SECTION XVIII

THE ANIMAL PARASITES, THEIR INCIDENCE AND SIGNIFICANCE

FRED D. WEIDMAN, M. D.

It is quite to be expected that animal parasites would be found in the

animals of zoological gardens, garnered as these beasts are from all

parts of the world, tropical and otherwise. It inevitably follows that

many of the forms should be strange and new, enticing one to the

fascinating determination of their identity, life history and hygienic

importance; and, developing from all this, one can easily imagine how

limitless the opportunities are for scientific work in parasitology in a

laboratory like ours.

As in other biological fields, the taxonomic range of parasites here is

wide. It extends from the lowly protozoa to the insecta, and, dropping

to the smaller subdivisions, includes not only most of the genera

familiar to human parasitology but many known only among the lower

animals. From the standpoint of the host, the biologic state of

parasitism extends from the lowest protozoa to homo.

The above will suffice to indicate the wide range of parasitism in

animals, but the extent of work actually done thus far in wild animal

material is a different story. Collated, consistent studies, so far as I

am aware, have been undertaken only at the London Garden, here at

Philadelphia, and at Washington, D. C., by Dr. Charles W. Stiles and

Albert Hassal. The data, collected by the last mentioned workers are

incidental to the Index Catalogue of Veterinary and Medical Zoology, and

embrace only the (index) phase indicated by the title, but it is so

valuable, and withal so altruistic, that it must be credited. What other

work there is is scattered where—not in literature—general biological,

medical and veterinary. That at London has been conspicuous through the

observations of Plimmer and of Beddard on filariæ and cestodes

respectively, while the work of Nicoll must not fail of mention.

That the reader may the better appraise the sections of our own work

which are to follow I wish at once to indicate their material basis.

Ordinarily only the larger parasites are looked for at the autopsy table

and there must be special indications to demand search for the finer

ones. Those of microscopic size, or so minute as to be overlooked in the

guise of seeds, vegetable fibres, etc., have not, both here and

elsewhere, been routinely studied as have macroscopic ones.[107] From

our autopsies there have accumulated records of nearly 900 parasites—

some determined generically, others but as to order. The parasites have

in greatest part been preserved and are available for further study; in

the past, special groups have been culled out from time to time and

examined. Where conditions have been pressing, as in certain epizoötics,

investigations have amounted to more than observations and descriptions,

and received detailed laboratory examinations with more or less animal

experimentation as the occasion demanded.

The foregoing may suffice to apprise the reader that the subject of wild

animal parasites has been but broached so that data are especially

incomplete on life histories—a phase most important in relation to

hygiene; but in spite of this and although the statistics are only

approximate, as is the case in most parasitological work, these data

have attained to sufficient proportions to justify at least a beginning

in the matter of collating and generalization. At any rate the time has

arrived to establish at least a nucleus for the accretion of data, which

can be later subjected to confirmation or correction. We draw just a

grain of comfort from the knowledge that the more fully worked field of

human parasitology is also vulnerable to criticism of very much the same

order.

THE VALUE OF PARASITOLOGICAL STUDIES IN ZOOLOGICAL GARDENS.

The foregoing chapters have made clear two fields of practical

usefulness of any study in such gardens. These—hygiene in relation to

the animals and comparison in relation to human beings—need therefore

only to be mentioned at present since it is obvious that both benefit by

our parasitological work. But there is yet a third—a scientific phase of

parasitology which may be considered purely academic. It consists in

morphological and other studies necessary for the identification of the

parasite, the determination of its life history, etc. These last studies

may still in a restricted sense include a modicum of the practical in so

far as they have a bearing on the disease with which they are

associated. But on the whole they are a source of danger for us since

such things as studies on the finer structures of worms, taxonomic

arrangements, descriptions of new species of commensals, etc., being

alluring, are likely to lead one so far afield that eventually an

attitude of stubborn resistance will have to be assumed in order to

conserve that precious, volatile laboratory asset—time—for the more

crying, practical problems ever reaching out to us.

However, in parasitological investigations as in other scientific work,

immediate abstract information may at some time prove to be of greatest

practical value. Thus for example if we can discover the exact facts

concerning one phase of the life history of a certain parasite, it may

be possible by hygienic measures, to break the cycle of development of

the parasite at one point thereby preventing its completion. This

information is perhaps obtained most readily in experimentation upon the

rôle of lower animal forms in the pathogenesis of disease but where

reliable evidence is lacking, help may be had by comparison with others

in the same taxonomic group. Undoubtedly systematic classification will

go far to help solve many of these riddles.

PATHOGENICITY OF ANIMAL PARASITES IN GENERAL.

The first question which arises in this connection concerns the actual

ability of animal parasites to produce disease in wild animals. At once

it will be seen that this must be a relative matter, for no one on one

side would contend that every symbiont in an animal is harmful—parasites

_sensu stricto_—nor on the other that none could possibly be, _i.e._,

that all are always commensals. It is evident that the issue boils down

to questions as to the extent to which they are harmful. Before

attempting the answer let us consider the means by which the parasites

may conceivably produce disease.

MODES OF DISEASE PRODUCTION (PATHOGENESIS).

The medical reader is familiar enough with the pathogenic powers of some

animal parasites, but may be sufficiently interested to glance over

specific wild animal instances illustrating them while they are being

listed for those less familiar with this subject.

1. MECHANICAL OBSTRUCTION.

I refer here particularly to simple blockage of normal body passages as

the result of bulk or mass. This occurs more commonly in the intestines

than elsewhere on account of the greater frequency, greater numbers and

larger size, in general, of parasites inhabiting this tract. Thus, we

have recorded a liothrix (_Liothrix luteus_)[108] where the combination

of a small host and consequently narrow gut and comparatively large

parasite induced obstruction. Plimmer[109] records microfilaria clogging

the brain capillaries. Shipley[110] mentions two specimens of _Ascaris

lumbricoides_ obstructing the nares of a chimpanzee (_Pan niger_).

Blockage may also be produced secondarily to the presence of the

parasite, even in the absence of notable numbers of them, and quite

apart from the element of verminous bulk. This occurs through

inflammatory swellings which the worms excite. We saw many serious

grades of this in our spiroptera epizoötic, the lumen of the

proventricle being narrowed by swelling of the mucosa and more or less

occluded by exudate and necrotic mucous membrane.

Yet another direction wherein a mechanical rationale pure and simple

obtains is by the production of diverticula. Worms encysted in the gut

wall may, by weight alone or by excitation of peristalsis, cause the

wall to bulge outwards (or inwards even) like a pocket. Such a

diverticulum has been noted in the gut of a Pale Cebus (_Cebus

flavescens_)[111] parasitized by acanthocephalus, but in this case there

were adhesions to the nearby stomach, and it is possible that in this

individual case the diverticulum was a traction one, _i.e._, pulled out

by the anchorage of adhesions externally.

[Illustration:

FIG. 71.—ACANTHOCEPHALUS (THREE SPECIMENS) PROJECTING FROM THE INCISED

INTESTINES OF A PIGMY MARMOSET. COMPARE THE SIZE OF THE PARASITES,

WHICH MAY BE DISTINGUISHED BY THEIR ANNULATIONS, WITH THAT OF THE

INTESTINES.

]

[Illustration:

FIG. 72.—BLOOD-RED NEMATODES PROTRUDING FROM FRONTAL SINUSES OF COMMON

OPOSSUM (DIDELPHYS VIRGINIANA). THE SKULLCAP HAS BEEN LIFTED OFF AND

THE POSTERIOR WALLS OF THE SINUSES BROKEN.

]

2. MECHANICAL IRRITATION.—In those instances where inflammation is the

manifestation which reflects the simple mechanical effects of parasites

it will be difficult indeed to prove, in the present state of our

knowledge, that it is not rather the effect of associated toxic

substances or excreta elaborated by the parasite. But instances of a

purely mechanical irritation there must be, although one can scarcely

put the finger upon them and say that this or that individual inflamed

mucosa did not become so from a toxic cause. Omitting these then, the

more certain, purer, more unequivocal examples will be those where

physiological processes become exalted as the result of the parasitic

irritation. An example in point is a case of volvulus in a Screech Owl

(_Otus asio asio_).[112] Here it is probable that the parasites excited

the gut to undue peristaltic action, and that during this process it

became twisted. Worms in such passages as the nose and nasal sinuses (I

have seen blood-red filariæ in the frontal sinuses of an opossum)

undoubtedly produce nervous effects by their presence and movements.

Those in the subcutaneous tissue (filariæ of wild cats) probably also do

so. It is difficult to judge those cases where doubtfully sensitive

parts are the ones affected. Probably the intestinal and intraperitoneal

worms, and less certainly the generally-migrating ones analogous to

_Filaria loa_, produce no nervous effects mechanically.

3. PRODUCTION OF HEMORRHAGES.—Hemorrhages large enough to kill suddenly

are theoretically possible, since worms occasionally produce aneurysms

which may rupture; we have seen such an accident in a Paradoxure

(_Paradoxurus leucomystax_). But certainly it is the long continued,

wasteful small hemorrhages that are important, inducing an anemia often

of severe and fatal grade. The hookworms are the shining offenders here,

yet we have seen very much the same effect from Acanthostoma in the

intestine of monkeys. Œsophagostomum has also been incriminated at the

London Garden in young Rhesus Macaques (_Macacus rhesus_)[113] where the

young forms of the parasite did the damage as they burrowed into the

wall of the gut.

4. OPENING UP AVENUES OF INFECTION.—This may be accomplished either by

passage of parasites from one position normally containing bacteria to

another which is susceptible to infection, or by devitalizing a tissue

which is ordinarily resistant to infection; _i.e._, creating a _locus

resistentiæ minoris_. The intestinal tract is the most common organ

concerned, but the illustrations to follow will give variety. Thus, the

mature examples of œsophagostoma in young rhesuses just referred to

above burrowed into the gut wall and led to both local and general

peritonitis. In one of our “spiroptera” parrots the worm had passed

through the proventricular wall and a chronic fibrosis resulted around

it. At the autopsy on a Rhesus Macaque Doctor Fox found a localized

abscess adjacent to the gut wall, and in it a whipworm was imbedded.

Passing from these examples of intestinal worms, I can mention the loss

of a valuable Philippine Spotted Deer (_Cervus alfredi_) as the result

of secondary infection of a cysticercus cyst of the lesser omentum which

led to a nearby peritonitis. Lung infections are not uncommon.

Murray[114] records that forty-four out of eighty-five young rhesus

monkeys dying from pneumonia showed an acarian, and he ascribed the

pulmonary irritation to certain crystals in the excreta of the mite. I

have studied a case of bronchopneumonia in a prairie dog where great

numbers of an arachnid were present. The reports of the London

Zoological Society are replete with notes of round worm pneumonias of

reptiles. These pulmonary cases must result from decreasing of tissue

resistance by the presence of the worms, and are easy to understand,

much more so than the intestinal infections when one recalls how

sensitive lung tissue is to foreign bodies, and that there seems to be

no indication that this tissue becomes accustomed to infestation such as

may be argued for the gut. All these citations must convince us that

parasites are most important predisposing agents to infection, and that

this is one of the most sinister phases of animal parasitism.

5. DESTRUCTION OF TISSUE.—This heading does not refer to the

comparatively trivial effects that accompany the more acute

inflammations secondary to parasites, albeit certainly the absorption of

their disintegrative tissue products has some effect on the economy; but

our ideas of such are so vague as to justify their being disregarded

here. What I refer to is the more massive destruction such as may occur

in the blood, for instance, from the action of protozoa. There is also

loss of mucosa in those chronic infestments of the stomach where we find

excessive fibrous tissue overgrowth. The most striking example of tissue

destruction we have seen was in the cirrhotic livers of prairie dogs

affected by _Hepaticola hepatica_, where in extreme cases, the amount of

functionating liver substance was reduced to a very small fraction of

its normal bulk.[115]

6. TOXINS.—We have no direct evidence to offer that noxious products of

parasites are concerned in producing disease in wild animals. The local

effects of such toxins are not distinctive enough—individual enough to

toxins or to the animal body—to separate them from the effects of such

accompanying factors as bacterial inflammations; nor can we separate the

general effects of these toxins from what might have been, for instance,

the effects of an accompanying anemia of hemorrhagic or other origin.

From a knowledge of what happens in human prototypes though, there is

scant doubt that some one of the multitudinous species must be capable

of producing toxins, but just which varieties are concerned cannot be

listed by anyone. By analogy we can at most only suspect the hookworms

and the dibothriocephalidæ. Under this same category of the toxins come

the worm-products which are reputed to have a destructive effect upon

the digestive enzymes in the gastrointestinal tract of the host, and

which would thereby interfere with the proper assimilation of pabulum,

resulting in malnutrition. For the same reasons as above indicated for

the toxins one is unable to speak for or against these “anti-enzymes.”

7. PRECLUSION OF NUTRITION.—This must be a very unimportant phase of the

activity of intestinal parasites, when one compares the bulk of food

which passes through the bowel and the average number of worms present;

and the same holds good for some interstitial parasites like the adult

filariæ. Even in amazingly heavy infestments of the intestines one will

be constrained to dismiss this idea when he compares the bulk of

parasites with that of the host, and recalls what the physiologist terms

the “factor of safety” inherent in this tract as elsewhere. But in the

case of blood parasites the matter may be different. Here we are

concerned with the withdrawal of refined foodstuffs—those which have

been worked over and over by subtle internal metabolic processes; and we

are not so sure, especially on recalling the enormous numbers of

parasites usual to blood infestments, that there is the capacity on the

part of these internal processes to meet increased demands that we count

upon for the intestinal functions. It is much more serious to be

deprived of the finished product than of the crude because it means the

undoing of “digestive” work all along the line, from gut to tissue cell.

Furthermore, a blood infestment guarantees that the parasite has been

feeding upon and depriving the animal of the precise foodstuffs the

cells require, and not by any chance upon, even in part, intestinal

substances that were wastes or residues. If we except the blood

parasites, then, it seems safe to conclude on the whole that the amount

of pabulum used by parasites is unimportant to the animal.

Having reviewed the manner in which parasites may conceivably be

harmful, it is time to return to the question of the actual exercise of

these powers.

The older appraisal of parasites in animals, namely that they were

rather innocent of disease production, was suggested by and borrowed

from the veterinarian, probably being engendered in him by their

frequency in what appeared to be normal domestic specimens. Yet it is

only proper to add that one of our former pathologists, and sometime

professor of veterinary pathology, Dr. C. Y. White, is a medical man and

is of much the same opinion. Older writers regarded worms even as

“guardian angels” of children. Very recently Schwartz[116] reviews some

work in this connection showing that, _in vitro_, some cestode extracts

were inhibitory to certain bacteria (_B. anthracis_, _B. pyocyaneus_ and

_B. dysenteriæ Shiga_). This relationship is so different from natural

conditions as to need no further comment.

At the London Garden the view appears to be different. In the 1910

report they charge five deaths against perforation by worms of the

stomach and intestines; in the 1911 report they record giant toads dead

from lung infestment; in 1912 “eighteen cases of enteritis were due to

worms”; and in 1917 they mention pneumonia in a toad and perforation of

the stomach of a puma. These reports represented evidently the more

striking, unequivocal examples of death from parasites which had

outspoken anatomical expressions, and omitted those in which the more

subtle agencies of parasitic pathogenesis were concerned. Their

experience has apparently been much the same as ours.

The ideal approach to a decision in reference to the importance of

parasites would appear to be a mathematical one, something as follows:

First, to determine what species infest animals and how commonly, then

to decide which ones are pathogenic and thirdly to estimate the severity

of the disease induced; so that finally, by an analysis and comparison

of the three results—a comparison and analysis judicial in the broadest

sense—we might hope to come to an opinion. Let us consider the three

avenues in order. At the first glance it must be evident that a list of

all possible parasitic varieties does not exist and may never be

compiled. The most that can be done is to tabulate the findings in

scattered laboratories, data usually recorded in terms of the individual

observer’s studies and often inadequate to give the compiler all the

facts desired. The same remarks apply to the percentage incidence of

parasitism. Not to prolong the academic discussion, suffice it to say

that very much the same obstacles present in the second avenue—that of

pathogenicity of the individual species. Our own data referring to this

second heading will be presented later, but after the failure of the

first avenue, the second and third lose greatly in value. At best,

statistics can be only suggestive. Unless critically and suspiciously

interpreted, and with a full appreciation of their limitations from a

foreknowledge of the way in which they were compiled, they would only

delude the reader and offend science, and so we abandon this line of

reasoning.

At present the best results of the study of pathogenesis by animal

parasites will probably be reached by a combination of methods, as

follows:

1. Direct. How commonly do we see clinical symptoms and morbid

anatomical changes that are incontrovertibly due to the parasite? We

restrict ourselves here to a narrow group of infestments indeed, and

think of such diseases as trichosomiasis in prairie dogs and

spiroteriasis in parrots.

2. By comparison with analogous infestments of domestic animals and man—

more thoroughly studied and therefore more accurately appraised, in

general, as to pathogenicity; a comparison from the standpoint of

disease production rather than natural habits of the parasite. Example,

coccidiosis and hookworm disease in foxes and dogs.

3. By inference through deduction. This is the most unsatisfactory

consideration of all, and should be well checked up and discounted. Here

we would evaluate the known propensities of the parasite first, such as

its size, motility, anatomic position in the host and the general

pathological traits of the genus and family to which it belongs, etc.,

and then compare these verminous properties with those of the host—its

size, temperament, physical stamina, etc. This third consideration must

necessarily overlap with or be supplementary to the first two. For

example, this consideration would have to be resorted to in many cases

of ascaris infestment where anatomical changes are generally not

demonstrable.

Acting on these three considerations, and after twelve years of

observation on parasites here in the Garden, a fresh review of our

records, and a recent review of the accessible relevant parasitological

literature I have come to the conclusion that, considering wild animal

collections the world over, there is no justification for an

unqualified, definite answer to the question of pathogenic parasitism

that will meet all conditions. We lack data on too many species that are

not sufficiently represented in collections or indeed not represented at

all. It is the liability to infestment of each order or family of beasts

that will have to be determined, and, depending on the assortment each

garden has on exhibition, will the importance of parasites to the garden

as a whole vary.

Speaking for the Philadelphia Garden, I have come to the conclusion that

on the whole parasitism does play an important part of our annual

losses. The financial loss which could be charged against spiroptera

alone is in the four figures, to say nothing of the difficulty of

replacement of rare species. And while touching the financial phase let

it be added that scientific work done now, it must be remembered, is not

restricted to the present time or place, but is to be measured in

dollars and cents with the yard stick applied to the future, and in

other places than that where the initial work is done. Even if we cannot

answer the question of the matter of importance the world over we can

guarantee that it is sufficiently so in the Philadelphia and London

Gardens to warrant a rigid supervision for parasitism; and since the

other larger collections are probably made up of similar animals, albeit

in different proportions, we surmise at least that it is likewise so

with them.

IMPORTANCE OF PARASITES IN OTHER FIELDS.—In addition to their importance

to exhibitions, animal parasites of wild animals are important first to

man. The animal hosts may serve as porters of infestation, and interfere

with attempts at eradication of the disease. The experience of the

European with African sleeping sickness attests to this. Not to go

farther than immediate examples I wish to note in this connection the

occurrence in this Garden of scabies in an orang which was transmitted

to a keeper, and of amebic dysentery in monkeys. Leiper[117] has called

attention to a guinea-worm in a leopard.

Parasites are important to certain wild animal industries. The ones that

have come to my attention are the fur seal (_Otoes alaskanus_) industry

of the Pribiloff Islands and fox-farming in Newfoundland. In both of

these instances the hookworm was concerned and entailed losses of

thousands of dollars. Lucas, who conducted a United States Government

commission to the seal grounds and after whom Stiles named the parasite,

has left very full notes of the former disease. I have identified the

same infestment in a young California hair seal (_Zalophus

californianus_) which was born and died in this Garden. This indicates

that the parasite might perhaps be found farther down the Pacific coast

than hitherto suspected.

To hunters parasitism of animals must be important, but to an unknown

and undoubtedly unimagined extent. The grouse plague of Scotland[118] is

an example to point. Who knows but that the disappearance of some of our

game animals, particularly birds, was not due more to disease than to

the ravages of man? There is at least food for thought here.

OCCURRENCE OF ANIMAL PARASITES IN THE WILD.—It would be unbelievable

that parasitism did not exist in the wild. It seems proper, however, to

record some evidence. Diesing’s _Systema Helminthum_ is replete with

references to Natterer’s Brazilian expedition. Nicoll speaks of a German

expedition to Spitzbergen in 1898, and a Swedish one to Egypt in 1901,

in both of which large numbers of parasitic forms were collected.

Nicoll[119] found _Trichosoma hepaticum_ in a hare shot in the wild, and

liver-flukes[120] in a kestrel shot on the coast of Scotland.

Leiper[121] found nine species of worms in hippopotami during an

expedition to Uganda, and[122] states that thirty-seven species of

helminths were collected on an Antarctic voyage by Surgeon Atkinson. In

an investigation of Grouse disease in Scotland, Fantham found many

different blood and intestinal parasites. Dr. Charles B. Penrose tells

me that all of the white-tailed deer he shot in the valley of the Swan

River, Montana, were infested with liver-flukes, so much so that the

liver was literally riddled by the disease, and yet the deer were fat.

The black-tail deer of the same valley were not thus parasitized and

were not as fat. In our own Garden we have found many tapeworms in wild

cats[123] which had been too recently captured for the worms to have

developed in captivity. Such instances might be still further

multiplied.

A more important consideration is the fate of the parasites thence

introduced into our Garden. Do they disappear of themselves? Naturally

we can never make sweeping predictions, for future events will depend

upon the life history of the individual parasite concerned. But by and

large, once introduced it is better to assume the attitude of pessimism,

and resign oneself against spontaneous disappearance and, what is worse,

realize that the parasitism is likely to become indigenous. We have

several pieces of evidence, however, that the infestment may

occasionally quite disappear. Thus, I have seen _Coccidium bigeminum_

spontaneously disappear from a Swift Fox (_Canis velox_) and _Spiroptera

incerta_ from a Macaw as proven at autopsy. Nicoll[124] remarks that

certain trematode infestations were heavier in newly arrived animals

than in ones long resident in the Garden. This is conceivable on the

basis of individual worms dying out, _i.e._, fulfilling their life spans

without the host becoming reinfested with fresh parasites. Precise

information on the subject is supplied by Ackert[125] who found that

cestodes disappeared from chickens in six to eight months when the birds

were confined, _i.e._, protected from reinfestment. Moreover, it is

known that worms can escape during acute infections, the infectious

state of the economy producing conditions obnoxious to the parasite. We

hear of many instances of their expulsion in human feces and vomitus

during malaria and the exanthemata of childhood and know of similar

discharge from animals during the death agony. I cite these data largely

because they explain the scarcity or absence of parasites at autopsy in

animals which were known to have been clinically infested.

FREQUENCY OF PARASITISM IN WILD ANIMALS

There can be little doubt that wild animals are more frequently infested

than man, and furthermore with a larger number of parasites. I have no

statistical basis for these opinions—they rest on personal observations

of human and animal autopsies, and reports of findings in the tropics

and elsewhere. They have therefore but the value of an individual

opinion. I should estimate rather cautiously that wild animals are

infested at least two or three times as frequently as man and much more

heavily.

The first step in the discussion of the incidence of parasites must be

that respecting the (host) classes and smaller taxonomic divisions—of

course as they have been studied in this Garden. Certain statistical

limitations were experienced and can be summarized as follows:

Data are not available on a sufficiently large number of animals to

justify conclusions as far down as genera and species, except for such

commonly and generously exhibited forms as monkeys and parrots. I have

therefore in tabulating and reviewing our records, distributed the

animals only as far as families—not into genera and species. The table

(24) to follow will be found not to contain every family because to do

so would needlessly enlarge it. Accordingly I have followed the policy

of only indicating those genera and species showing either frequent or

important infestment. I shall refer to those groups later as

“susceptible” groups. If no family is recorded in the table it means

that we have had no important numbers of infestments in it. The

“remarks” column shows the individual parasite that has been

particularly frequent or otherwise important. If there are no remarks it

means that the species of parasites found have been scattering.

RESULTS OF REVIEW AND TABULATIONS.

We now pass to an analysis and discussion of the findings brought out in

the previously mentioned review of our records and in Table 24. Viewed

broadly we find that there is a wide variation in the susceptibility of

different families to infestment. Those that are susceptible may be

located by consulting the table, and each will therefore not be

separately culled out and subjected to needless repetition. A few points

are however worthy of separate mention. While there is a familial or

generic susceptibility within certain orders it is unwise to generalize

too broadly. Thus for example the Corvidæ have a high percentage in

incidence for tropidocerca, syngamus and periproventricular worms, many

families of Ungulata harbor echinococcus, and Carnivora are prone to

show ascarids. On the other hand, among the copious exceptions to this

may be cited the irregular liability to infestment exhibited by the

Galli. Four varieties of these birds are represented but there are

missing such important kinds as curassows, guans, guinea fowl and

peafowl.

TABLE 24.

_Incidence of Parasites in Animal Groups._

══════════════════════╤═══════════════════════════════╤════════════════════

Animal │ MAMMALIA │ Remarks

──────────────────────┼───────────┬────────┬──────────┼────────────────────

„ │ Number of │ Number │Percentage│ „

│Autospecies│Infested│ │

──────────────────────┼───────────┼────────┼──────────┼────────────────────

Primates │ [126]538│ 51│ 9.4│

Cercopithecidæ │ │ │ │

Sooty Mangabey │ 34│ 4│ 11.8│

Cercocebus │ │ │ │

fuliginosus │ │ │ │

Rhesus Macaque │ 60│ 6│ 10.│

Macacus rhesus │ │ │ │

Callitrichidæ │ │ │ │

Marmosets │ 43│ 7│ 16.3│

Cebidæ │ │ │ │

Squirrel Monkeys │ 8│ 3│ 37.5│

Other Cebus │ 87│ 10│ 11.5│Eight had Filaria

Monkeys │ │ │ │ gracilis.

Lemures │ 86│ 6│ 7.│

Carnivora │ 498│ 84│ 16.9│

Felidæ │ │ │ │

American Wild Cat │ 28│ 11│ 40.│Stomach and

│ │ │ │ intestines, 22;

Felis ruffus │ │ │ │Bronchi, 4; Muscles,

│ │ │ │ 7.

Spotted Wild Cat │ 5│ 4│ 80.│

Felis ruffus │ │ │ │

texensis │ │ │ │

Canada Lynx │ 10│ 4│ 40.│Ascarids only.

Felis canadensis│ │ │ │

Lions │ 10│ 3│ 30.│Ascarids in stomach

│ │ │ │ and

Felis leo │ │ │ │intestines.

Ocelot │ 15│ 5│ 33.│Uncinaria.

Felis pardalis │ │ │ │

Canidæ │ │ │ │

Gray Fox │ 28│ 1│ 4.│Cestodes.

Canis cinereo │ │ │ │

argenteus │ │ │ │

Red Fox │ 17│ 2│ 12.│Uncinaria.

Canis vulpes │ │ │ │

pennsylvanicus│ │ │ │

Swift Fox │ 5│ 2│ 40.│Uncinaria.

Canis velox │ │ │ │

Gray Wolf │ 18│ 2│ 11.│Ascarids.

Canis mexicanus │ │ │ │

Mustelidæ │ │ │ │

American Badger │ 17│ 7│ 41.│Physaloptera.

Taxidea taxus │ │ │ │

Procyonidæ │ │ │ │

Raccoon │ 42│ 2│ 5.│

Procyon lotor │ │ │ │

Ursidæ │ │ │ │

Bears │ 37│ 6│ 16.│Ascarids.

Otariidæ │ │ │ │

Hair Seal │ 20│ 1│ 5.│Uncinaria.

Zalophus │ │ │ │

californianus │ │ │ │

Rodentia │ 198│ 32│ 16.│

Sciuridæ │ 44│ 4│ 9.│Scattered through

│ │ │ │ four

Castoridæ │ │ │ │different genera.

American Beaver │ 17│ 4│ 23.│In three cases

│ │ │ │ oxyuris

Castor │ │ │ │and flukes in cecum.

canadensis │ │ │ │

Hystricidæ │ │ │ │

Canada Porcupine │ 47│ 17│ 36.│Cestodes 8, filaria

│ │ │ │ 11, oxyuris 9,

Erythizon │ │ │ │in peritoneal cavity

dorsatus │ │ │ │ also intestine.

dorsatus │ │ │ │

Hyraces │ 7│ 2│ 28.│Cestodes in bile

│ │ │ │ ducts.

Cape Hyrax │ │ │ │

Procavia capensis │ │ │ │

Ungulata │ 365│ 44│ 12.│

Equidæ │ │ │ │

Zebras │ 7│ 7│ 100.│Nematodes,

│ │ │ │ intestine.

Cervidæ │ │ │ │

Axis Deer │ 6│ 1│ 17.│C. tenuicollis.

Cervus axis │ │ │ │

Barasingha Deer │ 8│ 0│ │

Cervus duvanceli│ │ │ │

Eld’s Deer │ 6│ 0│ │

Cervus eldi │ │ │ │

Fallow Deer │ 20│ 1│ 5.│Echinococcus cysts.

Cervus dama │ │ │ │

Hog Deer │ 21│ 0│ │

Cervus porcinus │ │ │ │

Japanese Sika Deer│ 14│ 0│ │

Cervus sika │ │ │ │

typicus │ │ │ │

Red Deer │ 14│ 0│ │

Cervus elaphus │ │ │ │

Elk │ 29│ 2│ 7.│Trichocephalus.

Cervus │ │ │ │

canadensis │ │ │ │

White tailed Deer │ 33│ 2│ 6.│Echinococcus in lung

│ │ │ │ (2).

Mazama │ │ │ │

virginiana │ │ │ │

Mule Deer │ 8│ 5│ 62.│Four Cyst.

│ │ │ │ tenuicollis.

Mazama hemionus │ │ │ │

Camelidæ │ │ │ │

Llama │ 14│ 2│ 14.│

Lama glama │ │ │ │

Camels │ 9│ 4│ 44.│Hydatid cysts.

Suidæ │ 19│ 2│ 10.│

Edentata │ 16│ 2│ 12.5│

Armadillos │ 10│ 2│ 20.│

Marsupialia │ 175│ 45│ 26.│

Didelphyidæ │ │ │ │

Common Opossum │ 84│ 40│ 48.│Physaloptera, 38;

│ │ │ │ oxyuris, 5;

│ │ │ │ cestodes, 5;

│ │ │ │ nematodes in

│ │ │ │ lungs, 3; cysts in

│ │ │ │ peritoneal areolar

│ │ │ │ tissue, 2;

│ │ │ │ trematodes in

│ │ │ │ ileum, 1.

Didelphys │ │ │ │

virginiana │ │ │ │

Macropodidæ │ │ │ │

Kangaroos and │ 70│ 0│ 0.│

wallabies │ │ │ │

──────────────────────┼───────────┴────────┴──────────┼────────────────────

│ AVES │

Passeres │ │ │ │

Corvidæ │ │ │ │

Common Crow │ 16│ 7│ 44. }│Tropidocerca and

│ │ │ │ occasional

│ │ │ │ intestinal

│ │ │ │ cestodes. Syngamus

│ │ │ │ in crows. Few

│ │ │ │ filaria.

Corvus │ │ │ }│

brachyrhynchos│ │ │ │

brachyrhynchos │ │ │ }│

Magpies │ 28│ 18│ 64. }│

Jays │ 41│ 22│ 55.│Periproventricular

│ │ │ │ filaria,

│ │ │ │ strongylus.

Pies, choughs, │ 35│ 12│ 33.│There is a striking

etc. │ │ │ │ consistency of

│ │ │ │ infestment in the

│ │ │ │ different members

│ │ │ │ of Corvidæ both as

│ │ │ │ regards degree of

│ │ │ │ infestment and

│ │ │ │ species of

│ │ │ │ parasite present.

Sturnidæ │ │ │ │

Starlings │ 63│ 19│ 30.│Periproventricular

│ │ │ │ filaria largely.

Turdidæ │ 25│ 8│ 33.│Periproventricular

│ │ │ │ filaria largely.

│ │ │ │Thrushes and Robins.

│ │ │ │ None in American

│ │ │ │ thrushes, one in a

│ │ │ │ robin.

│ │ │ │Finches. Not

│ │ │ │ examined closely

│ │ │ │ at autopsy, but

│ │ │ │ there is a

│ │ │ │ scattering of

│ │ │ │ periproventricular

│ │ │ │ filaria and

│ │ │ │ intestinal

│ │ │ │ cestodes through

│ │ │ │ most of the

│ │ │ │ species.

Canaries │ 24│ │ │Were free from

│ │ │ │ parasites.

Picariæ │ │ │ │

Picidæ │ │ │ │

Woodpeckers │ 4│ 2│ 50.│

Rhamphastidæ │ │ │ │

Toucans │ 30│ 9│ 30.│Spiroptera largely.

Striges │ 142│ 2│ 7.│Remarkably free of

│ │ │ │ parasites.

Psittaci │ [127]774│ 124│ 16.│

Loriidæ │ │ │ │

Lorys │ 24│ 5│ 20.│3 spiroptera, 1

│ │ │ │ hemoproteus, 1

│ │ │ │ intestinal worm.

Cacatuidæ │ │ │ │

Cockatoos │ 4│ 2│ 6.│2 spiroptera.

Crested Ground │ 45│ 4│ 9.│4 spiroptera.

Parrakeet │ │ │ │

Calopsitta novæ- │ │ │ │

hollandiæ │ │ │ │

Psittacidæ │ │ │ │

Old World (Totals)│ 453│ 65│ 14.3│

Undulated Grass │ 121│ 2│ 1.6│1 spiroptera, 1

Parrakeet │ │ │ │ coccidium.

Melopsittacus │ │ │ │

undulatus │ │ │ │

Pennant’s │ 21│ 6│ 29.│6 spiroptera.

Parrakeet │ │ │ │

Platycercus │ │ │ │

elegans │ │ │ │

Rosehill Parrakeet│ 48│ 21│ 44.│20 spiroptera, 1

│ │ │ │ cestode.

Platycercus │ │ │ │

eximius │ │ │ │

Other old world │ 86│ 12│ 14.│12 spiroptera.

parrakeets │ │ │ │

Old world parrots,│ │ │ │

lovebirds, │ 74│ 13│ 18.│13 spiroptera.

eclectus. │ │ │ │

New World (Totals) │ 321│ 69│ 21.5│

Macaws │ 26│ 9│ 34.│9 spiroptera.

Conures │ 62│ 16│ 26.│15 spiroptera, 1

│ │ │ │ hemoproteus, 1

│ │ │ │ blood larva.

Amazons │ 164│ 27│ 16.5│24 spiroptera, 3

│ │ │ │ nematodes.

Other new world │ 69│ 17│ 10.│7 spiroptera.

parrots │ │ │ │

Accipitres │ [127]201│ 13│ 6.7│

Falconidæ │ │ │ │

Buzzards │ 55│ 4│ 7.3│

Eagles │ 44│ 1│ 2.3│

Serpentaridæ │ │ │ │

Vultures │ 29│ 1│ 3.4│

Miscellaneous │ 73│ 7│ 9.6│4 were blood

│ │ │ │ protozoa.

Galli │ 299│ 42│ 14.│

Phasianidæ │ │ │ │

Pheasants │ 95│ 20│ 21.│Heterakis in ceca.

Partridges │ 14│ 3│ 21.│

Quail │ 70│ 10│ 14.│Heterakis.

Megapodidæ │ │ │ │

Wild Turkeys │ 39│ 7│ 18.│Intestinal cestodes.

│ │ │ │ Coccidia twice.

Columbæ │ [128]163│ 14│ 9.│Mostly intestinal

│ │ │ │ cestodes, but

│ │ │ │ several

│ │ │ │ spiroptera.

Fulicariæ │ [128]38│ 7│ 18.│

Alectorides │ [128]41│ 10│ 25.│

Gaviæ │ [128]21│ 3│ 14.│

Steganopodes │ [128]22│ 1│ 5.│

Herodiones │ [128]105│ 21│ 20.│

Anseres │ [128]319│ 28│ 8.8│

Swans │ 48│ 7│ 14.│No significant

│ │ │ │ groupings.

│ │ │ │ Parasites

│ │ │ │ scattering. Few

│ │ │ │ intestinal

│ │ │ │ cestodes.

Geese │ 83│ 13│ 15.6│

Ducks │ 188│ 8│ 4.│

Struthiones │ 36│ 1│ 2.8│

──────────────────────┴───────────┴────────┴──────────┴────────────────────

Nor do all members of a genus necessarily show the same susceptibility,

and the heterakis infestment in the pheasants illustrates this matter

very well. It was limited almost entirely to two species—Amherst’s and

Golden, whereas several frequently exhibited species showed none. The

following table brings this out in more detail:

TABLE 25.

_Heterakis in Pheasants._

════════════════════════════════════════════╤════════╤════════╤════════

Species │ Total │Infested│ Per

│ │ │ cent.

│ │ │infested

────────────────────────────────────────────┼────────┼────────┼────────

Golden Pheasant (Chrysolaphus amherstiæ) │ 18│ 12│ 67

Amherst’s Pheasant (Chrysolaphus pictus) │ 16│ 5│ 31

Silver Pheasant (Gennæus nycthemerus) │ 19│ 1│ 5

Reeves’ Pheasant (Phasianus reevesi) │ 16│ 1│ 6

Ringnecked Pheasant (Phasianus torquatus) │ 12│ 0│ 0

Swinhoe’s Pheasant (Gennæus swinhoii) │ 10│ 0│ 0

────────────────────────────────────────────┴────────┴────────┴────────

Enzoötics and environment played no part in the above figures. We have

had no real heterakis enzoötics, for in but two instances did three

heterakis deaths occur in a year, and two deaths per year have occurred

in but four instances in the past twenty years. During this time there

have been sufficient animals on exhibition and subjected to autopsy to

indicate definitely that the two species named—Amherst’s and Golden,

must be considered as more susceptible than the other varieties. Nearly

all of the heterakis in quail likewise occurred in one species—seven of

the ten cases occurred in a total of twenty-three Scaled Quail—but in

these birds the infestment appeared in enzoötic form and cannot be

viewed as indicating a preference for a species.

Psittaci are on the whole, not susceptible to worms. It is true that we

suffered a serious outbreak of spiropteriasis a few years ago, but if we

consider this a closed chapter we can accept the above generality as

stated. Among 774 parrots autopsied we have encountered but one cestode

and three intestinal round worms.

The deer, likewise, are singularly free from intestinal parasites. I

gave the detailed records of these animals in Table 24 to emphasize the

scarcity of parasites even when fairly numerous specimens had been

available for examination.

Other interesting features in the table are the outstanding infestments

of squirrel monkeys and marmosets among the monkeys, of gastric and

intestinal worms in the wild cats, and intestinal worms in the zebras.

The foregoing has had to do with parasitism from the standpoint of the

host. The next phase, that of the individual parasite itself, interests

more the strict parasitologist than the general zoologist; however, both

will see how it may have a very practical value.

TABLE 26.

_Distribution of Parasitic Cases According to Parasitic Groups._

═════════════════════════════════════╤════════════════╤════════════════

Nematodes │ 183[129]│

Spiroptera │ 145│

Filaridæ │ 138│

Ascaris │ 30│

Physaloptera │ 28│

Uncinaria │ 25│

Tropidocerca │ 23│

Heterakis │ 22│

Trichocephalus │ 11│

Syngamus │ 9│

Trichina │ 2│

Hepaticola │ 2│

Other Miscellaneous │ 4│

Total Nematodes │ │ 622

Cestodes │ 165[129]│

Echinococcus │ 9│

Cysticercus │ 7│

Tænia │ 4│

Miscellaneous │ 3│

Total Cestodes │ │ 188

Trematodes │ │ 22

Acanthocephalus │ │ 4

Protozoa │ │ 14

Arthropods │ │ 6

Unclassified │ │ 34

─────────────────────────────────────┼────────────────┼────────────────

Grand Total │ │ 890

─────────────────────────────────────┴────────────────┴────────────────

INCIDENCE ACCORDING TO PARASITIC GROUPS.

Inasmuch as it has been physically impossible to determine specifically

and classify efficiently the accumulations of verminous material from

our autopsies I will not be able to tabulate parasitic groups even as

closely as I did in the “animal host” table. Nevertheless sufficient has

been done to illuminate in part certain phases of parasitism and to

prevent a summary dismissal of the subject. Reviewing our cross index I

have distributed the data into the following Table 26, the parasites

being listed in the order of their frequency. It may serve only as a

panorama of the situation, inasmuch as determinative study of a group

amounts to a research in itself, and the multiplicity of them precludes

a consistent study of every one. The data are based upon “cases of

parasitism.” That is, each and every worm species occurrence has been

counted, regardless of whether it was the same species that has been

concerned over and over again, or in different anatomical positions (of

different individual hosts, of course) or whether it was in association

with other parasites.

ANALYSIS OF TABLE 26.

There is a grand total of 890 cases of animal parasitism embraced in the

above table, which is a sufficiently large number to give representative

value to some phases of the analysis.

In the first place nematode worms occur about three times as frequently

as all other forms of parasites. In gardens where spiroptera has not

figured so largely the proportion might be reduced to about two to one.

Cestodes rank a poor second, trematodes a worse third, and

acanthocephali a very bad last. This order agrees with our figures of

1913[130] and with the small series of Nicoll.[131] The latter worker

found that the order was not changed when pains were taken to include

also such smaller worms as could only be obtained from the host by using

sieves, etc. Cestodes were not likely to be overlooked, but very small

trematodes and nematodes were easily passed over.

VISCERAL DISTRIBUTION.

As to the individual organs which are most commonly parasitized our

records show that with Aves as well as Mammalia the intestines are the

parts most commonly affected. The stomach ranks second for both—the

proventricle rather than the gizzard of birds corresponding,

parasitologically speaking, to the stomach of mammals. We have found but

one parasitic species in the gizzard of birds, _i.e._, immature forms of

_Spiroptera incerta_ lying under the chitinous lining of the gizzard and

only discoverable after the lining has been peeled off. The peritoneum

comes third (air sacs of birds) due to the presence of filaridæ, and the

blood fourth for the same reason. It is to be emphasized that, in our

data, identical organs of mammals and birds should be about equally

liable to infestment with the possible exception of the lungs. But in

view of the small number of cases available there is no justification

for speculating about the reason for this last difference, albeit the

radical difference in the anatomy of the two classes is very inviting.

Now that our spiroptera enzoötic has subsided, the order above given

will be changed, and in view of like disturbing factors other gardens

should not expect the same order to hold invariably for their

collection, since their enzoötics will depend somewhat on the

preponderance of animals of one or another family which are likely to

compose their exhibits. A single such enzoötic may suffice to disarrange

the whole fabric, and if two or three are taken into account the order

of organ involvement can be quite disrupted. To attempt to construct

statistically an “order of frequency involved” which would stand for

every garden would only lead to interminable adjustments on the basis of

animals exhibited and of parasitic enzoötics, so that I have finally

been reduced to a combination of our Garden statistics and the

bloodparasitic ones of the London Garden. Doing this I have arranged in

Table 27 the frequency of organ involvement as follows and estimated the

percentage of animals infested. These figures are computed upon a

different basis from that of Table 24. They naturally cover all animals

and not the “susceptible” ones as in Table 24.

[Illustration:

FIG. 73.—HUGELY DISTENDED PROVENTRICLE OF PARROT DYING WITH

SPIROPTERIASIS. COMPARE ITS SIZE WITH THAT OF THE HEART WHICH IS

ABOVE AND TO THE LEFT, AND THAT OF THE GIZZARD BELOW AND TO THE

LEFT.

]

TABLE 27.

═══════════════════════════════════╤═══════════════════════════════════

Mammalia │ Aves

───────────────────────┬───────────┼───────────────────────┬───────────

│ per cent. │ │ per cent.

Intestines │ 9.0│Blood │ 6.5

Stomach │ 3.7│Intestines │ 3.5

Peritoneum │ 2.3│Proventricle │ 1.7

Blood │ 1.5│Air sacs │ 1.3

Lungs │ 1.0│Liver │ 0.3

Muscles │ 1.0│Gizzard │ 0.3

Liver │ 0.5│Scattering │ 0.4

───────────────────────┼───────────┼───────────────────────┼───────────

Total │ 20.0│Total │ 14.0

───────────────────────┴───────────┴───────────────────────┴───────────

The effect of this is at first sight startling in that it places the

blood parasites of birds so far in the fore, but it must be at once

recalled that the inquiries upon the blood parasites were much more

searching—microscopic, than in the case of the other organs. If similar

methods were applied to the others their percentage of parasitism might

be notably raised—particularly that of the intestines.

SPECIAL PARASITOLOGIC CONSIDERATIONS.

At this point the statistical considerations of parasitism will give way

to descriptions of certain specific infestments that have given us more

or less concern.

The occurrence of single parasitic varieties or of well known species in

an isolated host may occasionally be of practical importance, but

usually they amount to little more than an academic study, whereas the

repeated discovery of single parasitic kinds, or infestment of similar

hosts, especially when grouped, raises the matter to a very practical

level demanding attention. Such findings being not infrequent in our

experience, it has been possible to study our material in a manner

designed to show the frequency of various parasites in a certain host,

the susceptibility of certain animals to parasites in general and the

infestment of dissimilar hosts by the same parasite. The more important

of these now follow.

AVIAN SPIROPTERIASIS.

This disease concerned parrots particularly but toucans, pigeons, and

such widely separated species of birds as the starling, quail, thicknee

and barbet have been occasionally affected. To the naked eye the

parasite resembles the human hookworm, but differs in location, being a

resident of the proventricle where it produces a swelling of the mucosa

which interferes with the passage of food. Up to a hundred worms may be

present in the one bird, and immature forms are occasionally found under

the chitinous lining of the gizzard. The parasite burrows into the

mucous membranes, occasionally penetrates quite through the wall into

the air sacs, and on one occasion induced an adenomatous hyperplasia of

the mucous membrane, and an adjacent “peritonitis.” Mucus is sometimes

present in the droppings. Death may occur either acutely, or with

emaciation. Spiroptera incerta Smith[132] is the common parasitic

species of parrots, but I have found at least one other as yet

unidentified species in the toucan, and there are probably more. In the

eight year period 1906–1913 from 25 to 50 per cent. of our dead parrots

showed this parasite every year, the total loss being 113 birds for this

period—a most important infestment.

[Illustration:

FIG. 74.—HISTOLOGIC SECTION THROUGH PROVENTRICULAR WALL OF PARROT,

SHOWING SECTIONS OF SPIROPTERA IN THE LUMEN AND MUCOSA. THERE IS

SOME GLANDULAR HYPERPLASIA (ADENOMATOID) AND NECROSIS OF THE LUMINAL

PORTIONS OF THE MUCOSA.

]

[Illustration:

FIG. 75.—INFLAMMATORY ROUND CELL INFILTRATION AROUND NERVE TRUNK IN

WALL OF PROVENTRICLE. PARROT DEAD WITH SPIROPTERIASIS.

]

We approached the problem by diagnosing and isolating the infested birds

through a microscopic examination of droppings, finding that by boiling

the droppings in 5 per cent. NaOH solution we clarified them and made

examination easier and more certain without at the same time destroying

the parasitic ova. The result of the examination of all our parrots was

the isolation of 14 per cent. of the parrot population; and as these

died off the diagnosis of infestment was found confirmed at autopsy in

every case. The parrot house was thoroughly renovated and no newly

arrived parrots were admitted until after quarantining and examining

droppings for ova. The toucans and other species, being housed

elsewhere, were not quarantined. Following this, we were gratified to

experience no more spiroptera deaths in parrots for seven years. Then,

in 1920 and 1921, a new outbreak occurred in four toucans and several

other scattering species, including two parrots; but none of these came

from the main parrot house and probably represented a fresh importation.

We attempted to cure the isolated verminous birds by medication but were

unsuccessful. Likewise attempts at determining the life cycle of the

parasite brought us no farther than that the ova developed larvæ in

moist sand in six days. Feeding of ova, freshly passed and larvated did

not produce infestment in parrots or pigeons. On the whole we can quote

our experience with spiroptera as a most satisfactory example of the

value of hygiene and as a result which could never have been

accomplished by medication.

HEPATICOLA (TRICHOSOMA) HEPATICA IN PRAIRIE DOGS.

Bancroft[133] and Hall[134] have given us details concerning this

parasite and the disease it causes. It is threadlike, several inches

long, and permeates the livers of the gray rat, white rat and wild

hare.[135] We first saw it in the more or less cirrhotic livers of

several prairie dogs; later we observed it in a beaver and the gray rats

of the Garden. In the prairie dogs and beaver the liver resembled that

of fatty cirrhosis and was so considered on naked eye examination at our

first autopsy. We were only set right when we came to the histological

examination. It was remarkable how well conditioned some of the prairie

dogs were in in the face of very extensive liver destruction; but on the

other hand some were emaciated and a few of the spontaneously diseased

showed at autopsy an enormous ascites. The outstanding features at

autopsy were the large size of the liver and its pallor and hardness;

and fine yellow lines could sometimes be made out twisting over the

surface.

The disease affects wild rats differently from prairie dogs. In both the

spontaneous and experimental disease the infestment was insignificant,

amounting to perhaps three or four foci the size of a split pea near the

anterior margins of the liver. Diagnosis may be easily confirmed by

crushing the yellow infested portions of the liver between glass slides

and examining microscopically for ova.

We have seen such a small number of cases of this disease because so few

prairie dogs reach the autopsy table, yet there must be some important

mortal factor in our prairie dog enclosure, for the Superintendent

states that the population there does not increase in spite of the

frequent births and additions from dealers. The animals almost

invariably die under ground and their bodies are not recovered.

In order to test out the origin of the infestment we trapped two of our

exhibition specimens, and the liver of both was found infested on

surgical examination whereas six newly purchased ones had normal livers.

The latter were secured fresh from their native habitat in the West, and

their livers were examined through long surgical incisions and found

free of infestment. Later we fed the ova (embryophores) from rat livers

to these prairie dogs and on destroying them found them infested. We

were also successful in transmitting the disease in the opposite

direction, _i.e._, from prairie dog liver to white rat. From all this we

feel sure that the prairie dog disease in our Garden was transmitted

from the rat and that here is another reason for rat extermination in a

zoological garden.

[Illustration:

FIG. 76.—OVA OF HEPATICOLA HEPATICA IN LIVER OF PRAIRIE DOG. THEY HAVE

BIPOLAR OPENINGS. THERE IS DESTRUCTION OF LIVER TISSUE AND A LITTLE

INFLAMMATORY REACTION OF CELLULAR CHARACTER, BUT NO IMPORTANT

FIBROSIS.

]

[Illustration:

FIG. 77.—UNCINARIA SMITHI COILED IN INTRAHEPATIC BILE DUCTS OF

GIRAFFE. NOTE MARKED PERIDUCTAL FIBROSIS IN THE NEIGHBORHOOD OF THE

PARASITES.

]

The adult _Hepaticola hepatica_ of prairie dogs I have not seen in

sufficient entirety to compare with the rat species and therefore cannot

affirm that the two are identical species. It is presumably like that of

the rat, being threadlike and most difficult to separate from the liver

substance through which it ramifies. At maturity it dies and

disintegrates, leaving the ova distributed more or less in tracts

through the liver substance, so that we are limited to a certain period

wherein to obtain the mature form. The ova are not passed into the

intestine, but remain _in situ_, just as in the case of hydatid disease,

and therefore diagnosis cannot be achieved by examination of feces. For

the disease to be transmitted the host must die and its carcass be eaten

or otherwise so disintegrated that the ova are distributed abroad.

Another interesting observation is the long incubation period of the

ova. Confirming Bancroft, we found that the ova only became larvated

after they had lain in water at least three months.

HOOKWORMS.

These important parasites have been taken from several foxes: Gray Fox

(_Canis cinero argenteus_), Arctic Fox (_Canis lagopus_), Swift Fox

(_Canis velox_), Red Fox (_Canis vulpes pennsylvanicus_), a Gray Wolf

(_Canis mexicanus_), divers members of the Felidæ-Eyra (_Felis eyra_),

Jaguarundi (_Felis jaguarundi_), American Wild Cat (_Felis ruffus_),

Spotted Wild Cat (_Felis ruffus texensis_), Ocelot (_Felis pardalis_),

from two Giraffes (_Giraffa Camelopardalis_, _Giraffa capensis_), a

Malayan Tapir (_Tapirus indicus_), and a young California Hair Seal

(_Zalophus californianus_). It has been a most serious infestment in

American wild cats (_Felis ruffus_ and _Felis ruffus texensis_)—animals

which generally also harbor other species of worms. In view of the

petechial hemorrhages of the intestines and analogous circumstances in

dogs and human beings, it must be conceded that this worm is pathogenic.

At this point it is fitting to note the infestment as it affects hair

seals. The parasite concerned, _Uncinaria lucasi_, has long been a

scourge among the fur seals (_Otoes alaskanus_) of the Pribiloff

Islands. Its punctures are bloodless, being signalized instead by small

edematous plaques in the intestinal mucosa, The animal we autopsied was

a young California Hair Seal born in the Garden, and is singularly the

only hair seal in which we have seen it. The natural habitat of the hair

seal is the coast of California which means that the range of _U.

lucasi_ may extend farther southward than at first suspected. We have

none of the northern variety.

I point out two giraffe cases only because they are unique as to the

organ (liver) affected. So far as I know, mature hookworms have never

been reported from other organs than the intestines.

From the prophylactic standpoint it will be advisable to have as little

moist earth as possible, particularly sandy ground, in and around the

enclosures for the above mentioned susceptible animals because it is in

such soil that the earlier stages of the life cycle of the parasite are

passed.

We have never found any of the human hookworm species in our animals,

but it must be recognized that transmission is possible to a certain

degree. _Anchylostoma ceylanicum_ Lane[136] was found in man, cats,

dogs, and a lion; Leiper[137] reports _A. duodenale_ in a dog, and von

Linstow[138] states that the latter parasite also occurs in the

chimpanzee.

AMEBIC DYSENTERY IN MONKEYS.—We recently lost six monkeys in a small

outbreak of this disease—four black spider monkeys (_Ateles ater_), a

Pinche marmoset (_Leontocebus edipus_), and a woolly monkey (_Lagothrix

lagotricha_). Except for non-characteristic looseness of stools, there

were no symptoms until the usual terminal lethargy set in. Living amebæ

were found in feces. At autopsy only the colon was found to be

anatomically affected. It was hugely distended, fully an inch in

diameter, and there were numerous confluent ulcers of the mucosa covered

by a thick slough. The liver showed no abscesses. In the histological

sections amebæ were found in the interstices of vital gut tissue just as

they are in corresponding human lesions. I have not diagnosed the

species yet, but can vouch that it is not _Endameba histolytica_ or

_coli_.

[Illustration:

FIG. 78.—MICROSCOPIC SECTION OF LIVER OF GIRAFFE, SHOWING SECTIONS OF

UNCINARIA SMITHI IN BILE DUCT AND MARKED FIBROSIS AROUND THE DUCT.

]

[Illustration:

FIG. 79.—COLON OF MONKEY DYING WITH AMŒBIC COLITIS. HIGHLY ELEVATED

SLOUGHS COVER THE ULCERS.

]

According to Leidy’s recommendation, grated nutmeg was administered and

was followed by an improvement in symptoms. The animals became brighter

and the stools firmer, but the amebæ were not eradicated. Emetin

hypodermically and by mouth had no obvious effects on the disease or the

amebæ. One monkey thus treated with nutmeg recovered, but died the next

year of another affection and disclosed the scars of the old ulcers in

the colon. Our experience with this disease, however, is not unique. At

Washington, D. C.,[139] eight spider monkeys were affected, and sporadic

cases come to light from the West Coast[140], Manila, Khartoum and

Ceylon. Prowazek’s report concerned a young orang[141]. Liver abscesses

in addition to the intestinal lesions were found by three different

observers.

As to the transmissibility of monkey amebiasis to man, reporters are

divided. Both sides are probably right, in as much as _Endameba

histolytica_ was concerned in some cases and non-human species in

others. It is an infestment to be feared, and calls for examination of

stools from such newly arrived animals as are known to be susceptible

(spider and woolly monkeys, orangs).

PARASITES OF MARMOSETS AND SQUIRREL MONKEYS.—I give a special place to

this subject because Table 24 shows that these monkeys are so commonly

infested and because they are so commonly used as household pets. In

this connection the questions arising are, first, whether the infestment

is a menace to life, and second, whether it is existent outside the

Garden or only acquired here. The following lists set forth the

parasitic status as shown at autopsy. The figures indicate how long the

animal lived in the Garden:

═════════════════════════════════════════╤═══════════════════════════

Marmosets │ Squirrel Monkeys

─────────────┬───────────────────────────┼─────────────┬─────────────

Infested │ Not infested │ Infested │Not infested

─────────────┼───────────────────────────┼─────────────┼─────────────

1 day│ 6–15 days ( 4 animals)│ 2 days│ 3 months

1 day│ │ │

2 months│ 1 month ( 6 animals)│ 14 days│ 3 months

6 months│ 3–5 months ( 9 animals)│ 26 months│ 5 months

12 months│ 6 months ( 2 animals)│ │ 14 months

12 months│ 7 months ( 2 animals)│ │ 15 months

12 months│ 8 months ( 1 animal)│ │

13 months│ 9 months ( 2 animals)│ │

│ 10 months ( 1 animal)│ │

│ 12 months ( 1 animal)│ │

│ 14 months ( 1 animal)│ │

│ 15 months ( 1 animal)│ │

│ 17 months ( 1 animal)│ │

│ 18 months ( 2 animals)│ │

│ 20 months ( 1 animal)│ │

│ 21 months ( 1 animal)│ │

─────────────┼───────────────────────────┼─────────────┼─────────────

Totals 8 │ 35 animals│ 3 animals│ 5 animals

animals │ │ │

─────────────┴───────────────────────────┴─────────────┴─────────────

Reverting to the questions above raised, the data show that some of the

animals were certainly infested on arrival here, and that others

probably were; but since these animals were not examined for parasites

on arrival in the Garden the duration of infestment remains unknown, and

accordingly we are not justified in going farther in our conclusions. In

the case of the marmosets, though, if we confine ourselves to the non-

parasitized animals, it would appear that the “acclimatization” period

is within the first six months. I have attempted to arrive at a

conclusion on this basis, but the average lifetime of the four

parasitized marmosets which survived this period is the same as that of

the sixteen non-parasitized survivors, and we do not know at what time

the parasitized ones contracted the disease.

[Illustration:

FIG. 80.—ARACHNID (PNEUMONYSSUS FOXI) IN LUNG OF ADULT MONKEY (MACACUS

RHESUS). IT OCCUPIES THE CENTRE OF A CYST WHICH IMMEDIATELY

UNDERLIES THE PLEURA SEEN AT UPPERMOST PART OF THE ILLUSTRATION.

]

CYSTICERCUS TENUICOLLIS.—We have noted this bladder worm in the Aoudad

(_Ovis tragelaphus_), Red River Hog (_Potamochœrus porcus_),

domesticated Angora Goats and several deer (_Cervus alfredi_, _Capreolus

capreolus_, _Mazama mexicana_, _M. hemionus_) located with one exception

in the peritoneal cavity or membrane. One of the mule deer (_Mazama

hemionus_) exhibited the parasite also in the lung and liver. This

parasite is discussed because the very valuable Philippine spotted deer

(_Cervus alfredi_) died from a peritonitis secondary to an infected cyst

in the lesser omentum, and because the parasitism (_Tænia marginatum_)

is contractible from canidæ which are also on exhibition in the Garden.

It happens that the spotted deer did not become infested from the dogs,

but it is quite probable that the goats did, since they passed many

times daily in front of the wolf cages, drawing the children’s carriages

over the walks, and were stabled nearby. We have not discovered any of

the other tapeworm cysts in deer which might be transmitted to them from

the canidæ. Camels which are parked directly opposite them have only

exhibited echinococcus cysts, yet we have never found its adult form

(_Tænia echinococcus_) or its ova in the canine feces. The danger of

fatal disease from _C. tenuicollis_, even though the infestment be

present, is remote; but we feel that it is better, if possible, not to

exhibit the canidæ adjacent to susceptible animals.

PULMONARY ACARIASIS IN MONKEYS.—We have seen but two instances of this

affection in the Philadelphia Garden. The offending parasite in our

animals was a new species, _Pneumonyssus foxi_ Weidman[142]. It occurred

sparingly in small cysts under the pleura and was certainly benign in

our cases. The importance of the infestment consists in part in that

these lesions may be mistaken for tubercles.

At the London Gardens[143] acariasis was found in forty-four young

rhesuses dying of pneumonia, and the observers ascribed the inflammation

to irritation of certain doubly refractile crystals which occurred in

the excreta of the mite. There are four other recorded instances of such

disease in monkeys, all caused by different species of parasites.

As to pathogenesis of these arachnids, the London experience is most

illuminating in that it was young rhesuses that were affected. Our

specimens were mature, and nothing was stated to the contrary in the

other reported cases from various parts of the world. The parasites are

perhaps inhaled from the straw used as bedding, since such vegetable

material is a common habitat for mites. If the resultant acute pneumonia

is weathered the relics might remain only in the form of the subpleural

and parabronchial cysts such as we have seen at the Philadelphia Garden.

I am the more willing to accept the possibility that the simian

arachnids can induce an acute pneumonia after studying a very definite

case of bronchopneumonia in a prairie dog, which was induced by

_Cytoleichus penrosei_ Weidman 1916.[144]

PERIPROVENTRICULAR FILARIDÆ OF BIRDS.—Every year we report a number of

cases (up to twenty-three) of these worms, probably several species,

coiled under the serosa of the air sacs and most commonly around the

proventricle. Tentatively we have recognized two forms, a shorter (an

inch or so long) and a longer (three to four inches). The latter is most

inextricably coiled, but the former may be teased out. Microfilaria

occur in the blood of the latter cases, but not in that of the former.

The adults have been observed to penetrate from their position in the

air sac serosa into the lumen of the proventricle (goose), to have

caused rupture of the inferior cava (bulbul), to be associated with

subserous cysts of the intestine (weaver) and with profound anemia

(liothrix). The birds affected are mostly small, inexpensive ones, but

the infestment is important because of its frequency and deserves study

of the means of transmission.

[Illustration:

FIG. 81.—ARACHNID (CYTOLEICHUS PENROSEI) IN A BRONCHOPNEUMONIC FOCUS

IN THE LUNG OF A PRAIRIE DOG (CYNOMYS LUDOVICIANUS).

]

[Illustration:

FIG. 82.—FILARIAL WORM COILED NEAR PROVENTRICLE OF A FINCH.

]

PHYSALOPTERA IN OPOSSUMS AND BADGERS.—These worms were frequent findings

for a period of years and were particularly impressive on account of the

large number of parasites present. The stomach often contained scores,

more or less securely attached to the mucosa by the head. The worms

average an inch or two in length and perhaps an eighth of an inch in

thickness. _P. turgida_ is the only species we have identified (three

examinations). As to pathogenicity we have not observed that definitely

constant lesions are induced by the parasites. In several instances the

gastric mucosa has shown the mosaic appearance indicative of chronic

gastritis, a condition not necessarily incited by, but certainly

aggravated by, these worms; at least significant is the habit of the

worm to imbed its head in the gastric mucosa. In one instance the

microscope has revealed a most severe fibrosis of the submucosa. The

fibrosis was not so much diffuse as it was local or nodular, and in

favorable places the ova of physaloptera could be discovered in the

centres of the nodules, and thus betrayed the previous presence of the

adult worm there. In this individual animal the case against the

physaloptera is clinched by direct evidence. In other cases we have

circumstantial evidence. Whereas it is not a deeply burrowing parasite,

it is still a penetrative one, and this is sufficient to compromise the

all important “integrity of the mucosa.” It should therefore be

considered pathogenic in all cases, because open to suspicion in several

directions—abstraction of tissue juices, irritation by its products or

movements and by opening up an avenue for bacterial infection.

TROPIDOCERCA IN BIRDS.—This is a blood-red nematode of the size of a

mustard seed to that of a peppercorn which inhabits the depths of the

proventricular mucosa. At first sight its spheroidal form suggests that

of a fluke, but under the microscope it is found to be a nematode hugely

ballooned out by ova, and coiled up into a ball. In spite of its

dangerous appearance—being red—it is most likely quite innocuous, for

microscopic sections show no sign of inflammation around the worm.

Moreover, we know that a Concave Casqued Hornbill (_Dichoceros

bicornis_) now on exhibition has harbored the worms, as indicated by ova

in the droppings, for eight years and yet seems perfectly well. I have

made wax reconstructions of three of the worms and find that the coils

are not very intricate and that they assume no regular or constant

arrangement.

SYNGAMUS TRACHEALIS.—Our worst experience with this picturesque parasite

was in common crows (_Corvus b. brachyrhynchos_). In 1914 and 1915 alone

we lost five such birds. Some geese, swans and a pheasant complete the

short list of birds affected in addition to the crows. In no case was it

a young bird that was affected. Shipley[145] reports this parasite in

two grouse at the London Gardens, and Plimmer’s tables show that three

deaths were directly charged against them in one year[146].

EXTRA-INTESTINAL TAPEWORMS.—This discovery is worthy of record because

it is rare for cestodes to appear anywhere save in the intestines. We

have observed three instances where they had backed up into the bile

duct—twice in the Cape Hyrax (_Procaria capensis_) and once in a

Livingston’s Eland (_Taurotragus oryx livingstonii_). At the London

Gardens they were mentioned in the gall-bladder of a wallaby and in Cape

Hyraces. Beddard[147] carefully describes four new species of these

cestodes from the hyrax.

[Illustration:

FIG. 83.—PHYSALOPTERA IN STOMACH OF COMMON OPOSSUM (DIDELPHYS

VIRGINIANA). THIS IS NOT AN EXCEPTIONAL DEGREE OF INVOLVEMENT.

]

[Illustration:

FIG. 84.—ONE OF THE FIBROUS NODULES IN THE GASTRIC SUBMUCOSA OF AN

OPOSSUM. AN OVUM OF PHYSALOPTERA IS SEEN PRECISELY IN THE MIDDLE OF

THIS ILLUSTRATION.

]

TABLE 28.

_Occurrence of Blood Parasites._

(Adapted from Plimmer, nine year period)

_Animals examined—12,241 Mammalia—2,924 Aves—6,619 Reptilia—2,698._

══════════════════════════════════╤══════════════════╤════════╤════════

Parasite. │ Host │ No. │ %

│ │Infested│Infested

──────────────────────────────────┼──────────────────┼────────┼────────

1. Hemogregarines │Reptilia │ 316│ 11.8

2. Microfilaria │Mammalia │ 33│ 1.1

│Aves │ 191│ 3.

│Reptilia │ 24│ 1.

3. Hemoproteus │Aves │ 140│ 2.1

4. Trypanosomes │Mammalia │ 1│ 0.003

│Aves │ 28│ 0.4

│Reptilia │ 4│

│Amphibia │ 3│

5. Plasmodia │Mammalia │ 2│

│Aves │ 39│ 0.6

│Reptilia │ 5│

6. Leucocytozoa │Aves │ 16│ 0.2

7. Intestinal organisms[148] │Reptilia │ 16│ 0.5

8. Toxiplasma │Mammalia │ 1│

│Aves │ 1│

│Reptilia │ 1│

9. Spirochæta │Mammalia │ 1│

10. Babesia │Mammalia │ 1│

11. Hæmocystidium │Reptilia │ 1│

──────────────────────────────────┼──────────────────┼────────┼────────

Grand Total │ │ 824│

──────────────────────────────────┴──────────────────┴────────┴────────

SUMMARY OF TABLE 28.

═══════════════════════════════════╤═══════════╤═══════════╤═══════════

│Parasitized│ Animals │ %

│ │ examined │Parasitized

───────────────────────────────────┼───────────┼───────────┼───────────

Mammalia │ 39│ 2,924│ 1.5

Aves │ 415│ 6,619│ 6.5

Reptilia │ 367│ 2,698│ 14.0

───────────────────────────────────┼───────────┼───────────┼───────────

Total │ 821│ 12,241│ 6.7

───────────────────────────────────┴───────────┴───────────┴───────────

FILARIASIS IN WILD CATS (_Felis ruffus_).—This parasite was named

_Filaria fasciata_ because it coils in the fascia between the muscles—

generally those of the thigh and abdomen. The worms are easily detected

on skinning the animal and separating thigh and other muscles.

Microfilaria were always present in the blood. The grade of

pathogenicity is only conjectural.

PERITONEAL FILARIA IN MONKEYS.—Thread worms have been encountered eleven

times, largely in Cebidæ. In several instances _F. gracilis_ has been

the species identified, always inhabiting the peritoneal cavity, and in

one instance also the lung. Microfilaria were always present in the

blood. We have never seen lymphangitis or elephantiasis in our filarial

cases.

BLOOD PARASITES.—I justify this paragraph on the basis of the usefulness

it might have in the clinical direction, for while the taking of blood

specimens is not as easy as with man it can still be done with some

animals. From time to time we have encountered blood parasites in this

Garden, but the large numbers occurring in the experience of special

searchers in the London Garden and Plimmer’s particular interest in this

direction make their data much the more valuable. In one report of 6,430

animals examined he found 7 per cent. infested with blood parasites of

one sort or another. I have constructed the foregoing table (28) from

his various reports to show which animal classes were affected by the

several blood parasites.

This table (28) brings out that considering them as a whole and without

respect to host, just as the animals come day in and day out to the

autopsy table, blood parasites will be met in 6.7 per cent. of all

cases. They are seen most commonly in the form of hemogregarines of

reptiles (2.5 per cent. of all animals and 12 per cent. of all reptiles)

while microfilaria run a close second, being found in 2 per cent. of all

animals but much more commonly in birds. Hemoproteus of birds while

ranking third, should be emphasized on account of its acknowledged

blood-destructive properties. The remaining infestations were too

infrequent to be useful statistically.

Turning to individual groups of blood parasites, microfilariæ of birds

deserve special comment. They occurred four times more often in birds

than in other animals, or, put in another way, one out of every twenty-

two birds was affected, and only one out of every ninety other animals.

The high figure for birds is significant in relation to what we have

already said about periproventricular filaridæ in our Garden, indicating

that the same infestment probably also exists in London.

[Illustration:

FIG. 85.—ADAPTATION FROM RECONSTRUCTION OF TROPIDOCERCA CONTORTA. THE

WORM LAY IN THE WALL OF THE PROVENTRICLE OF A LOUISIANA HERON (ARDEA

TRICOLOR RUFICOLLIS).

]

[Illustration:

FIG. 86.—CESTODES (THREE) PROJECTING FROM THE SEVERED END OF THE BILE

DUCT OF A CAPE HYRAX (PROCARIA CAPENSIS).

]

A point brought out by Plimmer is to the effect that, of the several

blood parasites, the microfilariæ were the least harmful, and that of

these the adult forms were the only ones to produce symptoms; yet in one

place[149] he records microfilaria as plugging the cerebral capillaries

of birds. This is a very important lesion if permanent, and especially

so when affecting cerebral capillaries as do the organisms and pigment

of malaria. The adult forms were found in one-fourth of the cases where

microfilaria were demonstrated.

As to the pathogenicity of these blood parasites in general, it will be

unsafe to arrive at a definite conclusion, recalling the pitfalls that I

have already outlined in discussing pathogenicity of parasites in

general. Keeping in mind the wonderful adaptability on occasion of

animals to unfavorable circumstances we must hesitate to declare

unqualifiedly the importance of even blood parasites as morbid agents.

Where the parasite is known to destroy the blood cells of birds and

mammals it is otherwise, but even here experimental work would be

necessary to settle the question. The element of “racial” immunity and

of phylogeny is the fly in the ointment of our deductions.

TRANSMISSION OF ANIMAL PARASITISM FROM WILD ANIMALS TO MAN.

Examples of direct transmission will be only occasional, due to the

relatively infrequent contacts between the two hosts. Pets threaten the

most. Several such examples have been touched upon in the preceding

pages and it but remains to gather them into one place. There is one

concrete instance in the form of clear cut simian scabies being

transmitted to a keeper in this Garden[150] and a similar lot fell to

the keeper of a wombat at the Paris Garden[151] as well as to the

taxidermist who preserved its skin. We know that the skin and feathers

of our parrots and pigeons harbor mites[152] (plumicoles of Megnin) and,

recalling the occasional cases of poultrymen’s itch, a transient

affection might be conceded from pet parrots and other birds. Pediculi

are not as numerous on monkeys as popularly supposed—we see very few at

the autopsy table. We have seen _Trichinella spiralis_ in the polar bear

(_Ursus maritimus_)—an animal whose flesh is edible. The hydatid cysts

in the camel appear unimportant, but in the livers of deer it is

otherwise. Neither of these infestments is dangerous if the meat is

sufficiently cooked before eating.

Hookworm disease points thus far only to _Anchylostoma duodenale_ in the

chimpanzee and _Uncinaria ceylanicum_ in the lion and tiger. Both serve

as reservoirs of the disease, the ova being discharged by way of the

feces. Similarly the _Strongyloides intestinalis_ infestment which we

have seen in the orang might be transferred to man. Indirectly,

Europeans traveling in Africa have made the crucial test that certain

ungulates and other wild animals of Africa are the reservoirs of

_Trypanosoma gambiense_, the parasite of the well known African sleeping

sickness; for this example the blood stream of the beast is the

reservoir and a biting insect the means of transmission.

The above examples are cited to emphasize the possibility that parasites

of wild animals may have a pathogenic significance for man. They do not

exhaust the subject. Many more instances might be cited but the

foregoing bring out the important ones which have come to our attention.

TREATMENT.

The recognition of the existence of parasites during the life of an

animal, especially those of the skin and intestinal tract whose

discovery is easiest, suggests that some means of combating them should

be employed. But we are by now quite satisfied that medicinal and

disinfective therapeutic procedures, while they have their field of

usefulness, are much less to be depended upon for the protection of

exhibits than are preventive measures of general hygienic nature. Under

the latter heading come the prompt removal of excreta, frequent changes

of drinking water, routine examinations of feces of certain varieties,

autopsy examinations and incineration of autopsy remains—all of which

are part of the requirements of common cleanliness and general disease

prevention. I wish to amplify the matter of disposal of feces and

general cage-police. Our ideas as to what constitutes thoroughness in

this work have changed considerably since Fulleborn’s recent

demonstration that ascarid ova[153] could live in formaldehyde for four

or five years, and the older one of Galli-Valerio[154] that those of

_Hepaticola hepatica_ lived one month in 2 per cent. formaldehyde

solution. Evidently the same substances which disinfect do not

invariably disinfest; and if the occasion should arise for the most

exacting control in this respect, a special investigation of the

susceptibility of the individual ova in question would have to be

undertaken.

In addition to these general measures we have put up certain special

safeguards against parasites. Thus, each specimen of the large Carnivora

(lions, tigers, leopards, etc.), has received routinely a dose of

santonin every month over a period of several years. We have no figures

on which to base comparison with previous periods, but an examination of

feces of all the inmates of the Carnivora house in 1916[155] showed that

less than one-third of the animals were infested, and of these all save

the jaguars showed either small numbers of ova in the feces or

relatively non-pathogenic forms. The jaguars had been badly infested for

many years with dibothriocephalus. Prior to this examination we had been

under the impression that nearly every one of the felidæ ordinarily was

infested and if this impression was well founded, due credit must be

given, in company with general hygienic precautions, to the routine

santonin dosages. It goes without saying that where animals are detected

at autopsy with unequivocal transmissible and dangerous parasites

(coccidia, amebæ, etc.), the contacts are isolated, examined and if

necessary treated for the affection or even sacrificed.

To continue the preventive measures, it would be most desirable to

examine at least the blood and feces of all newly arrived animals, but

at present this is not practicable on account of the labor involved in

the laboratory and in collecting the material, and because all animals

do not stand the restraint involved when blood specimens are being

taken. At present we are limiting special examinations to the droppings

of newly arrived parrots and toucans for _Spiroptera incerta_ and to the

feces of certain monkeys for amebæ.

Further preventive measures will depend on the nature of individual

infestments as they crop up. Food inspection, screening, sulphur dips,

etc., are but a few examples of what might be found necessary

hygienically after investigating or establishing the life cycle of our

numerous parasitic groups. However we cannot forbear to emphasize again

the value of the blast lamp and of paint in the hygiene of animal

enclosures—means we believe to be much more potent and quite as

practicable as chemical disinfectants.

[Illustration:

FIG. 87.—TRICHINELLA SPIRALIS IN MUSCLES OF POLAR BEAR (URSUS

MARITIMUS). THIS WAS AN OLD INFESTMENT, AS INDICATED BY THE THICK

AND HYALOID CHARACTER OF THE CAPSULE.

]

Turning now to the active curative side of the subject, what medical

means we have against parasites appertain for the most part to the

intestinal ones. The treatment of tapeworms is very hazy and

unsatisfactory—areca nut is perhaps more useful in animals than any one

other drug. For round worms santonin is most to be depended on although

turpentine is useful against the round worm of the Equidæ. The dosage of

santonin per month has been—for large bears, ten grains; for lions,

tigers, large pumas, six grains; for jaguars, leopards, hyenas, four

grains; for wild cats, etc., two grains. The dose of areca nut

recommended for Carnivora is two grains per pound of body weight. Since

ungulates do not stand areca nut well, iron sulphate may be used. For

animals the size of a horse the dosage is two drams, and to this one or

two grains of arsenic trioxide may be added. On the basis of very

carefully controlled experiments on dogs, Hall recommends carbon

tetrachloride for hookworms in these animals—0.3 mils per kilo of body

weight, without purging. Its efficacy has been confirmed lately but we

have not had the occasion to test it.

From time to time we have broached other lines of medication against

worms which may be worth while relating if for nothing more than to

illustrate the uncertain ways of our vermifuges when applied to wild

animals.

I can speak first of thymol as employed on parrots parasitized by

_Spiroptera incerta_. The first thing that impressed us was the large

dosage which birds could endure. The lethal dose for pigeons was four

grains, suspended in mucilage of acacia. After we had established that

certain parrots withstood fourteen grains in mucilage, we administered

on one occasion twelve grains and on another sixteen grains, suspended

in glycerin. The drug is reputed to be absorbed when exhibited in the

latter vehicle and we hoped to get a certain anthelmintic effect on the

parasites from the blood side as well as from the lumen of the gut. The

bird itself, a very heavily infested cockatoo, showed no ill effects and

passed two dead female spiroptera and enormous numbers of ova. But

thereafter it passed even greater numbers of ova than before (we

estimated 182,000 per day for this bird over a five day period and

288,000 on a single subsequent day), and was obviously unimproved by the

treatment. The explanation of failure was clear, for the worms can

retire into the protecting mucus or mucous membrane lining the

proventricle until the thymol has passed by, and even though paralysed

may not be flushed out. In a later test on a toucan which died twenty

minutes after thymol administration we found at the autopsy that worms

deeply imbedded in the proventricle were translucent and motionless from

the effects of the thymol-glycerin mixture, _i.e._, saturated with the

medicament and apparently dead. Twenty minutes later they were placed in

normal salt solution in the incubator, and next morning were found

actively motile. Thymol evidently does not kill—it only stupefies, and

in the absence of means for flushing the parasites out, as we do in

human hookworm cases, this class of vermifuge will have to be abandoned

in work against this parasite.

Not with any serious hope of success, but feeling that arsenic was the

most promising drug available for parenteral use, we tried atoxyl

hypodermically and arsphenamine intravenously but without success. The

only positive results were to emphasize the tolerance of some lower

animals to arsenic. Thus in preliminary work pigeons received sixty

drops of Fowler’s solution by mouth without embarrassment, but five

minims killed a pigeon when administered hypodermically. The organic

arsenical, arsphenamine, was withstood intravenously by pigeons in six

times the proportional human dosage.

One of our drug trials was instructive in that it worked quite a

different effect from that in man, besides being most amusing. In

earlier diagnostic work on spiroptera we tested the practicability of

examining the vomitus for the worms, hoping thereby to get a greater

concentration of ova, which would facilitate the microscopic

examination. Hypodermic injections of apomorphine (0.1 grain) into an

amazon did not induce vomiting from the gizzard as hoped—only a

regurgitation from the crop, but it did cause some dizziness and most

ludicrous talking and laughter.

To illustrate further the difficulties of animal medication I quote our

experience with four red howling monkeys (_Alonatta seniculus_). One of

these died of intestinal obstruction from large ascarids—the case which

has been already cited. Ova were found in the stools of the remaining

three, and one of the monkeys was treated twice with santonin. It died

in thirty hours after the second dose—not of santonin poisoning, for

none of the clinical symptoms were present, but most likely from

absorption of toxic substances originating in the decomposing ascarids

which crowded the gut. It profits not to destroy these parasites, then,

unless we feel assured that they may thereafter be removed immediately.

If, for the sake of brevity, I were asked to state in a single sentence

the practical status of animal parasitic disease in this Zoological

Garden I would put it thus: Since there are various animal parasitic

diseases continuously present here of which we know, and since fresh

ones are from time to time cropping out, and since these are on the

whole of economic importance, it behooves us to continue and extend our

efforts against an issue extant—somewhat through therapeutic means, but

far more through clinical laboratory examinations, careful autopsy

searches, and by rigid general hygienic measures such as cage-police,

new quarters, isolation, or if necessary, destruction of the exhibit.

INDEX

Abortion, 305

Abscess of liver, 231

of lung, 155

Acariasis, lungs, 647

of monkeys, 647

Actinomycosis, 138, 568

in deer, 368, 568

tapirs, 568

treatment, 570

Adenoma, 474

Adrenal body, 336

Alimentary tract, 166

Amblyopia, 403

Amœbæ, 606, 644

dysentery from, 644

Amyloid, liver, 227

spleen, 128

Anatomy of labor, 290

Anchylostomum, see hookworms

Anemia, 87

primary, 98

secondary, 88

Aneurysms, 65, 80

Animal Parasitism, hygiene, 656

prevention, 656

treatment, 655

Animal Parasites, 614

disappearance of, 627

frequency, 628

of groups, 633

in blood, 652

incidence, 628–636

modes of action, 617

occurrence in wild, 627

transmission animals to man, 653

visceral distribution, 637

Angina pectoris, 49

Aorta, 72

fatty deposits in, 71

Arteries, 66

Arteriosclerosis, 71

Arteritis, 70

Arthritis, 347

gouty, 347, 411

Ascending nephritis, 276

Aspergillosis, 558

Aspergillus, varieties, 558

Ataxia, 375

Atrophy, acute of liver, 228

Autopsy list, 47

Avian spiropteriasis, 172, 640

Bacterial flora, 418

Basal cell carcinoma, 475

Beriberi, 439

Biliary tract, 225

calculi, 238

Birth canal, 287, 296

comparative anatomy, 287 et seq

obstructions to, 306

Blackhead, 206

Bladder, gall, 224, 238, 239

urinary, 286

Blood, diseases of, 83

Blood formation in birds, 98

Blood vessels, 66

Bone marrow, 83, 109, 111

Bones, diseases of, 343

effects of trauma, 343

tumors of, 368

Botryomycosis, 564, 602

Botulism, 604

Brain, 385

tuberculosis of, 378

tumors of, 384

weight of, 385

references to, 387

Breast, 312

Bronchi, 141

Bronchiectasis, 144

Cage palsy, 349

Calculi, biliary, 238

renal, 282

Carcinoma, 476

basal cell, 475

Cataract, 403

Cecum, 211

Cestodes, 637

Cholangitis, 239, 256

Cholecystitis, 239

Choledochitis, 239

Cholelithiasis, 238

Chondroma, 472

Cloaca, 211

Coccidiosis, 606

Cirrhosis of liver, 232

Comparative anatomy of uterus, 287

of pelvis, 297–303

Conjunctivitis, 402

Constipation, 209

Constitutional diseases, 410

Convulsions, 373

Cornea, 403

Coronary arteries, 49

Cowper’s gland, 313

Cretinism, 320, 331

Cysticercus tenuicollis, 647

Cystitis, 286

Cytoleichus penrosei, 647

Deficiency diseases, 438–443

Degenerations of kidney, 269

of liver, 228

Diabetes, 412

Diet, carnivorous, 452

herbivorous, 452

grain, 455

seed, 454

soft, 453

omnivorous, 402

relation to disease, 415

alimentary tract, 417

Dilatation of heart, 54

Diphtheria, 600

Dislocations, 345

Distemper, 599

Diverticula of intestine, 219

Diverticulitis, 219

Dysentery, amœbic in monkeys, 644

Dystocia, 292

Ear, 409

Echinococcus, 647

Emphysema, 161

Encephalomyelitis, 380

Endocarditis, 52

Endometritis, 305

Endothelioma, 165, 474

Enteritis, 177

in Aves, 202, 205

Mammalia, 185

Enterohepatitis, 605

Epithelioma, 475

Esophagus, 169

Exophthalmic goitre, 320, 323, 329

Eye, 402

tuberculosis of, 402

Fallopian tubes, 305

Fat infiltrations of kidney, 268

liver, 226

metabolism, 445

Fibroma, 472

Filaria, fasciata, 651

gracilis in monkeys, 651

in blood, 652

fascia, 651

muscles, 651

wildcats, 651

periproventricular, 648

peritoneum, 651

Food, 415

definition, 415

in relation to alimentary tract, 417

Food, disease, 422

poisoning, 457

Fowl cholera, 598

plague, 598

typhoid, 598

Fractures, 344

Gall stones, 238

Gas-bacillus infection, 602

Gastritis, 204

Gastroenterocolitis in Ungulata, 194

in Marsupialia, 198

Gangrene of lung, 155

Giraffe, hookworm in, 644

Gout, 53, 410

Heart, dilatation of, 54

hypertrophy of, 54

diseases of, 48

effects of, 55

effect of strain, 55–59

weight of, 63

relative vulnerability of, 61

Hemorrhagic septicemia, 598

Hemoglobinuric fever, 603

Hemorrhoids, 218

Hepaticola hepatica, 641

Hepatitis, 228

Hernia, 216

Heterakis in avian ceca, 606

Hookworms, 643, 654

in giraffe, 644

Hypernephroma, 339, 341, 342, 475

Hypertrophic periosteitis, 346

Hyperthyroidism, 320

Hypertrophy of heart, 54

in Aves, 60

Hypothyroidism, 320

Ileus, 213, 261

Infantilism, 433

Infiltrations of kidney, 268

liver, 226

Inorganic salts in diet, 427

Intestinal obstruction, 212

tract, 177

inflammation of, 181

mechanical obstruction of, 212, 617

relation to food, 422

Intestines, diverticula, 219

tumors of, 220

Iridocyclitis, 402

Kangaroo disease, 570

bacteriology, 576, 586

course of attack, 573

pathology, 575

prevention, 572

treatment, 591

Kidney, 263

abscess, 268, 278

calculi, 282

degenerations of, 269

hemorrhages, 271

hypertrophy of, 267

infiltrations of, 268

tumors, 284

weight of, 265

Labor from a comparative standpoint, 290

obstructions to, 306

Laryngitis, 139

Larynx, 138

Leontiasis ossium, 359, 472

Leucemia, 104

in birds, 108

lymphatic, 105

myeloid, 109

Leucocytes, 84–86

Limberneck of ducks, 604

Lipoma, 472

Liver, 222

abscess, 231

acute atrophy, 228

amyloid, 227

cirrhosis, 232

degenerations, 228

fatty changes, 226

infiltration, 226

inflammation, 228

chronic, 232

necrosis in, 230

tumors, 240

Lungs, 146

abscess, 155

congestion, 148

gangrene, 155

infarct, 160

tumors of, 162

Lymphadenitis, 117

Lymphatic leucemia, 105

tissue, 114

hyperplasia of, 115

in pharyngeal wall, 115, 138

Lymph nodes, 114

tuberculosis of, 121

tumors of, 122

Lymphomatosis, 118

Malnutrition, 424

Mammary gland, 312

Marmosets, parasites of, 645

Marrow of bone, 83, 109, 111

Meningitis, 376

Metabolism, carbohydrate, 443

fat, 445

inorganic, 427

protein, 447

Miliary tubercle, avian, 512

bovine, 510

human, 511

monkey, 511

Miscarriage, 305

Molluscum contagiosum, 601

Mönckeberg sclerosis, 74, 76

Monkey’s temperature, 520–528

Moon blindness, 405

Muscles, 370

Mycosis, 137, 558

of esophagus, 168

histology of, 561

hygiene, 563

incidence, 562

of lung, 562

method of action, 560

pharynx, 168, 564

types of, 560

Myelitis, 350, 381

Myeloma, 111

Myocarditis, 52

Myocardium, 49, 50, 65

Myxœdema, 320, 331

Necrosis, liver, 230

spleen, 130

Nematodes, 636

Neoplasms, 462

incidence of, 463, 468

embryonic origin, 471

in captivity, 469

in the wild, 462, 476

metastasis, 471

visceral origin, 477

Nephritis, 271

ascending, 276

effects of, 280

histology of, 279

toxic, 275

Nervous system, 372

Nocardia macropodidarum, 585

Nocardiosis, 570

Obesity, 446

Ophthalmia, periodic, 405

Osteitis, 346

Osteitis deformans, 359, 431

Osteoma, 368

Osteomalacia, 349

Ovary, cysts, 307

Pachymeningitis, externa, 331, 377

Paget’s disease, 359, 431

Pancreas, 244

degenerations, 250

tumors, 259

Pancreatitis, 250

Parasites, see animal parasites, 614

Parovarian cyst, 307

Pasteurelloses, 597

Pearl disease, 491, 501, 505

Pellagra, 441

Pelvis, comparative anatomy, 297–303

Penis, 313

Pericarditis, 53

Pericardium, position of effusion in, 54

Periosteitis, hypertrophic, 346

Periproventricular worms, 648

Perisplenitis, 131

Peritoneum, 260

tumors, 262

Peritonitis, 260

Pharyngitis, 168

Pharynx, 168

Phimosis, 313

Physaloptera turgida, 649

in opossums, 649

Plants, poisonous, 459

Pleura, 163

Pleuritis, 164

Pneumonia, 149

broncho, 152

fibrinous, 151, 153

in Aves, 153

origins of, 154

lobar, 151

Pneumonokoniosis, 159

Pneumonyssus foxi, 647

Poisonous plants, 459

Poliomyelitis, 380

Prostate gland, 313

enlargements of, 314

tuberculosis of, 315

tumors of, 314

Proventricle, 171

worms in, 172, 640

Psittacosis, 208, 597

Pyelonephritis, 277

Quail disease, 608

Rabies, 602

Rachitis, 349, 429

Rectum, prolapse of, 218

Reproductive organs, female, 287

male, 317

Respiratory tract, 134

Rhinitis, 135

Rickets, 349, 429

Renal calculi, 282

Salpingitis fallopii, 305

Santonin, 657

Sarcoma, 471, 474

Scurvy, 440

Seminal vesicles, 315

Sinusitis, 135

Skeleton, 343

Spinal cord, 373

Spiroptera incerta, 638, 640

detection, 640

eradication, 640

in parrots, 172, 208, 640

Spiropteriasis, 172, 640

Spleen, 114, 122

amyloid, 128

congestions, 125

enlargements, 124

hemorrhage, 125

inflammation, 126

in anemia, 130

in hepatic cirrhosis, 130

necrosis, 130

size, 124

tuberculosis of, 132

Squirrel monkeys, parasites of, 645

Starvation, 425

Stomach, 174

tumors of, 176

ulcers of, 175

Streptothricosis, 567

Suprarenal body, 336

Syngamus trachealis, 140, 650

Tænia echinococcus, 647

Tape worms, 637

in liver, 650

Temperature of monkeys, 520–528

Testes, 313

tumors of, 313

Tetanus, 602

Thrombosis, 69

Thymol, 657

Thymus, 120, 336

Thyroid body, 316

atrophy of, 330

hyperplasia of, 325

size of, 318

tumors of, 333

Tonsils, 115, 138

Trachea, 140

Tropidocerca contorta, 649

Tubercle bacillus, types of, 513

Tuberculin test on monkeys, 518

other animals, 549

dose, 529

effect on kidneys, 548

eye, 546

reaction, 530

skin, 546

Tuberculoma, 505

Tuberculosis of brain, 378

avian characters, 503, 512

Carnivora, 498

control, 514–548

diagnosis of, 514

discovery during life, 514

distribution in birds, 504

Tuberculosis of eye, 402

gelatinous, 504

histology, 510

hygiene, 516

in Aves, 503

in Mammalia, 492

in Primates, 492

in various avian orders 506–510

incidence, 489

intestinal in birds, 505

Lemures, 495

lymph nodes, 121, 494

nonsusceptible animals, 490

ordinate characters, 492

frequency, 489

pathological type, 490

Proboscidea, 502

Rodentia, 499

routes of infection, 485

Tuberculosis, sanitation of cages, 516

susceptible animals, 490, 515–517

Ungulata, 500

visceral distribution, 491

Tumors, see neoplasms

Ulcer, gastric, 175

Uncinaria, 643

Uremia, 281

Urethra, 315

Uterus, comparative anatomy, 287

inflammation, 305

tumors of, 308

Vitamins, 438

Waterfowl epizootic, 604

Zoological list, 43

A LIST OF THE PUBLICATIONS FROM THE LABORATORY OF COMPARATIVE PATHOLOGY

OF THE PHILADELPHIA ZOOLOGICAL SOCIETY 1909–1923

1. Results of Tuberculin Tests in Monkeys at the Philadelphia

Zoological Garden, by C. Y. White, M.D. and Herbert Fox, M.D.

_The Archives of Internal Medicine_, December, 1909, Vol. 4, pp.

517–527, Chicago, Illinois.

2. Note on the Occurrence of a Ciliate (_Opalinopsis nucleolobata,

n.s._) in the Liver of a Mammal (_Canis latrans_), by Allen J.

Smith, M.D. and Herbert Fox, M.D. _University of Pennsylvania

Medical Bulletin_, February, 1909, Philadelphia, Pennsylvania.

3. The Tuberculin Test in Monkeys: with Notes on the Temperature of

Mammals, by Arthur Erwin Brown, D.Sc., C.M.Z.S., Sec. Zool.

Soc., Phila. _Proceedings of the Zoological Society of London_,

1909, pp. 81–90.

4. Observations on the Occurrence of Neoplasms in Wild Animals, by C.

Y. White, M.D. and Herbert Fox, M.D. _Proceedings of the

Pathological Society of Philadelphia_, February, 1910.

5. Observations on the Comparative Anatomy of the Female Genitalia,

by Edward A. Schumann, M.D. _American Journal of Obstetrics and

Diseases of Women and Children_, Vol. LXIV, No. 4, 1911, New

York.

6. Observations Upon Neoplasms in Wild Animals in the Philadelphia

Zoological Garden, by Herbert Fox, M.D. _The Journal of

Pathology and Bacteriology_, Vol. XVII. (1912), pp. 217–231.

England.

7. A Study of Metazoan Parasites Found in the Philadelphia Zoological

Garden, by Fred D. Weidman, M.D. _Proceedings of the Academy of

Natural Sciences of Philadelphia_, March, 1913, pp. 126 to 151,

Philadelphia, Penna.

8. The Pathology of the Thyroid Gland in Wild Animals, by Herbert

Fox, M.D. _Journal of Comparative Pathology and Therapeutics_,

Vol. 27, p. 23. Edinburgh, Scotland.

9. The Mechanism of Labor From the Standpoint of Comparative Anatomy,

With a Report of Cases of Dystocia in Wild Animals, by Edward A.

Schumann, M.D. _American Journal of Obstetrics and Diseases of

Women and Children_, Vol. LXIX, No. 3, 1914, New York.

10. Cirrhosis of the Liver in Wild Animals, by Herbert Fox, M.D. _New

York Medical Journal_, December 19, 1914.

11. The Dynamics of the Female Pelvis; Its Evolution and Architecture

with Respect to Function, by Edward A. Schumann, M.D. _American

Journal of Obstetrics and Diseases of Women and Children_, Vol.

LXXI, No. 1, 1915, New York.

12. _Pneumonyssus foxi, Nov. Sp_. An Arachnid Parasitic in the Lung of

a Monkey (_Macacus rhesus_), by Fred D. Weidman, M.D. _Journal

of Parasitology_, September, 1915, Vol. II, pp. 27–45, Urbana,

Illinois.

13. _Cytoleichus penrosei_, A New Arachnid Parasite Found in the

Diseased Lungs of a Prairie Dog, (_Cynomys ludovicianus_).

_Journal of Parasitology_, December, 1916, Vol. III, pp. 82–89,

Urbana, Illinois. Fred D. Weidman, M.D.

14. A Method of Obtaining Duplicate Reconstructions from the One

Series of Wax Plates, by Fred D. Weidman, M.D. _New York Medical

Journal_, March 3, 1917, New York.

15. Papers: Read at the Meeting of the Pathological Society at the

Philadelphia Zoological Garden.

Pancreatitis in Wild Animals, by Herbert Fox, M.D.

Report of an Enzootic of Parasitic Proventricular Worms

(_Spiroptera incerta_, Smith) of Parrots, with Control of Same,

by Fred D. Weidman, M.D.

_Coccidium bigeminum_, Stiles, in Swift Foxes (habitat Western U.

S.), by Fred D. Weidman, M.D.

Distribution of Uncinaria Among the Lower Animals, by Fred D.

Weidman, M.D.

An Arachnoid (_Pneumotuber macaci_, Landois and Hœpke?) Parasitic

in the Lungs of a Monkey (_Macacus rhesus_), by Fred D. Weidman,

M.D.

A Note Upon the Lesions of the Female Genitalia in Wild Animals,

by Edward A. Shumann, M.D.

Amblyopia in a Young Monkey (_Macacus nemestrinus_), by H. M.

Langdon, M.D. and W. B. Cadawalder, M.D.

Remarks on Examinations of a Series of Brains, by W. B.

Cadawalder, M.D.

_Journal of Comparative Pathology and Therapeutics_, December,

1915, Vol. XXVIII, Part 4, pp. 298–336, Edinburgh, Scotland.

16. Reversionary Pseudobile Canaliculi Formation in the Cirrhotic

Liver of a Vulpine Phalanger, by Fred D. Weidman, M.D. _New York

Medical Journal_, March 9, 1918, New York.

17. A Contribution to the Anatomy and Embryology of _Cladorchis_

(_Stichorchis_) _Subtriquestrus_, Rudolphi, 1814 (Fischoeder,

1901), by Fred D. Weidman, M.D. _Parasitology_, Vol. X, No. 2,

January 22, 1918, Cambridge University Press, London, England.

18. Nutritive and Blood Changes in Rats on Cancer-Inhibiting and

Cancer-Stimulating Diets, by E. P. Corson-White, M.D.

_Pennsylvania Medical Journal_, March, 1919, Vol. XXII, p. 348,

Athens, Penna.

19. Pemphigus in an Orang Utan Infested with Strongyloides

(intestinalis?) and Dying from Advanced Tuberculosis, by Fred D.

Weidman, M.D. _Journal of Cutaneous Diseases_, March, 1919, Vol.

XXXVII, pp. 169–173, Chicago, Ill.

20. Arteriosclerosis in Wild Animals, by Herbert Fox, M.D. _American

Journal of Medical Sciences_, June, 1920, No. 6, Vol. CLIX, p.

821, Philadelphia, Penna.

21. Osteomalacia in Wild Animals, by E. P. Corson-White, M.D.

_Archives of Internal Medicine_, November, 1922, Vol. 30, pp.

620–628, Chicago, Illinois.

22. Osteitis Deformans in Monkeys, by E. P. Corson-White, M.D.

_Archives of Internal Medicine_, December, 1922, Vol. 30, pp.

790–796, Chicago, Illinois.

23. Certain Dermatoses of Monkeys and an Ape, by Fred D. Weidman, M.D.

_Archives of Dermatology and Syphilology_, March, 1923, Vol. 7,

pp. 289–302, Chicago, Illinois.

24. Acute Papular and Desquamative Exanthem in an Orang Utan, by

Herbert Fox, M.D., and Fred D. Weidman, M.D. _Archives of

Dermatology and Syphilology_, April, 1923, Vol. 7, pp. 462–464,

Chicago, Illinois.

-----

Footnote 1:

Those who are interested in the subject of disease in its effect on

evolution are referred to Morley Roberts, _Proceedings, Zoological

Society, London_, 1918, p. 247.

Footnote 2:

_Proceedings, Zoological Society, London_, 1911.

Footnote 3:

_Proceedings, Zoological Society, London_, 1911, p. 425.

Footnote 4:

_Proceedings, Zoological Society, London_, 1911, p. 620.

Footnote 5:

_Br. Med. Jour._, 1910, 2, 1161.

Footnote 6:

_Proc. London Zool. Soc._, 1907.

Footnote 7:

Total is the number of individual animals showing lesions, not the sum

of the listed changes.

Footnote 8:

_Comptes Rendus Soc. Biol._, T, 62–206.

Footnote 9:

This is done by determining the percentages of hypertrophy and

dilatation for the total number of each class examined at autopsy.

Footnote 10:

_Arch. für. Ges. Physiologie_, 1908, 125, 507

Footnote 11:

dal Piaz: Papers from the Department of Anatomy, University of

California, 1912. Bergmann: _Dissertation_, Munich, 1884. Loer: _Arch.

f. die gesamte Physiologie_, 1911, V. 140–293. Grober: _Arch. f. die

gesamte Physiologie_, 1908, V. 125–507. Grober: _Deutsch Archiv f.

Klin. Med._, 1907, V. 91, 502. Welcher and Brandt: _Arch. für

Anthropologie_, 1903, V. 28. Vierordt: _Tabellen_, 1906. Parrot:

_Zoologischer Jahresbericht_, 1893. Hasenfeld and Romberg: _Arch. f.

Exp. Path. und Pharmacol._, 1897, V. 39–333. Joseph: _Jour. Exp.

Med._, 1908, V. 10–521.

Footnote 12:

These values are obtained in part from the literature, in part from

our own specimens. At this laboratory the hearts of animals killed or

dying from a short illness, organs showing no pathological change,

were removed by cutting at the base of the vessels, washed free of

blood and weighed. The weight of the whole animal was obtained after

death.

Footnote 13:

These figures are obtained by determining mathematically the

percentage of each feature in each class and then reducing the numbers

to their lowest value.

Footnote 14:

_Verh. deutsch Path. Gesel._, 1906, X, 149.

Footnote 15:

With Coronary sclerosis only.

Footnote 16:

With Coronary sclerosis only.

Footnote 17:

_Proc. London Zool. Soc._, 1916.

Footnote 18:

_The Leucoses of Fowls_, London, 1922.

Footnote 19:

Lubarsch-Ostertag, _Ergeb. aus der Allg. Path._, 1908.

Footnote 20:

Vide Sisson’s _Veterinary Anatomy_ and Owen’s _Anatomy of the

Vertebrates_.

Footnote 21:

Ball, _Jour. Vet._, 1907.

Footnote 22:

See Magnan, _Compt. Rendus d. l’ Acad. de Science_, 1910 and 1911,

Vol. 150, 151, 152.

Footnote 23:

_C. R. Soc. de Biologie_, Paris, T. 73–526. _Bull. Mus. Hist. Nat.,

Paris Ann._, 1911, 492 et seq.

Footnote 24:

See Woodland, _Proc. London Zool. Soc._, 1906, and MacLeod, _Chemical

and Physiological Medicine_, Chicago, 1923.

Footnote 25:

_Proc. Zool. Soc. London_, 1905.

Footnote 26:

_Bull. Soc. Anat._, 1898, 73, 491

Footnote 27:

_Amer. Med._, 1903, 996

Footnote 28:

_Surg. Gyn. and Obst._, 1919, 28, p. 529.

Footnote 29:

_Jour. A.M.A._, 1921, 77, 194.

Footnote 30:

_Ibid._, 197.

Footnote 31:

Garrod, _Schorstein Lect._, 1920.

Footnote 32:

_Anatomical Record_, 1917, 13, p. 305, On the morphology of the renal

tubule in the vertebrates.

Footnote 33:

Policard, _C. R. Assoc. Anat._, 1910, 12, 57.

Footnote 34:

Huber, _Anat. Record_, 1916, 10, 201.

Footnote 35:

_Bull. Mus. Hist. Nat._, 1911, 493 and 1912, 527, and C. R. Acad. Sc.,

155, 182.

Footnote 36:

_C. R. Soc. Biol._, 1898, 5, 188.

Footnote 37:

_Monatsh._, 1893.

Footnote 38:

_Inaug. Diss. Giessen_, 1911.

Footnote 39:

_Arch. f. Tierheilk._, V. 38–99.

Footnote 40:

Comparative Anatomy of the Female Genitalia, _Am. Jour. of Obstet._,

Vol. LXIV, No. 4, 1914. Mechanism of Labor from a Comparative

Standpoint, _Ibid._, Vol. LXIX, No. 4, 1914. Dynamics of the Female

Pelvis, its Evolution, etc., _Ibid._, Vol. LXXI, No. 1, 1915.

Footnote 41:

_Proc. L. Z. Soc._, 1919, p. 16.

Footnote 42:

_Journ. Phys._, Vol. 34, 295.

Footnote 43:

_Am. Jour. Phys._, Vol. 30, 129.

Footnote 44:

Carlson, Rooks and McKie, _Loc. cit._

Footnote 45:

Vincent and Jolly, _Loc. cit._

Footnote 46:

See Blair and Brooks, Osteomalacia of Primates in Captivity, _Ninth

Annual Report, New York Zoological Society_, 1904, p. 135.

Footnote 47:

Campbell and Cleland, _Jour. Comp. Path. and Ther._, Vol. 32, p. 95.

Footnote 48:

_Med. Chir. Trans._, Vol. 60, 37, 1877.

Footnote 49:

_These de Lyon_, 1901.

Footnote 50:

_Verein Freibürger Aerzte_, May, 1902.

Footnote 51:

_Arch. f. Wiss. u. Prak. Tierhk._, Vol. 36, 652, 1910, and Vol. 39,

164, 1913.

Footnote 52:

_Vet. Med. Inaug. Diss. Giessen_, 1913.

Footnote 53:

_Traite d’ Anatomie Path._, 1883.

Footnote 54:

_Jour. Med. Res._, Vol. 24, 43, 1911.

Footnote 55:

_Publ. Jefferson Med. College_, Vol. 6, 1, 1915.

Footnote 56:

We have observed later, however, one case with very definite

degenerative arterial disease; it will be discussed under the

affections of the eye since the most definite and indeed only lasting

sign of trouble was amblyopia, the attack being ushered in by a

nondescript fit.

Footnote 57:

_Chemistry of the Proteins_, Mann.

Footnote 58:

_Ann. Inst. Past._, 1899, XIII, 558, and _Skandinavisches Arch. f.

Physiol._, 1904, XVI, 249.

Footnote 59:

_Skandinavisches Arch. für Physiologie_, Vol. 17, p. 211, 1905.

Footnote 60:

_Jour. Physiologie et Path._, Vol. 14, 108, 1912.

Footnote 61:

_Carnegie Institute Publication_, No. 203, p. 247, 1915.

Footnote 62:

_Jour. Biol. Chem._, Vol. 14, p. 59, 1913.

Footnote 63:

_Publication of the Jefferson Medical College and Hospital_, Vol. 6,

p. 1, 1915.

Footnote 64:

_These de Lyon_, 1901.

Footnote 65:

_Verein Freiburger Aerzte_, May 30, 1902.

Footnote 66:

_Vet. Med. Inaug. Diss. Giessen_, 1913.

Footnote 67:

_Chemistry of Food and Nutrition_, Macmillan, 1918.

Footnote 68:

Ohio Agricultural Experiment Station Bull., 295.

Footnote 69:

_Skandinavisches Archiv. f. Physiologie_, Vol. 17, p. 211, 1905.

Footnote 70:

_Bull._, 185, Experiment Station, U. S. Dept. Agriculture, 1907.

Footnote 71:

_Physiological and Pathological Chemistry_, Blakiston, 1902.

Footnote 72:

_Journ. Physiol._, 1912, XLIV, 425.

Footnote 73:

Die Vitamine und ihre Bedeutung für die Physiologie und Pathologie mit

besonderer Berücksichtigung der Avitaminoses, Wiesbaden, 1914.

Footnote 74:

_Newer Knowledge of Nutrition_, Macmillan, 1919.

Footnote 75:

_Bull._, 34, Bureau of Amer. Ethnology.

Footnote 76:

_Jahrhuch. Kinderheilk._, 1904, LIX, 175.

Footnote 77:

_Journ. Am. Med. Assoc._, 1917, LXVIII, 1516.

Footnote 78:

_Arch. Path. Anat._, 1897, CXLVIII, 523.

Footnote 79:

_Lancet_, London, March 12, 1910, 733.

Footnote 80:

_Lancet_, London, 1911, II, 1266.

Footnote 81:

_Bull._, Dept. of Agriculture, Dec. 13, 1915.

Footnote 82:

Bureau of Animal Industry, 1895–96, 172.

Footnote 83:

_Z. Hyg. u. Infektionskrankh._, 1913, LXXV, 334.

Footnote 84:

_Jour. Biol. Chem._, 1917, XXXI, 229.

Footnote 85:

_Jour. Infect. Dis._, 1916, XIX, 478.

Footnote 86:

_Jour. A.M.A._, 1922, 79, 2132.

Footnote 87:

_Pflüger’s Arch._, 1909 (129), 63.

Footnote 88:

_Chemical Pathology_, Philadelphia, 1918.

Footnote 89:

These botanical names are taken from Chestnut’s _Poisonous Plants of

America._

Footnote 90:

_Textbook of Histology_, 1920.

Footnote 91:

_Zeitch. für Krebsforsch_, Vol. 15, p. 1.

Footnote 92:

_Proceed. Phila. Path. Soc._, 1910, and _Journal of Pathology and

Bacteriology_, Vol. XVII, 1912.

Footnote 93:

Figures in parentheses are numbers of animals with captivity known.

Footnote 94:

See Gould’s _Birds_, Vol. II, p. 83.

Footnote 95:

_Am. Jour. Med. Soc._, 1907, 133–769.

Footnote 96:

_Jour. Path. and Bact._, Vol. XVII, 1912.

Footnote 97:

Totals and percentages for class, including all members.

Footnote 98:

Grand Totals, all autopsies.

Footnote 99:

Totals used for analysis after deduction of cases insufficiently

described.

Footnote 100:

_Rev. de Med. Vet._ T. 89, p. 221.

Footnote 101:

White and Fox, _Archives of Internal Medicine_, 1909, Vol. IV, p. 517.

Footnote 102:

The temperature in the axilla is often .5°F. higher than by rectum,

but the difficulties of the axillary method render it impracticable.

Footnote 103:

A. E. Brown, _Proc. London Zool. Soc._, June, 1909, p. 81.

Footnote 104:

Simpson and Galbraith, _Trans. Royal Soc._, Edinburgh, XIV, p. 1, 65,

1906.

Footnote 105:

This term will be used in the following pages to mention the organism

since by many persons it is better known than Nocardia and moreover

describes the form better. I believe genus Nocardia is the correct

nomenclature for reasons given on a subsequent page.

Footnote 106:

Those interested in the investigation of the cause of Blackhead are

referred to the recent literature by Tyzzer and by Smith, in the

_Jour. of Exp. Med._ and _Jour. of Med. Research_, 1918–1922.

Footnote 107:

There are certain exceptions to this, as with Nicoll’s (_Proc. Zool.

Soc. London_, 1912, p. 858) careful search for trematodes with sieves,

but this means a separate research, and is incompatible with the all-

round, general policies of present routine laboratory organization.

Footnote 108:

_Phila. Zool. Soc. Rep._, 1920, p. 28.

Footnote 109:

_Proc. Zool. Soc. London_, 1910, p. 134.

Footnote 110:

_Proc. Zool. Soc. London_, 1905, p. 252.

Footnote 111:

_Phila. Zool. Soc. Rep._, 1920, p. 29.

Footnote 112:

_Phila. Zool. Soc. Rep._, 1921, p. 31.

Footnote 113:

_Proc. Zool. Soc. London_, 1919, p. 15.

Footnote 114:

_Proc. Zool. Soc. London_, 1919, p. 15.

Footnote 115:

_Phila. Zool. Soc. Rep._, 1916–1921.

Footnote 116:

_Journal of Parasit._, June, 1921, p. 194.

Footnote 117:

_Proc. Zool. Soc. London_, 1910, p. 147.

Footnote 118:

Fantham, _Proc. Zool. Soc. London_, 1910, p. 672.

Footnote 119:

_Loc. cit._, 1911, p. 674.

Footnote 120:

_Loc. cit._, 1915, p. 87.

Footnote 121:

_Loc. cit._, 1910, p. 233.

Footnote 122:

_Loc. cit._, 1914, p. 222.

Footnote 123:

_Phila. Zool. Soc. Rep._, 1912, p. 40.

Footnote 124:

_Proc. Zool. Soc. London_, 1914, p. 140.

Footnote 125:

_Jour. Parasit._, June, 1921, Vol. VII, p. 198.

Footnote 126:

This figure and a number of others in the tables do not correspond

with those in other sections of this book because certain injured,

decomposed and newly arrived animals were available and accepted for

my purposes, but were objectionable for the general medical statistics

and therefore excluded.

Footnote 127:

For foot note see page 630.

Footnote 128:

For foot note see page 630.

Footnote 129:

Not generically diagnosed.

Footnote 130:

_Proc. Acad. Nat. Sci. Phila._, March, 1913, p. 127.

Footnote 131:

_Proc. Zool. Soc. London_, 1912, p. 858.

Footnote 132:

_Proc. Acad. Nat. Sci. Phila._, 1913, p. 133.

Footnote 133:

_Proc. Roy. Soc. N. So. Wales_, Sydney, Vol. 27, pp. 86–90, 1893.

Footnote 134:

_Proc. U. S. Nat. Mus._, Wash., D. C., Vol. 50, 1916, p. 31.

Footnote 135:

_Proc. Zool. Soc. London_, 1911, p. 674.

Footnote 136:

_Indian Med. Gaz._, June, 1913, p. 217.

Footnote 137:

_Jour. Trop. Med. Etc., London_, 1913, XVI, p. 334.

Footnote 138:

_Am. Med. Phila._, V. 6 (16), 1903, p. 611.

Footnote 139:

Eichhorn and Gallagher, _Jour. Inf. Dis._, XIX, No. 3, Sept., 1916, p.

395.

Footnote 140:

Macfie, _Ann. Trop. Med. and Parasit._, 1915, 9, p. 507.

Footnote 141:

_Arch. f. Protistenk_, Jena, V. 26 (2), 22, July, p. 241.

Footnote 142:

_Jour. Parasit._, Sept., 1915, V. 2, pp. 37–45.

Footnote 143:

_Proc. Zool. Soc. London_, 1919, p. 14.

Footnote 144:

_Jour. Parasit._, Dec., 1916, V. 3, pp. 82–89.

Footnote 145:

_Proc. Zool. Soc. London_, 1909, p. 335.

Footnote 146:

_Loc. cit._, 1912, p. 236.

Footnote 147:

_Loc. cit._, 1912, p. 576.

Footnote 148:

The exact taxonomic position could not be stated,-probably an ameba.

Footnote 149:

_Proc. Zool. Soc. London_, 1910, p. 134.

Footnote 150:

Weidman (F. D.), “Dermatoses of Monkeys,” _Arch. Derm. and Syph._,

Chicago, March, 1923, p. 289.

Footnote 151:

Railliet Traite de Zool. Med. et Agric. Paris—Asselin et Houzeau,

1895, p. 659.

Footnote 152:

Megnin, Les Parasites Articules, 1895, Masson et Cie, Paris.

Footnote 153:

Quoted by Jensen (V.), _Hospitalstidende_, Copenhagen, 1922, 65, No.

28, p. 457.

Footnote 154:

Centr. f. Bakt. u. Parasitk., (etc.), Jena 1—Abt. V. 35 (1), 5, 1903,

orig. p. 89.

Footnote 155:

_Phila. Zool. Soc. Rep._, 1917, p. 36.

------------------------------------------------------------------------

TRANSCRIBER’S NOTES

● Typos fixed; non-standard spelling and dialect retained.

● Used numbers for footnotes, placing them all at the end of the last

chapter.

● Enclosed italics font in _underscores_.

● Subscripts are shown using an underscore (_) with curly braces { },

as in H_{2}O.