about the third or fourth day. Leucopenia and

polymorphonuclear reduction are constantly noted. Apathy and a mild

neurasthenic state may continue into convalescence.

=Synonyms.=—Dandy Fever (the word dengue is supposed to be derived

from the Spanish equivalent of dandy or denguero), Break-bone Fever,

Bouquet. German. Dengue-fieber.

HISTORY AND GEOGRAPHICAL DISTRIBUTION

=History.=—While Hirsch gives the credit for the first mention

of the disease to the chronicler Gaberti, who described a disease

with certain resemblances to dengue as existing in Cairo in 1779,

yet, for the reason that certain clinical features of this epidemic

would hardly appear to belong to dengue, as we now know it, there

would seem to be good ground upon which to give the credit of

priority to Benjamin Rush, who, under the designation break-bone

fever, gave us a true picture of dengue as it manifested itself in

Philadelphia in 1780.

Gaberti was particularly impressed with the knee involvement so

that from his description the disease was known as the disease of

the knees. He further noted swelling of the fingers and that the

pains continued for more than a month. The sudden onset and the

sweating would seem to belong to relapsing fever as well as to

dengue and in support of the view that the disease described by

Gaberti might have been relapsing fever we have the statement of

Sandwith that bone pain, chiefly of the knee, is the symptom most

complained of by the Egyptian native with relapsing fever.

Boylon, who reported an outbreak of an epidemic disease in Batavia

in 1780 stated that everybody was attacked and that the symptoms

were almost the same as those ushering in plague—headache,

lassitude and pains in the joints. He noted, however, that this

epidemic had no bad consequences, patients getting rid of it in

three days under moderate diet and copious beverages.

Ashburn and Craig, in 1907, proved that the disease could be

transmitted by injections of blood, unfiltered as well as filtered.

=Geographical Distribution.=—The disease may occur in epidemic

form in almost any part of the tropical or subtropical world. It is

very common in the countries about the China Sea and in the West

Indies.

ETIOLOGY AND EPIDEMIOLOGY

=Etiology.=—One can only state that the disease is caused by a

filterable virus which is present in the patient’s blood from the

second to the fifth day. Graham reported a piroplasm-like organism as

the cause but other workers have failed to confirm this. Reports as

to bacterial causative organisms have not been verified. Cleland and

his colleagues inoculated guinea pigs and rabbits without result and

were unable to find spirochaetes. Couvy has reported the presence of

short spirochaetes in the blood 2 or 3 hours before the onset of the

fever,—never later. They had two or three turns and fine extremities.

=Epidemiology.=—As regards the epidemiology of dengue there seems

to be a general acceptance of the idea that dengue is transmitted

by the common culicine mosquito of the tropics, _Culex fatigans_.

There is not, however, that definiteness which attaches to the

transmission of yellow fever by _Stegomyia calopus_ or to pappataci

fever by _Phlebotomus papatasii_, in both of which a certain period

of development of the unknown filterable virus in the arthropod host

is necessary before the insects become capable of transmitting the

infections.

It will be remembered that in the nine experiments as to dengue

transmission, conducted by Ashburn and Craig, the authors threw out

five of the cases for such reasons as previous immunity or refusal

of the experimental mosquitoes to bite. Of the four remaining

volunteers only one developed dengue. This man, however, had been

on duty at the Division Hospital in Manila and the statement is

made that he had not been exposed to the disease so far as could

be determined. This of course rather militates against the value

of this isolated experiment and furthermore the mosquitoes which

bit him had fed on the blood of a dengue patient only two nights

previously. If this is to be considered as a valid experiment, we

must believe that only a short sojourn of the virus in the mosquito

is requisite, which is rather at variance with the twelve days for

the yellow fever virus and eight days for that of pappataci fever.

In the recent Australian epidemic (1916) experiments failed to show

_C. fatigans_ capable of transmitting the disease. _Stegomyia_,

however, gave success in 4 out of 7 cases, the volunteers

developing dengue in from six to nine days after being bitten.

_Stegomyia_ mosquitoes are often termed the domesticated ones,

since they are observed to breed and pass their lives in the

immediate environment of man and further to be distinctly urban,

rather than rural, in their distribution. For their breeding places

they choose artificial collections of water, such as cisterns,

barrels, pails, bottles and cans, in or near dwellings.

These mosquitoes are small in size, silver-striped, vicious feeders

and very alert. The female alone bites, blood apparently being

necessary for ovulation. It feeds especially during the morning

and afternoon hours,—much less commonly at night unless there is

a light. The life history of _Stegomyia_ is discussed more fully

under yellow fever.

As regards the transmission of the disease by blood filtered through

a diatomaceous filter it will be remembered that Ashburn and Craig,

by proving this fact, placed the dengue virus in the same category

with the filterable viruses of the two diseases just considered.

Cleveland found the virus in the washed cells as well as in the

serum. The virus maintains its potency for several days outside the

body it being present in the blood at periods of from 18 to 90 hours.

Lavinder injected dengue blood from cases in the second to fifth

day into rhesus monkeys without noting any variation in their

temperature or blood findings.

Graham in Beirut carried out some experiments, one of which would

seem almost positively to demonstrate mosquito transmission. He

took mosquitoes which had fed on dengue patients, to a village in

the mountains where no case of dengue existed. He caused these

mosquitoes to feed on two natives of the village and both men

became sick with dengue four and five days respectively after

being bitten by the mosquitoes. Graham’s claims to have noted

piroplasma-like organisms in dengue blood have not been verified

and do not receive credence.

The most convincing evidence as to mosquito transmission of dengue

is that afforded by the absence of dengue in Port Said during the

years 1906 and 1907 notwithstanding the prevalence of the disease

in adjacent parts of Egypt. This was attributed to the absence of

mosquitoes, these having been destroyed in the fight to make Port

Said malaria-free. This campaign was commenced in May, 1906.

Other species of culicine mosquitoes, among which may be noted

_Stegomyia_, have been incriminated. In the Philippines I was

convinced that _Culex microannulatus_ might transmit the disease

as well as _C. fatigans_. In one of his experiments Graham claimed

to have produced dengue by injecting an emulsion of the salivary

glands of a mosquito which had fed on a dengue patient one or two

days previously.

PATHOLOGY

As death almost never occurs from the disease there is nothing to

note other than the marked leucopenia.

SYMPTOMATOLOGY

After a period of incubation of from four to fifteen days the disease

manifests itself with striking suddenness, in fact the patient can

generally recall almost the hour of the onset.

The temperature rapidly rises and in a few hours reaches a maximum

of from 102° to 105°F. Associated with this primary fever we have

frequently a blotchy congestion of the face—the so-called initial

rash.

We also have intense headaches, principally supraorbital and

postorbital. The pulse rate is slightly accelerated at first but

soon becomes slow and may fall to 50 from the fourth to fifth day.

There is no involvement of the joints, and the so-called joint pains

are really pains of the muscular insertions about the joints.

The backache of dengue is usually a well marked feature. Pain on

motion of the eyeballs is a prominent symptom—it is a deep soreness.

Insomnia, characterized by frequent dropping off to sleep to be

awakened immediately by disturbing dreams, is often noted.

The depression, mental and physical, is altogether out of

proportion to the lack of seriousness of the disease.

Malaise and anorexia are marked. Constipation is the rule at first.

About the third or fourth day the temperature drops to normal or

about that and remains so lowered for from twelve hours to three

days. At this time the patient feels much better and views his

affection in a less serious light. After this variable intermission

the temperature rises to possibly a greater height than primarily,

although as a rule it is less marked. This interval, or intermission,

separating two periods of fever gives us a chart designated

“saddle-back.” There may be only one rise of fever.

This second febrile attack is attended with pains and possibly

greater depression than the first accession. It is usually,

however, of shorter duration and during this period the terminal

rash appears. This is the most characteristic feature of the

disease. It generally manifests itself about the dorsal surface

of hands and feet advancing up forearms and legs. Later on it may

involve all extremities, face and trunk. The eruption is much like

that of measles but lacks the dusky red appearance of the measles

rash. It may however be punctiform and thus resemble the rash of

scarlet fever.

With the appearance of the terminal rash we may have crises such as

profuse sweating or marked diarrhoea or epistaxis.

The desquamation is furfuraceous in character and may be attended by

marked itching.

In some patients (European) there is a rosy carmine flush of palms

of hands and soles of feet. Some authorities have reported glandular

enlargements in dengue.

[Illustration: FIG. 137.—Temperature charts of dengue and

dengue-like fevers.]

Convalescence is apt to be protracted, being especially

characterized by malaise and nervous depression, practically

neurasthenia.

Leucopenia and polymorphonuclear percentage reduction appear by the

second day.

_Clinical Types._—In different epidemics it is noted that some one

clinical feature may seem outstanding. Of these we may note:—

(1) The pulse rate is slow for the temperature rise, thus reproducing

a phenomenon common in yellow fever (Faget’s law). It is in recent

epidemics particularly that clinical descriptions have recorded the

frequency of a very slow pulse, most of the older authorities having

noted a pulse rate which corresponded to the elevation of temperature.

(2) In some epidemics the feature of glandular swelling is prominent,

while in others the swelling is so slight as to be overlooked.

(3) The characteristic “saddle-back” temperature chart seems lacking

in the general run of cases in certain outbreaks. It is possible that

such epidemics, showing atypical temperature curves, may have been

due to phlebotomus fever, or seven-day fever, instead of dengue.

(4) In some epidemics, the rash is insignificant or very slight in

most cases. This observation is possibly dependent on the ephemeral

character of the eruption in certain groups of cases.

(5) From the chart Fig. 138, analyzing the symptoms in one epidemic,

it will be noted that Lane observed cold, clammy, dusky extremities

in 17 per cent of his cases. This is an unusual finding.

Symptoms in Detail

_Onset and the Temperature Chart._—Dengue probably sets in more

abruptly than any other disease. The temperature chart is typically

saddle-back.

_The Pains._—Very marked soreness deeply seated about the place of

origin of the ocular muscles so that every movement of the eyeballs

is at once complained of as giving pain.

General pains all over the body, more especially of the back and

about tendinous insertions of the muscles which cause the pains to

be referred to the joints. The knee-joint pains are probably the

most frequent. The rachialgia may be as great as that in variola or

yellow fever.

_The Eruption._—The characteristic eruption does not appear until

about the time of the intermission or with the accession of the

terminal fever.

The fall of fever about the third or fourth day is often attended

by a critical epistaxis, sweat or diarrhoea, to be succeeded by an

intermission of from one to three days of a feeling of well-being.

About this time or with the secondary rise of fever the true dengue

rash appears. It is at first noted about the bases of the thumbs

and extending over the dorsal surfaces of the wrists. Almost

simultaneously a measles-like rash appears over the dorsal and

internal surfaces of the big toe extending to the ankle, especially

over the internal malleolus. Later on the elbows and knees may be

involved or the rash may cover thickly the entire body. A carmine

flush of the palms of the hands and soles of the feet is not

uncommon. A furfuraceous desquamation with much itching at times

follows the eruption. The so-called primary eruption is nothing

more than an initial flushing of the face, it is ephemeral. The

true dengue rash may also be quite ephemeral but usually it lasts

for two or three days, or possibly four or five days.

_The Nervous System._—Besides the headaches we have insomnia and

depression which extends through convalescence. Apathy is marked.

_The Blood._—This shows a leucopenia of about 4000 from shortly

after the onset together with a reduction of the percentage of

polymorphonuclears to about 45%. During the attack the eosinophiles

are decreased but there is an increase during convalescence.

DIAGNOSIS

The two diseases with which dengue can be most easily confused are

influenza and yellow fever. In fact when the great pandemic of

influenza (1890) first made its appearance in France, many regarded

it as an atypical form of dengue.

[Illustration: CLINICAL CHART ONE HUNDRED CASES OF DENGUE FEVER

FIG. 138.—Dengue. Analysis of Symptoms, from 100 cases occurring in

epidemic at St. Thomas, V. I. (After Lane, from U. S. Naval Medical

Bulletin.)]

The respiratory involvement of influenza and the eruption and

comparatively slow pulse of dengue are the principal points of

difference. It must be remembered that affections in the tropics,

diagnosed as influenza, have shown but slight respiratory symptoms,

the cases being more of a nervous or intestinal type. The eruption

of dengue may fail to appear or be missed in the study of the case.

The blood findings should aid in differentiation from influenza as

is also true of yellow fever, a disease which likewise has blood

findings of practically a normal character. Other than the blood

picture we have in yellow fever (1) albuminuria, coming on about

the second day, and (2) jaundice appearing about the third day.

In dengue the eruption appears from the third to the fifth day.

Albuminuria is absent in dengue.

Dengue may be mistaken for measles, but the early coryza, Koplik

spots and marked rash, first appearing about the face, should

differentiate.

In scarlet fever the rapid pulse, angina and leucocytosis should be

sufficiently differentiating.

Confusion with articular rheumatism may arise when the pain

about wrists, knees and ankles has been mistaken for true joint

involvement.

The headache and backache of smallpox may be confusing until the

eruption about the forehead appears. The leucopenia of dengue is

the main differential point in these first three days of doubt.

PROPHYLAXIS AND TREATMENT

=Prophylaxis.=—This would seem to rest entirely upon the question of

destruction of mosquitoes and prevention of the mosquito from biting

a patient. In dengue the virus is apparently in the blood for four or

five days so that screening of patients is necessitated for a longer

period than for yellow fever or phlebotomus fever.

=Treatment.=—The malaise and depression are generally so great that

the patient keeps his bed voluntarily. A light diet is indicated

although the anorexia is so marked that it is difficult to persuade a

patient to take food.

Cold spongings, provided the patient is not disturbed by being

moved, are of value for the insomnia. Phenacetine may be given for

the relief of the headache and backache. It is rarely necessary to

give morphine.

During convalescence tonics are indicated and if there is any

condition where a good wine is of value, it is in this, to

counteract the terrible depression. It has been suggested that

adrenal insufficiency may account for the asthenic, protracted

convalescence and from this standpoint adrenalin has been

recommended.

DENGUE-LIKE FEVERS

PHLEBOTOMUS OR PAPPATACI FEVER

=Etiology and Epidemiology.=—This fever, which is often called

three-day fever, on account of its running its course in this period,

is caused by a filterable virus. This virus only seems to be in the

blood of the patient’s peripheral circulation during the first

twenty-four hours of the illness, blood abstracted toward the end of

the second day and injected into a well person failing to reproduce

the disease.

If the blood is filtered through a Pasteur candle F, the filtrate

will set up an attack just as well as the unfiltered blood, in this

respect being like dengue and yellow fever. Couvy reports having

found spirochaetes in the blood 3 hours and 24 hours after the

onset.

The transmitting agent is a moth midge, _Phlebotomus papatassii_.

This midge, as is true of the psychodid family, to which it belongs,

is very hairy. It has long slender legs and narrow wings. The

proboscis is as long as the head and the lancets project beyond the

labium.

The female alone bites, which act takes place chiefly at night;

cool, moist, shady places, away from sleeping rooms, being

preferred in the day time. The insect is a persistent, vicious

feeder, difficult to escape from, as mosquito nets offer no

protection. It takes from six to eight days after feeding on a

patient in the first day of the fever before the midge is capable

of transmitting the disease, this being in accordance with the

twelve-day developmental period in the mosquito, that holds

for yellow fever. Doerr thinks that the pappataci virus may be

transmitted hereditarily by the insect to the egg.

At present, of the genera of the three families of midges, only

_Phlebotomus_ is known to transmit disease. _P. papatasii_

transmits phlebotomus fever in the Balkans. _P. minutus_ is the

host at Aden. Another species, _P. perniciosus_, can transmit the

disease. These moth midges are 2 mm. in length and have the body

densely covered with long yellow hairs. The second longitudinal

vein has three distinct branches. The antennae have 16 restricted

joints and the proboscis is as long as the head. The species of

_Phlebotomus_ are separated by slight variations in wing venation,

palpal lengths, etc., thus the second segment of palpi of _P.

papatasii_ is a little longer than the third one, while with _P.

perniciosus_ these segments are of equal lengths. In _P. minutus_

the second segment is only half the length of the third. The insect

lays about 40 eggs in damp dark places. The period of metamorphosis

from egg to insect is about one or two months, according to

temperature.

_Phlebotomus_ larvae die out in dry soil and very wet earth is

unfavorable. Moderate moisture and protection from light seem

necessary for their development. The remains of dead insects also

seem to make good breeding places. It is in cracks of old damp brick

or stone walls that the female most often deposits her eggs. Caves

are also selected.

Blood seems necessary for the fertilization of the eggs but lizard

blood seems more common in the stomach of _P. minutus_ than human

blood. They have also been observed to feed on other reptilian

bloods. The female insect has been kept alive in captivity up to

forty-six days.

Cases first appear in the late Spring and the disease becomes

epidemic during the Summer.

An attack produces quite an immunity.

The disease has chiefly been studied in the Balkan States but

undoubtedly it is widespread.

The disease is almost never fatal so that we know nothing of its

pathology.

=Symptomatology.=—The symptoms will answer perfectly for cases

of dengue one sees in a dengue epidemic in which, instead of the

saddle-back course of fever, we have a three-day primary rise and

then a fall to normal without any secondary fever rise. Cases of

phlebotomus fever are occasionally reported where the fever continues

seven or eight days.

The symptoms as usually given are as follows: After a period of

incubation of from three to six days there is an abrupt onset with

congested face and injected conjunctivae. There is pain in head,

eyes and back. There is marked malaise with great depression of

spirits. There is anorexia with coated tongue and rarely vomiting

and diarrhoea. There may be some congestion of the pharynx and

even a slight bronchitis. So much in common with influenza has it

clinically that a synonym is summer influenza. The liver and spleen

are normal. Mental depression is frequently noted. Epistaxis is

rather common.

There is a leucopenia and polymorphonuclear percentage decrease. The

two points which are chiefly advanced in its clinical differentiation

from dengue are (1) slow pulse, a bradycardia, and (2) only three

days of fever and absence of eruption.

SEVEN-DAY FEVER

Rogers first described a dengue-like fever which occurred in India

during the summer months as seven-day fever. The fever course was at

times typically saddle-back and again would be of continuous type.

A pulse relatively slow for the temperature is generally recorded,

together with sudden onset and general malaise. The spleen is at

times enlarged and there is a definite leucopenia and polynuclear

percentage reduction. The eruption is only occasionally present

(about 10%) and is an erythema which makes its appearance on the

extensor surfaces of the forearm about the fourth day after the onset.

=Etiology.=—In cases similar clinically to the seven-day fever of

Rogers, Ido, Ito and Wani have found a spirochaete resembling that

of infectious jaundice and designated _Leptospira hebdomadalis_.

It can be differentiated from _L. icterohaemorrhagiae_ by immunity

reactions. It is found in the blood during the fever period and young

guinea pigs can be infected by such blood either subcutaneously

or by mouth. The organism can be cultured by Noguchi’s method. The

spirochaete is to be found in the urine towards the end of the

disease and the urine is probably the source of infection. In Japan

field mice seem to be the carriers of this spirochaete. In about 3%

of such rodents the spirochaete can be found in the urine and the

disease is limited to the sections in which the field mice are found.

There is practically no mortality and the treatment is symptomatic.

SAND-FLY FEVER, AND THREE-DAY FEVER

These dengue-like fevers of India are practically identical

clinically with phlebotomus fever. The usual idea is that dengue

epidemics are far more explosive in character than is true of

epidemics transmitted by the sand-fly.

The strongest point in differentiation of sand-fly fever and dengue

is that neither confers any immunity for the other disease.

The distinctions of enlarged glands and break-bone pains are often

advanced as characteristic of dengue and not of sand-fly fever. I

have never observed other than slight glandular enlargement in dengue

cases.

SIX-DAY FEVER

Deeks has described a disease from Panama with a dengue-like clinical

course.

There were but slight changes from normal in the pulse rate or blood

findings. Some of the cases showed a late scarlatiniform eruption.

It was considered that the continuous fever for six days and

the enlargement of the spleen, which accompanied the disease,

differentiated it from dengue.

CHAPTER XXXVII

TSUTSUGAMUSHI

DEFINITION AND SYNONYMS

=Definition.=—This is an acute febrile disease caused by the bite of

the larval Kedani mite of the region where the infection prevails.

The onset is characterized by headache and giddiness, a rather

rapidly rising temperature and swelling of the lymphatic glands

draining the region in which is situated a small necrotic ulcer

marking the site of the bite. With injected conjunctivae, continuous

fever and hyperaesthesia, the disease goes on for about a week when

a macular eruption appears about face, then chest, extremities and

trunk. About ten days after the appearance of the eruption there is a

fall of fever by lysis.

[Illustration: FIG. 139.—The Kedani mite. _Trombidium akamushi._

(From Ruge and zur Verth.)]

=Synonyms.=—Flood fever, Japanese River fever, Kedani mite disease.

Shimamushi.

HISTORY AND GEOGRAPHICAL DISTRIBUTION

=History.=—There are records which would indicate that the disease

has been known for more than 1000 years.

=Geographical Distribution.=—It is only in the western part of the

island of Nippon, when the banks of the Shinanogawa are inundated

each spring, that we find the disease. The disease is supposed

to be confined to Japan although Ashburn and Craig have thought a

disease observed by them in the Philippines as possibly identical.

ETIOLOGY AND EPIDEMIOLOGY

The cause is unknown, but has been attributed by some to various

bacteria and by others to a protozoon.

Nagayo attaches importance to piroplasm-like forms found in the

spleen and lymphatic glands.

Kawamuro and his colleagues could not demonstrate any organism by

any method of examination. The virus is in the blood and even as

small an amount as 0.001 cc. may infect a monkey although 0.1 cc.

is usually required. The virus is present also in the enlarged

lymph glands. Heating the blood at 50°C. for 10 minutes destroys

the virus. Recently Hayashi has reported as cause minute rod,

ring-shaped or spheroid bodies which when stained with Giemsa’s

stain are brought out in the lymphocytes and endothelial phagocytes

of lymph nodes and spleen. They also occur in the blood plasma

and in severe cases in red blood cells. He has transmitted the

disease to monkeys, guinea pigs and rabbits. These bodies resemble

bacteria, in this respect resembling the organisms of typhus and

spotted fever of the Rocky Mountains. Hayashi regards the organism

as resembling _Theileria parva_ and _Bartonella bacilliformis_,

and believes he has shown the field mouse to be a reservoir of the

virus.

The disease is not communicable from person to person and

only follows the bite of a larval mite, _Trombidium akamushi

(Leptotrombidium akamushi)_. This is a minute orange-red arachnoid

which can scarcely be seen with the naked eye. This mite is only a

source of danger in the region of the inundated river banks, its

bite not producing the disease elsewhere.

Persons harvesting hemp during August are liable to contract the

disease if bitten by the larval mite.

The mite is found in large numbers on the ears of field mice, these

hosts, however, not appearing to be suffering from any particular

disease.

PATHOLOGY

Other than the local ulcer and the swollen regional glands, there is

little that is definite. The spleen shows enlargement and there is

also swelling of the mesenteric glands. The lower part of the ileum

may show injection.

SYMPTOMATOLOGY

=A Typical Case.=—About one week after receiving the bite of

the larval mite, which may not have been noticed by the patient,

there develop chilliness, giddiness and headache, with a rising

temperature. In two or three days from the onset, painful glands are

noticed in certain regions as of groin, axilla or neck. From these

glands we can often by following inflamed lymphatics find the small

necrotic ulcer which is often located in the armpit or in the region

of the genitals. There is a dark red areola about the ulcer which is

only slightly tender. The glands are not very much enlarged and are

not excessively tender. There may be general glandular enlargement

following that of the primary swellings. The pulse rate is only from

80-100, notwithstanding the rise of the fever to 104°F. or even 105°F.

The body is decidedly hyperaesthetic and the conjunctivae are

injected. There is frequently deafness. About the seventh day a

macular eruption appears first on the face and then spreads to

chest, extremities and trunk. The eruption never becomes petechial.

The tongue becomes dry and cracked. There is often a cough. The

blood shows a leucopenia. The eruption disappears in from seven to

ten days and the fever becomes remittent or intermittent and, after

a few days, reaches normal. Parotitis may occur as a complication.

Schüffner has described a similar disease from Sumatra. The mortality

is, however, only 3% as against the 30% in Japan. He thinks it is

transmitted by a tick. In his cases the necrotic ulcer and glandular

enlargements were followed by a roseola which reached its maximum

on the eighth to tenth day and was most marked on the trunk and

flanks. The nervous symptoms resembled typhoid fever and there was a

lymphocytosis.

Symptoms in Detail

_The Nervous System._—There is marked giddiness and headache at

the onset. Hyperaesthesia of the body is quite characteristic.

There is often delirium at night. Deafness is frequently noted.

_The Cutaneous System._—A small necrotic ulcer about ⅙ inch in

diameter, with a dusky red areola, is noted at the site of the bite

of the larval mite. The healing of the ulcer is delayed well on

into convalescence.

About one week after the onset a dusky macular eruption appears

first on the face (cheeks), then going to the chest, legs, forearms

and trunk. It is not marked on neck, arms or thighs. It never

becomes petechial.

_Fever Course._—The temperature, which on the first day or

two reaches only 101° to 103°F., becomes later on higher and

continuous. About the tenth day from the appearance of the eruption

it begins to fall, becoming remittent and then intermittent.

_The Lymphatic System._—Very characteristic is the swelling of the

glands proximal to the initial ulcer. The connecting lymphatics may

be inflamed. Later on other glands may show slight swelling and

tenderness.

The spleen is usually enlarged.

_The Blood._—There is no change in the red cells but there is a

leucopenia.

DIAGNOSIS

In the differential diagnosis the limited geographical distribution

should prevent error and, in particular, where one has the initial

necrotic ulcer, with enlargement of the glands draining the region

in which it is located, there should be little confusion. Of course

plague may have a primary vesicle or ulcer with enlargement of

neighboring glands; these glands however are matted together and are

exquisitely tender.

Then too the eruption of tsutsugamushi and the early and more

stuporous state of plague should differentiate, even without the

aid of the laboratory.

It is usual to consider tsutsugamushi, typhus fever and spotted

fever of the Rocky Mountains as having many characteristics in

common. These diseases may best be differentiated by the fever

course and eruption as shown in the following table:

------------------+-------------------------+---------------------------

| Fever course | Eruption

------------------+-------------------------+---------------------------

_Tsutsugamushi_ |Fever increases each day |Begins on face, then chest,

| until reaching maximum | legs, forearms and trunk.

| about 4th or 5th day. | Does not become petechial.

| Fall by lysis after | First appears about 7th

| fading of eruption. | day.

------------------+-------------------------+---------------------------

_Tabardillo._ |Onset and termination |Begins on abdomen, sides of

_Typhus fever._ | of fever characterized | chest, thence going to

_Brill’s | by considerable | extremities. Petechial

disease._ | abruptness. | tendency. First appears

| | about 5th day.

------------------+-------------------------+---------------------------

_Spotted fever |Gradual rise during a |Begins on forearms and leg.

of the Rocky | week with lysis. | Petechial tendency. May

Mountains._ | | have gangrene of prepuce

| | and scrotum. First appears

| | on 2d to 5th day.

------------------+-------------------------+---------------------------

TREATMENT

There is no specific treatment. It may be necessary to use drugs to

combat the insomnia.

The serum of monkeys which have recovered from the disease seems to

have some value.

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.

[Illustration: FIG. 140.—Generalized eruption of spotted fever of

the Rocky Mountains. (Kindness of Doctor Frick.)]

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.

[Illustration: FIG. 141.—Female D. andersoni. 2. Head showing (a)

hypostome, (b) chelicerae, (c) palps. 3. Male.]

=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.

CHAPTER XXXIX

TYPHUS FEVER

DEFINITION AND SYNONYMS

=Definition.=—Typhus fever is an acute infectious disease, possibly

caused by _Rickettsia prowazeki_. There is a fairly abrupt onset,

with a continued fever lasting about two weeks, followed by a

critical fall or rather rapid lysis of temperature. About the fifth

day a rose spot eruption, similar to that of typhoid, first appears

about the loins and abdomen later on extending over the trunk and

extremities. The rash tends to become petechial and stands out rather

prominently on a general cutaneous mottling. The stuporous state is a

marked feature of the disease. It is transmitted by lice.

=Synonyms.=—Jail fever; Ship fever; Putrid fever; Petechial fever;

Typhus exanthematicus. Ger. Fleckfieber; Fr. Typhus exanthématique;

Sp. El tabardillo; Ital. Typho-esantematico.

HISTORY AND GEOGRAPHICAL DISTRIBUTION

=History.=—Hirsch notes that the history of typhus fever belongs

to the dark pages of the world’s story, at times when war, famine,

and misery of every kind are present. It is reasonable to suppose,

according to this author, that many of the pestilences of ancient

times and the Middle Ages were typhus fever. This disease was

prevalent among the Spanish soldiers at the time of the conquest of

Grenada and the designation of the disease then used (Tabardillo)

is the one now given typhus fever in Mexico.

The disease was first described with sufficient accuracy by

Frascatorius, in the 16th century, to enable us distinctly to

differentiate it from plague; the stuporous states of the two

diseases having previously caused them to be confounded. In

England, in the 16th century, the disease was very prevalent in

the jails and court officials attending the trials of prisoners

often contracted the disease and died; hence the designation “black

assizes.”

During the Thirty Years War, in the 17th century, typhus fever

spread over central Europe.

Typhus fever was very prevalent at the time of the epidemic of

plague known as the great plague of London and it is a matter of

practical interest that the two diseases were not infrequently

confounded by medical men. There were some very severe epidemics of

the disease in Ireland in the 19th century.

Typhoid fever and typhus fever were only separated as distinct

diseases by Gerhard, 1837. Huxham, however, had previously noted

the marked difference between putrid malignant fever and slow

nervous fever.

Until very recent times it was declared that typhus fever was among

the most contagious diseases of man and innumerable instances were

cited of frequent contagion of those attending or visiting typhus

patients. In 1909, Nicolle, in North Africa, demonstrated that the

disease was transmitted by lice and the recent experiences in the

Balkan war and in the Servian epidemic of 1915 show that in the

absence of such vermin the disease does not appear to be contagious.

=Geographical Distribution.=—The disease has largely been

eradicated from European and other countries where hygienic

measures leading to the destruction of vermin have existed.

During the recent war the disease became one of importance, owing

to the difficulty of preventing the spread of body lice to the

soldiers.

In the tropics the disease, when present, is usually found in

regions of high altitude. In Mexico tabardillo, as typhus is there

designated, is a disease of the elevated regions. This is also true

of India.

Sporadic cases of typhus, known as Brill’s disease, have appeared

from time to time in New York.

During the great war typhus first appeared in Servia, thence

extending to Austria, Germany and Russia. Its nonappearance on the

Western battle line must be attributed to the active measures of

the Germans in attacking the lice problem. It is now widespread in

Russia and Poland.

ETIOLOGY AND EPIDEMIOLOGY

=Etiology.=—Recent work by Anderson and Ricketts has shown that the

blood of human cases is infective for monkeys. The virus does not

seem to pass through a Berkefeld filter and the epidemiology points

to the body louse as the sole transmitting agent. Nicolle reported

the filterability of the virus. More recently he has considered this

filterability as doubtful.

The guinea pig is susceptible to the virus as well as the monkey

but only shows temperature rise. Nicolle has shown that lice do not

become infective until about the tenth day after feeding on typhus

blood. The virus is found in the blood of man and in the spleen and

blood of monkeys and guinea pigs.

Plotz has isolated a Gram-positive pleomorphic bacillus from

the blood of typhus patients which has been named _B. typhi

exanthematici_. This organism is of historical interest only and

apparently has nothing to do with the causation of typhus fever.

Hort states that only blood recently taken from typhus patients

will cause the disease in monkeys while the same blood which

has been incubated several hours or days fails to produce the

disease. Others, as well as Hort, doubt the etiological relation

of the organism of Plotz to typhus fever or to the mild form of

the disease as seen in New York City and there known as Brill’s

disease. Tabardillo or Mexican typhus is the same as typhus.

Rocha-Lima insists upon the etiological importance of short oval

bodies, often showing polar staining with Giemsa preparations, and

found in the epithelial cells of the alimentary tract of lice which

have fed on the blood of typhus patients.

Ricketts noted similar bodies in such lice. They differ from the

Plotz organism in that they are Gram-negative and apparently cannot

be cultivated. Lice feeding on blood other than that of typhus

patients fail to show these bodies and furthermore the blood of

typhus cases during the period of convalescence fails to infect

lice. When guinea pigs are inoculated with emulsions of lice

containing such bodies they show the temperature reaction of typhus

fever. Plotz states that his organism may be Gram-negative at first

and believes these organisms to be the same. Wolbach and Todd

take the view that the bodies described by Rocha-Lima and called

_Rickettsia prowazeki_ are the cause of typhus fever. Similar

bodies have been found in trench fever and even in certain normal

lice. These bodies, however, are extracellular and are more oval

and stain more intensely than the typhus bodies. These Rocha-Lima

bodies require a Romanowsky stain to bring them out. In man these

bodies are found in the endothelial cells of the small blood

vessels, occurring singly or in clumps. In the louse the epithelial

cells of the intestine may be found distended with masses of these

organisms.

It is not certain whether the virus is transmitted by the bite of

the louse or by inoculation of faeces. Monkeys and guinea pigs can

be infected by injection of emulsions made from infected lice.

Loewe and others have succeeded in cultivating the virus of typhus,

using deep tubes containing 10 cc. of a rich ascitic fluid and a

piece of sterile rabbit kidney. The medium was inoculated with 2

cc. of typhus blood, after which 0.3 cc. of a 20% dextrose solution

was added and the culture sealed with liquid petrolatum. Its

reaction was pH 7 to 7.4. Cultures were incubated at both room and

body temperature.

As proving the culturing of the virus, it was noted that 1 cc. of

a fourth-generation culture would infect a guinea pig. This would

represent 0.00000016 cc. of the original typhus blood. The bodies

cultivated differ in morphology from the bacillus of Plotz in

that they are even more minute, of slight hazy outline and do not

assume polymorphous involution forms. They vary also in cultural

characteristics. Concerning the question as to the identity of the

bodies with _Rickettsia prowazeki_, no definite decision is as yet

permissible, nor were the authors able to decide whether the bodies

are of bacterial or of protozoan nature.

=Epidemiology.=—Until recently authorities stated that typhus fever

was the most contagious of all diseases. We now know that in the

absence of body or possibly head lice the disease is only slightly,

if at all contagious.

At the same time recent experience has shown that it requires

the greatest care on the part of those having charge of louse

destruction to avoid being infected while attending to this duty.

The same is true of those examining patients with the disease prior

to the eradication of the body lice of the sick.

A knowledge of the life history of the body louse is necessary. The

body louse, _Pediculus vestimenti_, is slightly larger than the head

louse, _P. capitis_, and is the species concerned in the transmission

of Indian and North African relapsing fevers as well as typhus fever,

although it is probable that the head louse can also transmit these

infections.

While the head lice live among the hairs of the head and show

their presence chiefly by the appearance of their pear-shaped

eggs (nits) projecting from the hair shaft, the body lice attach

themselves to the under surface of the garments worn next the skin,

and holding fast to the undershirt, feed about twice daily on the

human host. They are but rarely found on the skin. The female body

louse is about ⅐ inch long and about 1/15 inch broad (3.5 mm. ×

1.5 mm.). The antennae are somewhat longer than those of the head

louse. Warburton found that the egg stage, in experiments, lasted

from eight to forty days, the larval stage about eleven days, and

that the male louse lived three weeks and the female four weeks.

Of course, under natural conditions these periods may not hold.

Development of the eggs takes place best at a temperature of 30°C.

Lice feed at once after being hatched and a young louse will die

unless it feeds within 24 hours.

Lice will leave their host only when he has fever or when he dies

but they may drop off a host or be brushed off. They are not apt to

be found in bedding.

PATHOLOGY

Fraenkel, in 1914, first called attention to proliferative changes

in the endothelium of the arterioles and arterial capillaries,

followed by necrotic changes. These changes are chiefly manifest in

the vessels of the skin, central nervous system and myocardium. In

addition to the proliferation of the endothelial cells we have a

perivascular infiltration of small round cells. Kurt Nicol notes that

there is a combination of proliferative and inflammatory changes.

These are microscopical and there is absence of characteristic

macroscopic findings.