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Trichinosis 
 by Benjamin Schwartz 
 (Benjamin Schwartz is Chief of the Zoological Division, Bureau of 
Animal Industry.) 

U. S. Yearbook of Agriculture, 1942 

 Italic numbers in parentheses refer to Literature Cited, p. 801. 


The microscopic roundworm parasites that occur at times in the 
muscles of human beings, swine, dogs, cats, rats, mice, and many 
other omnivorous and carnivorous animals are known to the general 
public as trichinae and to biologists and medical scientists as 
Trichinella spiralis. These parasites, when present in sufficient 
numbers in a suitable host, produce a disease known as trichinosis 
or trichiniasis. 

Although trichinosis is probably never diagnosed in swine and 
seldom in other animals during life, the disease as it appears in 
man presents a more or less definite chain of symptoms, 
principally fever, muscular pains, and swelling of the eyelids. It 
may terminate in death and, in fact, is known to produce fatal 
results in about 5 percent of the cases. Because infected pork 
eaten raw or imperfectly cooked is the main source of human 
trichinosis, the occurrence of trichinae in swine has a far 
greater significance as a possible hazard to human health than as 
a cause of sickness in the affected animals. 

In the discussion that Follows trichinae are considered, 
therefore, largely as a menace to human health. The public-health 
aspect of swine trichinosis, which has been widely publicized in 
recent years, has produced considerable repercussions in this 
country to the detriment of swine producers and the meat industry. 

Trichinae were named and described in 1835, a quarter of a century 
before they were shown definitely to have any influence on human 
and animal health. There is some reason to believe that these 
parasites were actually observed in England in 1822 and again in 
1828, In fact it appears quite certain that trichinae in their 
cysts, or capsules, were found in England by Hilton in 1832 in 
the abdominal muscles of a human cadaver. Hilton, who was a 
demonstrator in anatomy in Guy's Hospital, London, did not 
investigate the contents of these cysts, and the credit for doing 
this for the first time belongs to his fellow countryman, Paget, 
who made his observations 3 years later. In 1835 Paget, a medical 
student, discovered, while dissecting the muscles of a Human body, 
small gritty spots that took the keen edge off his scalpel. 
Fortunately he had enough curiosity to investigate these spots 
with the aid of a microscope and, with technical assistance from 
others, determined that the spots were actually cysts containing 
organisms. He turned the material over to his professor, Sir 
Richard Owen, who in the same year published an account (10) 2 of 
the encysted parasites now known as Trichinella Spirosis. 

Following their discovery, trichinae, later recognized to be 
roundworms, continued to be encountered from time to time in 
dissecting rooms and for the next 25 years were regarded by most 
medical workers as relatively harmless zoological curiosities. The 
discovery by Leidy of trichinae in pork in the United States in 
1846 (6) and a similar discovery in a cat in Germany some time 
later apparently threw no light on the possible origin of these 
muscle parasites. How they got into the muscles and how they 
propagated remained a complete mystery for two and one-half 
decades following their discovery, though speculation on these 
points was not lacking. 

Like some other important discoveries in parasitology. those 
relating to trichinae were begun with simple observations that 
were followed later by experiments to determine the essential 
facts in the life cycle. In 1851 Herbst published an account of 
experiments in which he fed to dogs meat from a badger that, 
presumably, had been infected experimentally with trichinae; some 
time later he discovered encysted trichinae in the dogs' muscles. 
Investigations carried out in Germany a few years later by 
Leuckart, Zenker, and Virchow demonstrated conclusively that 
trichinae in the muscles of man and animals are actually 
incompletely developed worms, distinct from all others known up to 
that time as parasites of man and animals, and capable of 
undergoing further growth and development in the intestines of 
suitable hosts Finally, these three investigators, working at the 
same time but independently, elucidated the essential facts in the 
mode of transmission of trichinae and established beyond doubt 
that the worms that occur in the muscles are the infective stages 
of parasites that can grow to maturity in the intestines of 
susceptible host animals that have ingested trichina-infected 
meat. 

That pork is a source of human infection came to light in 1860 
under rather dramatic circumstances: 

While conducting a necropsy, or post mortem examination on a 19-
year-old girl who died in Dresden, Germany, early in 1860, of a 
disease that was diagnosed before her death as typhoid fever, 
Zenker failed to find the usual post mortem picture characteristic 
of that disease. He found, however, numerous unencysted trichinae 
in the girl's muscles. Part of this material he sent to Leuckart. 
and part Virchow, the former an outstanding zoologist and 
parasitologist and the latter known the world over as the founder 
of cellular pathology These investigators determined by animal 
experimentation that the trichinae found in the muscles of the 
girl developed to maturity in the intestines of suitable hosts, 
the mature parasites, in turn, evidently producing a new 
generation of young worms that ultimately invaded the muscles. 
Meanwhile Zenker discovered mature trichinae in the girl's 
intestines. He learned, moreover, that she had eaten raw sausage a 
month or so before her death. Fortunately some of the sausage was 
still available in the household where she had been a servant, and 
an examination showed that it was heavily infected with trichinae 
Moreover, Zenker elicited the information that others in the 
household who had eaten this sausage had also become sick. 

Thus in the year 1860 trichinae were shown to be pathogenic 
(disease producing) to man and capable of causing death; infected 
pork was shown to be a source of human trichinosis; and the mode 
of transmission of trichinae from one animal to another was 
conclusively established by rigid scientific experimentation. 
Perhaps the strangest occurrence in the unraveling of the story of 
trichinosis was the demonstration by Leuchart and Virchow, on. the 
same day but quite independently of one another (8), of the 
presence of unencysted trichinae in the muscles of test animals to 
which infected meat had been fed several weeks earlier. The 
unencysted worms which Leuckart found in the muscles of an 
experimentally infected hog and Virchow found in those of an 
experimentally infected rabbit were in the same stage of 
development as those found by Zenker in the muscles of the girl 
whose death was the first to be definitely recorded in medical 
literature as due to human trichinosis. 

 LIFE HISTORY OF TRICHINAE 

 The life history of trichinae is shown graphically in figure 1. 
It is evident that infection results from eating meat that harbors 
trichinae. As a rule, human beings acquire trichinae by eating raw 
or imperfectly cooked trichinous pork in one form or another; 
swine become infected by eating offal or garbage containing scraps 
of raw infected pork or by eating the flesh of infected rats, 
mice, or other animals (fig. 1, sec. 5); rats and mice, in turn, 
acquire trichinae by eating raw, trichina-infected pork or other 
infected meat in garbage or elsewhere, or through cannibalism; 
dogs, cats, and other carnivorous animals acquire parasites by 
eating the flesh of other animals already infected. Regardless of 
the source of infection, the course of events following the 
consumption of trichinous meat is briefly as follows: 

As the trichina-infected meat is digested in the stomach of a 
human being, hog, or other suitable host, the encapsulated worms 
(fig. 1, sec. 4), are freed from their lemon-shaped or spherical 
capsules, or cysts, which are, approximately one-fiftieth of an 
inch in maximum diameter and therefore microscopic in size. The 
worms themselves, spirally coiled within the cyst, are cylindrical 
in shape and measure about one twenty-fifth of an inch from end to 
end. Once they are free in the cavity, or Iumen of the stomach 
they pass rapidly into the small intestine and become localized 
among the folds and villi (minute projections of the inner 
lining). Here they increase in size and attain sexual maturity in 
2 days or earlier (3). Following the mating of the sexes, the 
worms continue to grow, and they attain their maximum size 4 to 5 
days later, or 6 to 7 days after they reach the host's stomach. 
When full grown, the females measure from one-eighth to one-sixth 
of an inch in length; the males are only about half as long (fig. 
1, sec. 1). The fertilized eggs are not discharged by the female 
worms as are those of most other parasitic roundworms that occur 
in man and domestic animals but develop within the maternal uterus 
where they hatch and from which they escape as larvae. 

The birth of the larvae begins about 5 days after infection (3) 
and may continue for several weeks; though many more young are 
born during the first 2 weeks of the worms fertile period than 
subsequently. The adult trichinae in the intestine tend to die and 
pass out after their reproductive functions have been fulfilled 
though adult worms have been found several weeks after infection 
and some of them at least may persist for 3 months or so. The 
newborn larvae (fig. 1, sec. 2), of which several hundred can be 
deposited by a single female trichina (9), measure about one two 
hundred and fiftieth of an inch in length. Owing to the fact that 
the female worm is rather deeply imbedded the intestinal lining 
the larvae are deposited directly in the lymph spaces of the 
intestinal wall. The larvae thus caught in the lymph channels 
migrate with the lymph stream ultimately reaching one of the large 
lymph vessels known as the thoracic duct. This ties into a large 
vein from which the blood flows to the right side of the heart. 
The larvae are distributed by the circulation from the right side 
of the heart to the lungs and thence to the left side of the heart 
and by the arterial circulation to all parts of the body. It is 
known that trichina larvae reach various tissues and organs but 
they become localized for the most part in the voluntary muscles
(the flesh), the fibers of which they penetrate (fig. 1, sec. 3, 
A) and in which they ultimately become encapsulated. 

Within 10 to 14 days after their penetration into the muscle 
fibers the larvae have attained their maximum length, which is 10 
times their original length (fig. 1, sec. 3 B). Encystment begins 
about I month after infection, and a thin-walled capsule is 
readily recognizable about 2 weeks later. About 6 months after 
infection the capsules may begin to calcify, calcium being 
deposited first at their poles or ends. Living trichinae commonly 
occur in such calcified capsules. It is not known precisely how 
long trichina larvae may live within their cysts but there is 
reason to believe that they can do so for many years at least in 
some cases. Sooner or later however the worms within the capsules 
may calcify and break down into crumbled masses or they ma die 
before the process of calcification has set in and become absorbed 
However even though the worms remain alive they are incapable of 
further growth within the capsules. In many respects the live 
encysted worms are comparable to seeds which are capable of 
further development only under favorable conditions. These 
conditions are fulfilled for trichinae when the flesh or meat in 
which they are present is eaten by an animal in which they are 
capable of developing to sexual maturity, as previously described. 

 HOSTS OF TRICHINAE 

 Trichinae have been recorded from a variety of animals besides 
those mentioned. Bears in particular can play an important role in 
the transmission of trichinae to man, severe cases of this 
infection in Europe having been traced to the eating of uncooked 
bear meat. In the United States there have been instances in which 
jerked bear meat has been found to be a source of human 
trichinosis. Various other carnivorous animals, such as the fox, 
the badger, the martin the raccoon, the otter, the mongoose, and 
others are known to be hosts of trichinae. Several wild rodents, 
such as the mole, the hedgehog, the ground squirrel, and others, 
also have been reported as hosts of these parasites. In the 
laboratory, rabbits, guinea pigs, white rats, and mice are readily 
infected experimentally with trichinae, and much of the available 
information about these parasites is a result of the experimental 
infection of these rodents. The herbivorous domestic animals--
cattle, sheep, goats, and horses also are susceptible to 
experimental infection with trichinae. Under normal conditions, 
however, these animals would not become infected, since they do 
not eat meat, and so far as is known, their susceptibility is only 
of theoretical interest and without any practical significance. 

In certain European countries the flesh of various fur-bearing 
animals, in addition to that of bears, is sometimes eaten raw or 
incompletely cooked, with the result that some cases of human 
trichinosis have been traced to this source. In the United States, 
however all cases of trichinosis that have been definitely traced 
to their source, with the exception of a few known to have 
resulted from eating uncooked bear meat, were found to have been 
caused by the eating of raw or rare pork or some pork-containing 
meat food product, such as sausage, insufficiently processed to 
destroy trichinae. Cases of trichinosis usually occur after 
parties, picnics, and family gatherings in which raw ham or 
sausage or some. other insufficiently cooked or inadequately cured 
pork-containing food is eaten by relatively large groups, only 
those who abstain from eating the food in question escaping 
infection (16). 

 THE DISEASE 

 Symptoms 

The disease trichinosis manifests itself in man and animals by 
various symptoms, the severity of which is usually correlate with 
the number of worms swallowed in the infected meat. The 
consumption of lightly infected pork or other meat by man or 
animals produces no visible symptoms unless large quantities of 
such meat are eaten. On the other hand, the consumption of even 
relatively small quantities of heavily infected meat may produce 
serious illness and even death. 

The clinical manifestations of trichinosis in swine have been 
established by experimental feeding of large quantities of 
trichinous meat. In the severest cases intestinal irritation, 
fever, muscular pain and stiffness, difficult in chewing and 
breathing, and severe emaciation have been noted. In more moderate 
infections the symptoms are indefinite. Trichinosis in pigs is not 
diagnosed during the life of these animals, even though the 
symptoms are striking for the reason that other, more familiar 
febrile diseases-that is, diseases accompanied by fever --of swine 
are characterized by similar clinical manifestations. 

In many the clinical picture of trichinosis has been ascertained 
in various parts of the world since 1860. The classical accounts 
of this disease as recorded in the medical literature are briefly 
as follows: 

During the development of trichinae in the intestine and the 
production of their young, known as the stage of ingression, 
there may be nausea, vomiting, diarrhea, and abdominal pain, or 
these symptom, may be entirely lacking. Other manifestations 
during the first week or so of infection are a general torpor, 
accompanied by weakness, a sensation of tension or pain in the 
muscles, muscular, itching, and, towards the end of this period, a 
swelling of the face and eyelids, particularly the latter. 

The next stage of the disease, known as the stage of digression 
corresponds to the distribution of the larvae throughout the body 
and their penetration into the muscles. The symptoms of this stage 
appear after the first week, about 8 days to 2 weeks after initial 
infection, and continue for the next 2 weeks or so. They are 
characterized by severe muscular pains, the muscles becoming 
swollen, hard, and tense. Moving the eyes and the tongue and 
chewing, breathing, swallowing are likely to be painful because of 
the penetration of trichina larvae. 

The third stage, known as the stage of regression, corresponds to 
the encystment of the parasites within the muscles and may be 
accompanied by an intensification of the symptoms of the second 
stage and the appearance of pronounced swelling of the legs, 
forearms, abdominal wall, and face. Anemia and cutaneous (skin) 
eruptions may appear, and pneumonia is a probable complication. 

Fever sets in during the first stage, becomes more pronounced 
during the second, stage, and may persist, usually with 
remissions, for several weeks. Apathy or mental disturbances may 
set in, and in some cases the mental symptoms may become 
aggravated to the point of delirium. 

The symptoms outlined represent, no doubt, a composite picture of 
the disease. All of them would not be present in all cases, nor 
would they appear necessarily in the order mentioned. Actually the 
clinical picture may show striking variations, as indicated in 
accounts of a recent outbreak of trichinosis in England (5, 20) 
involving about 500 clinical and an undetermined number of 
subclinical cases. 

 Diagnosis 

In a few cases practicing veterinarians have diagnosed trichinosis 
in pet animals, largely on the basis of fever associated with 
muscular stiffness. In man a presumptive diagnosis of trichinosis 
is frequently made on the basis of symptoms, particularly if the 
clinical manifestations can be traced to the consumption of raw 
pork or some pork food product not sufficiently processed to 
destroy trichinae. Not infrequently, however, the clinical 
manifestations of trichinosis in man have been confused with those 
of other febrile diseases, especially typhoid fever, undulant 
fever, influenza, nephritis, tuberculous meningitis, 
gastroenteritis, colitis, rheumatic endocarditis, syphilis, 
tuberculosis, and other diseases. 

Of the more important diagnostic aids that are used to corroborate 
a presumptive diagnosis of trichinosis, eosinophilia (an increase 
in certain white blood cells-the eosinophilic leucocytes of the 
blood), a positive skin test and blood serum test, and the 
discovery of trichinae in small pieces of muscle (biopsy 
material), are the most important. 

 INCIDENCE OF TRICHINAE AND OF TRICHINOSIS IN MAN 

Investigations conducted in the United States during the last 12 
years and still in progress have disclosed a surprisingly high 
incidence of infection with trichinae in the general population of 
this country. The investigations under consideration have been 
conducted by means of one or both of two techniques: (1) 
Digesting, in an incubator, the diaphragm or other muscle tissues, 
or sizable portions of them, obtained from the bodies of persons 
that have died in hospitals from various causes other than 
trichinosis, and recovering and trichinae present from the 
sediment of the digestive fluid; (2) repeated, painstaking 
microscopic examinations of fresh preparations, of diaphragm or 
other muscle tissue in which trichinae are known to be localized 
in large numbers. 

Queen (11) reported in 1931 that the muscle samples from 59 of 344 
unselected persons (17.2 percent), who died in Rochester, N.Y., 
and those from 16 of 58 persons (27.6 percent) who died in Boston, 
Mass., contained trichinae; other investigators working in or 
obtaining their material for the most part from large metropolitan 
hospitals afterward published more or less similar results. In 
some of these cases the reported incidences of infection with 
trichinae were even more striking than those recorded by Queen. A 
recent report issued by the United States Public Health Service 
(4) cowers the examination for trichinae of 2,330 human diaphragms 
obtained from hospitals in Washington, D. C., and 670 from various 
Federal hospitals in other cities. Of the total number examined, 
488 (16.3 percent) were infected with trichinae. It is important 
to note, however, that 425 contained trichinae in rather small 
numbers probably too few, in most cases, to have produced any 
signs of illness during life. Only 8 of the 488 positive 
diaphragms contained more than 100 larvae per gram of muscle 
tissue examined, and it is not unlikely that these were from the 
only individuals who showed signs of illness caused by trichinae 
during life. In general, the observations recorded by other 
investigators in the course of the recent surveys of over 5,500 
human diaphragms also show a high incidence (14 percent) and a low 
intensity of infection. Practically none of the investigators who 
conducted the surveys were able to obtain from the medical history 
of the persons involved any conclusive evidence of clinical 
trichinosis during life. 

The number of cases of clinical trichinosis in the United States 
actually recorded as such in the medical literature is very small 
when compared with the high incidence of infection with trichinae 
already discussed. In 1938 Sawitz (13) concluded from a study of 
the statistical data published by the United State's Public Health 
Service and records available in medical journals that the total 
number of cases of clinical trichinosis ever recorded in the 
United States amounts to between 5,000 and 6,000. It cannot be 
properly concluded, however, that all cases of trichinosis that 
have occurred in this country since 1842, when these parasites 
were first found in the body of a person who had suffered 
rheumatic pains in the arms and legs, have found their way into 
medical statistics or into the medical literature (16). 

Investigations on the incidence of trichinae in human beings in 
foreign countries, comparable to those made in the United States, 
are only fragmentary. The recent examination of 200 diaphragm 
samples from as many persons who died in England from various 
causes disclosed only two lightly infected ones, thus giving an 
incidence of 1 percent (24). Recently an examination of 420 
diaphragms in Canada (2) revealed 7 that were infected with 
trichinae, an incidence of 1.6 percent. 

In England up to 1940, the number of cases of clinical trichinosis 
and those involving the post mortem discovery of trichinae in 
foreign cadavers was well below 100 (2.4). Because of this the 
general opinion has prevailed that that country was singularly 
free from the disease. However, a serious epidemic of trichinosis 
came to light in England in December 1940, as previously noted, 
with an estimated number of at least 500 clinical cases and an 
undetermined number of non clinical infections. It is quite 
evident, therefore that as long as infected animals exist as a 
reservoir of the disease, the danger of its spreading to man is 
ever present. 

 OCCURRENCE AND FREQUENCY OF TRICHINAE 
 IN SWINE IN THE UNITED STATES 

The first recorded discovery of trichinae in swine was made in the 
United States in 1866 by Leidy, who discovered the cysts while 
eating a slice of cooked pork in his home in Philadelphia (7). 

In 1862, 2 years after the discovery of the transmission of
trichinae to man as a result of the consumption of raw, infected 
pork, an epidemic of trichinosis, with the mortality of 16 
percent, came to light in a small town in Germany. Two years later 
another and even more serious epidemic of this disease occurred 
iii another small town in that country, with the result that pork 
began to acquire the stigma of being capable of producing a 
serious and painful human disease that had a strikingly high 
mortality. These and other epidemics of trichinosis in Europe were 
not without effect on the American meat industry, which by 1879 
had developed a rather flourishing export trade to certain 
countries in Europe. By 1881 Italy, Germany, Austria and France 
had promulgated sanitary regulations prohibiting the importation 
of pork from the United States Because of the alleged danger of 
acquiring trichinosis from this meat. 

It is not surprising, therefore, that under the Federal meat-
inspection act of 1891 provision was made for the microscopic 
examination for trichinae of pork intended for export to foreign 
countries in order to surmount the sanitary barriers that had been 
set up against the importation of this commodity from the United 
States. This led to the systematic microscopic examination of 
samples of muscle tissue from millions of Hogs intended for 
export, and the microscopists of the Bureau of Animal Industry 
engaged in this work determined that a small percentage of these 
animals were actually infected with trichinae. In a total of over 
8 million hogs samples of which were examined microscopically from 
1898 to 1906, nearly 1.5 percent were found to contain live 
trichinae, and in addition slightly over 1 percent were found to 
contain what were, presumably, trichinae in various stages of 
disintegration. 

With the passage of a new meat-inspection act by Congress in 1906, 
microscopic inspection for trichinae of pork intended for export 
was discontinued, largely because this inspection was inherently 
imperfect. According to statements published by European meat-
inspection experts, reinspection of samples of pork from this 
country certified as being free from trichinae in accordance with 
the results obtained by microscopic inspection here showed some of 
the pork to be infected. The incidence of trichinae in swine in 
this country from 1906 up to quite recently was unknown but was 
assumed to be the same as that brought to light by the systematic 
microscopic examinations of 1898-1906. 

In 1933 the writer initiated an investigation to determine the 
current frequency of infection of swine with trichinae, using for 
this purpose a procedure that gives far more accurate results than 
the microscopic inspection previously used. The new procedure 
consists in digesting in artificial gastric juice in an incubator 
the diaphragms of hogs, selected at random, and determining the 
number of trichinae, if any, present in each diaphragm in relation 
to the quantity of meat digested. Since the diaphragm is known to 
be one of the preferred locations of trichinae, it is believed 
that the procedure outlined establishes the true incidence of 
these parasites in swine to a higher degree of probability than 
any other known method of examination. 

Out of more than 13,000 diaphragms from as many farm-raised hogs 
shipped to the most important meat-slaughtering centers of the 
United States, only 126 (0.95 percent) were found to be infected 
with trichinae. Nearly two-thirds of these contained the parasites 
in exceedingly small numbers (only I to 5 larvae per 100 grams-
about 31/2 ounces-of meat), so small, in fact, that it is doubtful 
whether any method of inspection other than the one used would 
have resulted in their discovery except by sheer accident. 
Considering the fact that in microscopic inspection of pork for 
trichinae only 3 samples from each carcass, each sample about the 
size of an oat grain and certainly no larger than a small pea, are 
examined or can be examined satisfactorily. from a practical 
standpoint, it is quite evident that the chances of detecting such 
light infections are exceedingly slight. Data not previously 
published show that out of about 9,000 samples of pork from as 
many hogs originating on the Atlantic and Pacific seaboards and 
known to have been fed almost exclusively on untreated garbage, 
554 (6.11 percent) were found to be infected. Not only was the 
incidence of infection in the garbage-fed hogs greater than that 
in the farm-raised hogs fed forage, grain, and other feeds, but 
the intensity of infection in the garbage-fed series also was much 
greater. Only something over one-third of the diaphragms from the 
garbage-fed samples contained the were light infections that 
occurred in about two-thirds of the positive diaphragms of farm-
raised hogs. In one series, including nearly 4,500 diaphragms from 
garbage-fed hogs in one of the Pacific Coast States, the incidence 
of infection was over 3.5 percent. In another series including 
over 2,500 diaphragms from as many Hogs from one of the Atlantic 
Seaboard States, the incidence of infection was about 10.5 
percent, while in about 2,000 diaphragms from hogs in another 
State on the Atlantic coast the incidence was nearly 6 percent. It 
is evident, therefore, that the average frequency of trichinae in 
garbage-fed hogs is more than 6 times that in farm-raised hogs. 
Pork from hogs fed garbage is, therefore, a far greater danger to 
human health than that from hogs raised on the farm and fed on 
forage, grain, and the usual supplements of tankage and minerals. 

In the course of examinations to determine the incidence of 
trichinae in swine fed on different types of feeds, over 2,200 
diaphragms were obtained from hogs known to have been fed cooked 
garbage only. Of these, only 11 (slightly less than 0.5 percent) 
were found to be infected, the numbers of trichinae in the 
positive hogs being very small. It is evident, therefore, that the 
danger inherent in garbage as a feed for swine, from the 
standpoint of trichinosis is the presence in it of pieces of raw 
pork or other meat containing trichinae. Cooking destroys nearly 
all of these parasites, as shown by the data just presented, and 
would destroy all of them if sufficient heat were applied. 

The occurrence of trichinae in nearly 1 percent of farm-raised 
hogs affords conclusive evidence that the animals must have had 
access at one time or another to offal, garbage, kitchen scraps, 
or possibly other sources of trichinous meat. In the absence of 
such sources of infection, these pigs would not acquire trichinae 
unless, because of some dietary deficiency or other reason, they 
happened to eat infected rats or mice. 

According to information published recently (14), trichinae are 
now exceedingly rare in swine in Germany, as shown by the fact 
that in 1936 samples of only 135 hogs were found to be infected 
out of nearly 19 million swine, samples of which were examined 
under the microscope as a regular routine. The indicated frequency 
is about 7 infected hog in every million examined. In Poland, 
where pork is not microscopically inspected for trichinae, the 
incidence of these parasites in swine was reported in a German 
publication in 1941 to be about 70 times greater than in Germany 
(14). In Canada, where swine-husbandry practices are more nearly 
similar to those prevailing in the United States than are those in 
European countries, an examination of 995 diaphragms from as many 
garbage-fed swine from the Provinces of Quebec, Ontario, and 
Manitoba disclosed 2 that were infected, the incidence being, 
therefore, 0.2 percent (1). This low figure is not surprising 
since the Dominion laws require the sterilization by heat of all 
garbage fed to swine. In a previous investigation in Canada 
involving nearly 2,300 diaphragms the incidence of infection was 
0.57 percent, very close to the figure derived from the data on 
the results of examinations in the United States of diaphragms of 
swine fed only cooked garbage. 

 CONTROL OF TRICHINOSIS 

Since there is no specific treatment for the removal of adult 
trichinae from the intestine or for the destruction of their 
larvae in the blood or muscles before or after their encystment, 
the major emphasis must be placed on prevention. Preventive 
measures must be directed against trichinosis in swine as well as 
in man because the successful control of the infection in pigs 
will result in a diminution in the number of human cases and might 
bring about its ultimate, elimination from the list of human 
diseases. Actually, trichinosis in man is an easily preventable 
disease, since prevention consists merely in thoroughly cooking 
pork in all its forms. Its persistence despite repeated warnings 
of the danger inherent in raw pork is proof that warnings have not 
reached the public or that they have not been heeded by persons 
whose taste for raw pork in one form or another is such that they 
will eat it even in the face of the danger of acquiring a painful 
serious, and possibly fatal illness. 

Different countries have met the problem in different ways, the 
preventive measures adopted in any particular country being 
governed to a greater or less extent by the prevailing habits of 
the population with respect to the cooking and curing of pork and 
its products. Some countries have no trichinosis problem so far as 
is known, presumably because their populations do not eat raw pork 
in any form. Other countries, particularly on the continent of 
Europe, followed the leadership of Germany and long ago adopted as 
part of their meat-inspection procedure the plan of microscopic 
examination of samples of pork from all hogs slaughtered for human 
consumption, including those slaughtered on the farm for home 
consumption. In adopting this procedure, the meat-inspection 
authorities of the countries concerned recognized that they had to 
cope with the custom of eating pork in the raw state, a habit so 
deeply rooted in the general population that it could not, in 
their opinion, be eradicated by education. The countries that have 
practiced microscopic inspection, particularly Germany and 
Denmark, point with pride to the fact that, largely as a result of 
this, the incidence of trichinae in swine has declined steadily 
and that this decline has been reflected in a sharp diminution of 
trichinosis in man. 

In the United States microscopic inspection for trichinae was 
resorted to, as previously noted, only in the case of pork intended 
for export to countries in Europe that made such inspection 
mandatory. The motives were economic rather than hygienic. At no 
time did American meat-inspection authorities give serious 
consideration to the adoption of microscopic inspection of pork for 
trichinae as part of the general procedure under Federal meat 
inspection. Investigations have shown that in numerous instances 
trichinous pork had been examined microscopically as many as 20 to 
30 times Before the parasites were found. Since it would be 
impracticable under any inspection scheme to make so many 
examinations, the unreliability of inspection for trichinae is quite 
obvious. Stiles (23) determined that out of 6,329 cases of 
trichinosis that occurred in Germany between 1881 and 1898, 2,042 
(over 32 percent) could be traced to pork which had been inspected 
microscopically and passed as free from trichinae. This evidence 
shows that microscopic inspection is inherently imperfect and is 
fraught with the danger of giving persons who are fond of raw pork 
and its products a false sense of security, encouraging the 
consumption of raw pork and defeating in a measure the very purpose 
for which the inspection was intended. 

It must be borne in mind that Federal meat inspection in this 
country is limited to plants that engage in interstate or foreign 
commerce. Slaughtering and meat-processing plants not engaged in 
interstate or foreign commerce do not come under the provision of 
the Meat Inspection Act and are therefore either without 
inspection or subject only to State or municipal inspection. 
Slaughtering done on the farm is exempt from inspection. Since 
only a few States and comparatively fen-municipalities have a 
rigid system of meat inspection, not all pork from hogs 
slaughtered in this country would be subjected to microscopic 
inspection even if such inspection were enforced iii Government-
inspected establishments. Actually, only about 60 percent of the 
hogs consumed in this country are slaughtered in Federally 
inspected establishments. It cannot be supposed that consumers 
would take the trouble in most instances to differentiate between 
pork inspected microscopically by Federal or other authorities and 
pork not so inspected. This situation would tend to nullify, at 
least in part, the good that might result from microscopic 
inspection of pork for trichinae. In addition, the cost of 
microscopic inspection by the Federal Government alone would 
involve an expenditure of about 10 million dollars annually (17), 
approximately twice the present outlay for all Federal meat 
inspection. In view of the fact that this investment of public 
funds cannot be expected to yield entirely satisfactory results, 
for the reasons already given, the drain on the Public Treasury 
that it would entail hardly appears to be warranted. 

Following the publication of results of investigations showing 
that rabbits experimentally infected with trichinae gave clear-cut 
reactions to the injection into the skin of various test materials 
(antigens) prepared from trichina larvae research work was 
undertaken by specialists in the Bureau of Animal Industry and 
elsewhere to determine the feasibility of detecting infection with 
trichinae in hogs prior to slaughter. Although several workers 
have recommended; at least by implication, the adoption of this or 
a similar biological test to weed out trichina-infected swine, the 
work reported by investigators of the Bureau of Animal Industry 
(18, 19, 21, 22) shows that the skin test, when applied to swine, 
is not sufficiently specific to warrant its use for the purposes 
indicated. 

In the absence of any known practical method of inspection of hogs 
for trichinae, the regulations governing meat inspection by the 
United States Department of Agriculture provide that no article of 
a kind prepared customarily to be eaten without cooking shall 
contain any muscle tissue of pork unless the meat has been 
subjected to a temperature sufficient to destroy all live 
trichinae, or to other treatment prescribed by the Chief of the 
Bureau of Animal Industry. The treatments prescribed for all meat 
food products containing pork muscle tissue that are prepared to 
be eaten without cooking are (1) heating, (2) special 
refrigeration, and (3) special processing. When heating is done, 
it is required that all meat food products of the kinds mentioned 
must be so heated that they will attain in all parts a temperature 
of not less than 137ø F., this temperature having been determined 
by investigation to be lethal to trichinae (12). The required 
refrigeration involves the subjection of pork or of articles 
containing pork muscle tissue to a temperature of not less than 5 
deg F. for a continuous period of not less than 20 days, or the 
subjection of the meat or articles to lower specified temperatures 
for shorter specified periods. Special curing methods in lieu of 
the required heating or refrigeration are designed to effect the 
destruction of trichinae by the action of curing ingredients, 
especially salt, by smoking at temperatures lower than 137ø F. for 
definite periods, and by drying. The prescribed curing methods are 
known, as a result of numerous trials, to be effective in 
destroying the vitality of trichinae. 

All the methods approved by the Bureau of Animal Industry as 
effective in destroying life in trichinae are based on extensive 
scientific research carried out in the laboratory and in meat-
packing establishments and were subjected to repeated trials 
before they were adopted for official use. Under Federal meat 
inspection, therefore, the public is safeguarded against the 
danger of acquiring trichinosis from meat food products containing 
pork muscle tissue that are usually eaten without cooking. In 
preparing fresh pork and ordinary varieties of cured pork- that 
have not been specially processed, under competent inspection, to 
destroy trichinae, the only safe rule to follow is to cook the 
pork until it is well done throughout. 

Inasmuch as data that- have been presented in this article show 
that garbage-fed hogs have an average incidence of trichina 
infections more than six times that of farm-raised hogs and that 
cooking garbage renders it safe as a swine feed so far as 
trichinae are concerned, the control of garbage feeding by States 
and municipalities through the enforcement of heat-sterilization 
requirements, or the voluntary adoption by feeders of the practice 
of sterilizing garbage by heat, would go a long way toward 
reducing the rather high incidence of trichinae in swine in the 
United States. 

On the farm, three precautions would further reduce the incidence 
of swine trichinosis: (1) Do not feed offal, kitchen scraps 
containing raw pork, or the contents of the slop barrel to swine; 
(2) do throw dead rats and mice into the hog pens; (3) bury deeply 
in quicklime or burn the carcasses of hogs and other animals that 
die on the farm. 

These steps, together with the control of garbage feeding 
indicated above, would eliminate to large extent practically the 
only source of human trichinosis in this country. 


 LITERATURE CITED (See the book referred to at the top.)