Transcript Trichinella spiralis

TRICHINELLA SPIRALIS
• Intestinal helminths, and other tissue Nematode
• Intestinal infection ,in which adult worms are found in the mucosa
of the intestine and encysment of larvae are found in the muscle.
. Parasite of carnivorous mammals, especially common in rats and
in swine fed uncooked.
• ONE SPECIES, Trichinella spiralis, IS A PARASITE OF MAN.
• ANOTHER SPECIESES :
* Trichinella nativa ( Kutub )
* Trichinella nelsoni ( Africa )
* Trichinella britovi ( Europe )
* Trichinella pseudospiralis
Trichinella spiralis
MORPHOLOGY
THE CAUDAL END OF THE FEMALE IS BLUNTLY ROUNDED, WHILE THE MALE IS CURVED AND HAS
A SINGLE SPICULE.
THE FEMALE SINGLE OVARY AND THE VULVA IS NEAR THE LEVEL OF THE BASE OF THE
ESOPHAGUS.
. THE FEMALES ARE VIVIPAROUS
THE ADULT INHABIT IN THE INTESTINE AND THE LARVAE IN THE MUSCLE OF MAMMALS.
The adult is a small worm with a slender anterior end.
THE MALE
• From 1.4 to 1.5 mm long and
0.04 mm broad.
• The cloaca is at the ventrally
curved posterior end between
two lobular caudal
appendages which serve
during copulation.
picture
Trichinella spiralis
MORPHOLOGY
The adult is a small worm with a slender anterior end.
THE FEMALE
• From 3 to 4 mm long and
0.06 mm broad.
• The vulva is in the anterior
fifth of the body, and a
single ovary is near the
bluntly rounded caudal end.
• The small terminal mouth is
nonpapillae and leads into
the pharyngeal esophagus.
picture
Trichinella spiralis
MORPHOLOGY
THE LARVA
 With a spearlike burrowing tip at its tapering anterior end
measure 80 to 120  by 5 to 6  at birth and grows but little
until it has entered a muscle fiber where it attains a size of 800
to 1,300  by 35 to 40 .
 The mature larva has a digestive tract similar to that of the
adult, and while the reproductive organs are not fully
developed, it is often possible to differentiate the sexes.
Trichinella spiralis
REPRODUCTION
Each viviparous female produces from 1350 to 1500 larvae.
VIABILITY
• Endcysted larvae are killed at temperature above 550C.
• The infectivity is reduced by refrigeration at 50C for 27
hours.
• By exposure to pepsin for 12 hours.
• Irradiation of the larvae inhibits the reproductive capacity
of the ensuing adult worms.
• Storage at – 15 C for 20 days or – 30 C for 6 days will kill
endcysted larvae.
TRICHINELLA SPIRALIS
HOSTS
Trichinella spiralis is found chiefly in :
 Man
 Hogs
 Rats
 Bears
 Foxes
 Dogs
 Cats, but any carnivorous or
omnivorous animal may be infected.
TRICHINELLIASIS
ETIOLOGY:
Trichina spiralis another name isTrichinella spiralis hominis
DISEASES :
TRICHINOSIS; TRICHINIASIS; TRICHINELLIASIS
HISTORY :
• Trichinella spiralis is Non Soil Transmitted Helminth and
tissue Nematode
• The encysted larval worm in man was first noted in
Germany in 1822 and later in England in 1828 and 1833.
• The larval worm was described in 1835 named it Trichina
spiralis.
• T spiralis is cosmopolitan and high pathogenecity
• T pseudospiralis , cosmopolitan, does not encyst,
infectious to birds and pathogenicity in humans not well
characterized
TRICHINELLIASIS
GEOGRAPHIC DISTRIBUTION
• Cosmopolitan. It occurs more frequently in the Northern
Hemisphere and less frequently in the tropic.
• It is particularly prevalent in countries where pork is eaten
raw or insufficiently cooked, and thus is rare in Moslem
and Hindu.In Indonesia especially in Bali.
• Survey in Jaya Wijaya Papua Indonesia indicate that
infections with Trichinella sp in pigs are present.
Trichinelliasis
LIFE CYCLE
• The same animal acts as
both final and intermediate
host, harboring the adult
parasite temporarily and
the larva for a long period.
• In order to complete the
life cycle, flesh containing
the encysted larvae must
be ingested by another
host.
picture
Trichinelliasis
LIFE CYCLE
• The adult worms are attached or hidden in the intestinal
mucosa.
• Found in the small intestine from the duodenum to the
ileocecal valve and sometimes in the cecum and first
portions of the colon.
• When infective stage are ingested by humans, usually in
raw or poorly cooked pork ,they pass to the upper small
intestine, where the capsules are digested and the larvae
released in a few hours by the action of digestive
juice.The liberated larvae immediately invade the
intestinal mucosa.
• They rapidly penetrate into the epithelium of the
duodenal and jejunal mucosa
• The amount of damage to the intestinal lining is depend
on the number of invaiding organisms and the time and
number of previous exposures.
Trichinelliasis
LIFE CYCLE
* In 18 to 24 hours may be differentiated in male and
female
* Within two days the worm reach sexual maturity and
mate in the small intestine
* After copulation gravid female increases in size and
in about 48 hours, burrows deeply into the mucosa of
the intestinal villi from the duodenum to the caecum
and even in the large intestine in heavy infections
* About the fifth day female worm begins to deposit
larvae into the mucosa and sometimes directly into
the lymphatics from which they reach the thoracic
duct and enter the blood stream and the larvae are
carried to all parts of the body.
.
Trichinelliasis
DEVELOPMENTAL CYCLE
* After passing through the hepatic and pulmonary
filters the larvae are carried to all parts of the body.
* Burrow into the muscle fiber, and capable of
encysting and developing only in streated muscle
Trichinelliasis
DEVELOPMENTAL CYCLE
• Larvae have been found in the skeletal muscles, lungs,
myocardium, brain, retina, intestine, bone marrow, blood,
cerebrospinal fluid, various serous cavities and other
tissues.
• They have a predilection and usually only develop in
striated muscles.
• They rarely settle in other tissues and if so they soon
disintegrated and are absorbed.
Trichinelliasis
DEVELOPMENTAL CYCLE
• Larvae have been detected in myocardial lesions as early
as the fifth day (Dunlap and Weller, 1934).
• The invasion of the muscle usually begins from 6 to 9 days
after infection.
• The larva burrows into the muscle fibers by means of a
spear-shaped apparatus at its anterior end.
• The larva grows in the long axis of the muscle fiber; it
begins to coil for encystment by the seventeenth day, when
it has become resistant to pepsin and capable of infecting a
new host.
Trichinelliasis
DEVELOPMENTAL CYCLE
• It attains its maximal size about the 20th day.
• Encapsulation begins about the twenty-first day and the
larva becomes encapsulated in a lemon-shaped capsule of
sarcolemmous origin, 0.4 by 0.25 mm.
• The cyst rarely contains more than one larva.
• The permanent capsule is completed in about 3 months.
• Calcification begin as early as 6 months or within 2 years
• Calcification is usually completed within 18 months, but
the encysted have may remain viable for long periods; a
duration of 11 years in the hog and 31 years in man has
been recorded.
• Adult female dies after passing her larvae and then is
digested or passed out of the intestine.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY
* Can be occurred because of :
- The intestinal lessions caused by the adult worm
- The presence of the larvae in the striated muscles
and vital organs.
-The reaction of the host to their activities, antigenic
products, and possible toxic reaction
* In 3 to 4 days after invasion of the larvae ,the muscle
fibers increase in size, and become edematous .
* The nuclei increased in size and number
*The adjacent muscle fibers undergo hydrophic
degeneration and hyaline necrosis.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY
• These organs show widespread focal necrosis and an
intense eosinophilic reaction.
• Evidently the reaction of the host to the parasite rather than
the effect of the parasite on the host is responsible for the
clinical manifestations.
• The clinical picture suggest that the damaging factors are
the result of an antigen-antibody reaction or have a toxic or
allergic background.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY
* The distribution of larvae in mild and severe infections
follows the same pattern with heaviest concentration in the
skeletal muscle of the forearm, intercostals and tongue, and
no larvae in the viscera, brain, or circulatory system.
* The lodgement of the migrating larvae in the capillaries
and perivascular sites throughout the body produces an
inflammatory cellular reaction, necrosis, edema,
hyperemia, petechiae, and infarction.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY
The pathologic changes in man involve many organs :
* Gastrointestinal tract
* Lungs
* Skeletal muscles
* Heart
* Central Nervous System
* Miscellaneous organs
Trichinella spiralis
TRICHINOSIS
PATHOLOGY IN MAN
Gastrointestinal tract
• In man who rarely dies in less than three weeks, the
early gastro-intestinal changes are not significant.
• The activities of the adult worms and larvae may
produce a catarrhal enteritis with hyperemia, petechial
hemorrhages, edema and occasionally slight ulceration
of the mucosa.
• The hyperplastic mesenteric lymph nodes are
hyperemic or gelatinous.
• The accompanying symptoms of gastro-intestinal
irritation, edema, and urticaria are usually attributed to
the activities or proteic products of the worms, although
the possibility of a toxic secretion has been suggested.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY IN MAN
Lungs
• During passage through the lungs some larvae may leave
the pulmonary capillaries and produce petechiae and
small foci of pneumonitis.
• Hemorrhages, nodular consolidations.
• Blood-tinged pleural effusions, small hemorrhagic foci,
pulmonary
edema
and
infiltration,
bronchitis,
bronchopneumonia, and pulmonary infarction and
embolism have been observed in man.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY IN MAN
Striated muscles
• The muscle fibers, particularly in the tendon of the
muscle, are invaded by the larvae.
• Three or four days after the invasion, the muscle fibers
increase in size, become edematous, develop a spindle
shape, lose their cross striations and undergo basophilic
degeneration.
• The nuclei increase markedly in number and size, become
oval rather than rod-shaped, stain less intensely, and
migrate from their normal position beneath the
sarcolemma to the interior of the muscle fiber.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY IN MAN
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The metabolism of the muscle is somewhat altered, with a
decrease in glycogen and an increase in protein and lactic
acid.
There is an acute interstitial inflammation about the
parasitized muscle fiber, which reaches its peak in five or
six weeks, with edematous swelling, and cellular
infiltration of polymorphonuclear neutrophils,
eosinophils, lymphocytes, and at times foreign body giant
cells.
Later the inflammation and edema dissapear, but the
adjacent muscle fibers undergo hydropic degeneration and
hyaline necrosis.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY IN MAN
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The larva is gradually enclosed in a lemon-shaped cyst,
which is composed of an inner mantle of basophilic
degenerative muscle plus epithelioid cells and fibroblasts
and an outer hyaline capsule derived from the
sarcolemma.
The latter is probably the expression of an antigenantibody reaction.
The permanent capsule is completed in about three
months.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY IN MAN
Heart
• Exudative changes in the heart are caused by the
migrating larvae, which although they never encyst in the
myocardium, are either killed there or enter the general
circulation.
• Macroscopically the heart is soft, and reddish brown, and
sometimes the pericardium is injected and contains
increased fluid.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY IN MAN
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The myocardium and endocardium show mild edema,
passive hyperemia, petechial hemorrhages, and numerous
focal areas of interstitial infiltration with neutrophilic and
eosinophilic leukocytes, lymphocytes, macrophages,
plasma cells, and at times fragmentation, fatty
degenartion, and necrosis of the muscle fibers.
These lesions, which are the result of a nonspecific
reaction to the migrating larvae, account for the transitory
cardiac symptoms in trichinosis and apparently do not
represent permanent changes.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY IN MAN
Central Nervous System
• Lesions of the central nervous system are fairly common
but inconstant.
• They may represent an acute nonsuppurative meningitis
with edematous hyperemic meninges, or may serious
focal cerebral damage.
• Larvae have been found in the spinal fluid, which shows
increased pressure.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY IN MAN
Eyes
• The eyes frequently exhibit a characteristis chemosis of
the bulbar conjuctiva with round-cell infiltration, necrosis,
edema, and accumulation.
• In the choroid there is a marked accumulation of
leukocytes and a proliferation of the endothelial cells of
the capillary walls, which frequently are thickened,
hyalinized, and dilated.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY IN MAN
Miscellaneous organs
• The larvae may invade the lungs, pleura, pancreas,
gallbladder, kidney, and other organs, producing local
inflammation and edema.
• The heart, kidneys, and liver may show fatty
degeneration. There may be hyperplasia of the bone
marrow with an increase in eosinophils.
Trichinella spiralis
TRICHINELLIASIS
PATHOLOGY IN MAN
Laboratory Examination :
• The leukocyte count may range from 4.000 to 34.000 but
generally is from 7.000 t0 17.000.
• The percentage of eosinophils starts to increase in the
second week, and after the third week usually runs from
15 to 40 % but may be as high as 89%.
• It gradually declines to about 5 % in six months and to
normal in one year, but sometimes remains elevates for
years.
Trichinella spiralis
TRICHINELLIASIS
SYMPTOMATOLOGY
•
Five factors determine the variability of clinical
symptoms:
 The number of worms
 The size and age of the patient
 The tissues invaded
 The general resistance of the patient
 The presence of concominant pathological condition.
Trichinella spiralis
TRICHINELLIASIS
SYMPTOMATOLOGY
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The essential symptoms probably arise from the toxemia
and activities of the parasite, but some workers consider
them allergic.
The disease is commonly divided into three cllinical
phases corresponding to the periods of :
 Intestinal invasion by adult worms
 Migration of the larvae
 Encystment and repair.
The incubation period varies from 2 to 30 days, but
usually ranges from 5 to 17 days.
Trichinella spiralis
TRICHINELLIASIS
SYMPTOMATOLOGY
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During the period of invasion the encysted larvae and
adult worms may produce symptoms of gastro-intestinal
irritation and intoxication: nausea, vomiting, and a watery
diarrhea without blood or mucus.
The early gastro-intestinal phase, resulting from the
mechanical or toxic action of the worms, is often
overlooked.
Fever, profuse sweating, rapid cardiac and respiratory
rates, edema of the face, and urticarial manifestation, also
occur.
Trichinella spiralis
TRICHINELLIASIS
SYMPTOMATOLOGY
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At the start of migration, some 5 days after infection, the
previous symptoms recur from toxic effect of the larvae.
The fever, rarely over 1040F and frequently below 990F, is
typhoidal in type; there is edema of the face and eyelids,
headache, and sometimes delirium.
Respiratory, ocular, and cardiac symptoms and more
rarely a maculopapular erythema or petechial rash may
appear.
The second stage usually lasts from 8 to 15 days, but
because of the continuous production of larvae the
symptoms of the second and third stages overlap so as to
produce a confusing clinical picture.
Trichinella spiralis
TRICHINELLIASIS
SYMPTOMATOLOGY
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When the muscles are invaded, a marked interstitial
myositis is established, producing rheumatoid symptoms
with muscle tenderness and spasm.
After the third week the leading symptoms in order of
prevalence are : eosinophilia, edema chiefly orbital,
muscular pain, and tenderness, headache, fever, generqal
weakness, joint pain, and rarely hyperethesia.
In severe case patients may show cachexia.
The cardiac symptoms that arise from the pathological
changes produced by the larvae in the myocardium during
their migration are usually transient.
Trichinella spiralis
TRICHINELLIOSIS
SYMPTOMATOLOGY
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Extensive myocardial damage, may result migration and
death.
The symptoms are a feeble or dicrotic pulse, suffled heart
sounds, an apical systolic murmur, tachycardia,
palpitation, hypotension, and edema.
About one sixth of the patients show electrocardiographic
changes; evidence of myocardial damage by the slurring
of the peak of the Q.R.S. complex, premature contractions
the prolongation of the P-R interval and flattening or
inversion of the T waves.
Trichinella spiralis
Correlation of Clinical findings with Parasite Development
in Trichinosis
•
•
•
•
Young adult migrating into mucosa of small intestine (24 – 72 hours)
Nausea; Vomiting; Diarrhea; Abdominal pain.
Larvae in bloodstream and invading muscles (10 – 21 days)
Periorbital edema; Conjunctivitis; Fever and chills; Muscle pain;
Headache; Eosinophilia; Skin rashes; Painful breathing; Elevated
muscle enzymes.
Larvae in Myocardium (14 – 21 days) Tachycardia; Edema of legs;
Hypotensia; ECG changes; Elevated muscle enzymes.
Larvae in brain and meninges ( 14 – 28 days)
Headache;
Delirium; apathy, or altered conciousness; Stiff neck.
Trichinella spiralis
TRICHINELLIASIS
CLINICALLY
 Thus a rising eosinophilia associated with fever, edema of
the face, myalgia, and gastrointestinal disturbances
provides strong presumptive evidence of trichinosis.
LABORATORY EXAMINATION
 Based on the detection of the larval worms in the muscle
by biopsy and serologic and intracutaneous test.
Trichinella spiralis
MUSCLE BIOPSY
 Biopsies of the tendinous portions of the deltoid, biceps or
gastroenemius muscles offers a specific though late
method of diagnosis and if positive, affords definite proof
of infection.
 A positif diagnosis cannot be made before two weeks, and
is seldom obtained, particularly in light infections, before
three weeks.
 The excised muscle is observed microscopically after
compression between two slides or a special compressor,
sectioning or digestion in an artificial gastric juice in
order to concentrate the larvae.
Trichinella spiralis
SEROLOGIC AND INTRACUTANEOUS TEST
•
•
Especially useful in diagnosis and in surveys, they include
1. Precipitation
2. Circumlarval microprecipitation
3. Complement fixation
4. Flocculation
5. Agglutination
6. Hemagglutination
7. Fluorescent antibody
8. Intracutaneous
Most workers consider that these tests are of greater
diagnostic value than the detection of larval worms and
that they have a relatively high degree of sensitivity.
Trichinella spiralis
TRICHINELLIASIS
DIFFERENTIAL DIAGNOSIS
Trichinosis resembles many conditions :
Due to the association with fever : Typhoid , Encephalitis ,
Myositis and Tetanus
Association with a high eosinophilia : the tissue stages of
Schistosomiasis ( Katayama syndrome ), Hook worm
infection , Strongyloidiasis and other helmintic infections.
Trichinosis may also resemble with collagen disorders
such as : Periarteritis nodosa and Acute Rheumatoid
arthritis.
Trichinella spiralis
TRICHINELLIASIS
TREATMENT
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Spesific Treatment and symtomatic treatment is very important. There
is no specific chemotherapeutic treatment for trichinosis.
Medical treatment is largely palliative, symptomatic and supportive,
designed to tide the patient over the critical period.
The administration of chemotherapeutic agents againts the adult or
larval worms has not been successful.
Benzimidazol most effective for Trichinella larvae before become
cyst stage.
Albendazol is the drug of choice because absorbtion is good and free
from side effect ; 400 mg twice a day for 8 to 14 days.
Mebendazole is allternative drug recommended 200mg – 400 mg
three times a day furthermore 400-500 mg three times a day for ten
days .
In intestinal phase Corticosteroid is contra indication. In muscle
invasion phase the patient with severe symptom must be take care in
hospital and must be given corticosteroid high dose for 24-48 hours to
be continuied with low dose for some weeks or months. In this phase
the symptoms caused by inflamation and allergic reaction so
corticosteroid is very important and anthelmintik is unnecessary.
Trichinella spiralis
TRICHINELLIASIS
PROGNOSIS
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Although unfavorable in severe infections, is ordinarily
good.
If survive the first 6 weeks of the acute illness, it will
recover slowly and show no residual ill effects, although
muscle pains may persist for 6 months.
Depend upon the location and number of larval trichinae,
the age and physical condition of the patient, severity of
symptoms, involvement of cardiorespiratory system, and
complications.
In overwhelming infections death may take place in the
second or third week, but more often it occurs in from 4 to
6 weeks.
Trichinella spiralis
TRICHINELLIASIS
PREVENTION
 The ultimate eradication of trichinosis in man is
dependent upon its elimination in hogs.
 The prevalence can be greatly reduced by sterilizing
garbage containing raw meat scraps, and by improving the
sanitation of piggeries and slaughter houses.
 The prevention of human trichinosis is dependent upon :
 inspection of hogs in slaughter and packing houses,
 the processing and refrigeration of pork products,
* storage of pork in deep freeze units at - 37 *C
* The cysts are destroyed by storage at -15*C for 20
days or more
* pork must be cooked at temperature not lower than
58,3 *C
Irradiation with cobalt-60 which kill the cysts.
 the education of housewife with regard to the through
cooking of pork.
Trichinella spiralis
TRICHINELLIASIS
EPIDEMIOLOGY
EPIDEMICS
Trichinosis has a cosmopolitan distribution but is rare or
absent in India, Australia and some Pasific islands.
In recent years small and large epidemics have occurred,
among these are :
 Greenland in 1947 with 300 cases
 Poland in 1951 and 1959 with 92 and 308 cases
 Germany in 1951 with 436 cases
 Liverpool, England in 1953 with 53 cases
 Romania in 1955 with 24 cases.
There has been an increase in small outbreaks in the United
States of America since 1930, the last being in
Pennsylvania in 1961.
Trichinella spiralis
TRICHINELLIASIS
EPIDEMIOLOGY
EPIDEMIOLOGY FACTORS
 In general the incidence of trichinous infection is less in
the tropics and subtropics than in the temperate zones,
chiefly owing to lower consumption of pork products.
 Religious bans on eating pork explain the absence of the
infection in certain countries and races.
 Trichinosis shows seasonal fluctuations, reaching its peak
during the winter months when there is greatest
consumption of pork.
 The incidence of infection in cadaver increase with age. A
high rate is found at autopsy in the older age group and a
relatively low rate in the younger age groups and in
Negroes.
Trichinella spiralis
TRICHINELLIASIS
EPIDEMIOLOGY
TRANSMISSION
Can be influenced by economic, cultural, and religious factors.
Prevalence of the disease is generally less in the tropics and
subtropics
 Trichinosis is acquired by man from hogs, particularly from
garbage-fed animals.
 In nature the enzootic disease is maintained by cannibalistic
rats.
 Hogs become infected chiefly from eating uncooked meat
scraps in the refuse from slaughter houses, markets, and
private homes, occasionally they may eat infected rats.
 Rats acquire the infection by eating garbage and discarded
offal from slaughter houses and by cannibalism, while the
large carnivora become infected by feeding on rodents and
meat scraps.
 Bear meat may serve as a source of human infection.
 Congenital infection rarely occurs in man
Trichinella spiralis
Antigens
 Specific and sensitive antigens are a requisite for
serologic diagnostic test.
 The presence of trichinous antigens has been
demonstrated in the serum and urine.
Antibobodies
 Complement-fixing, precipitative, agglutinative,
flocculative, protective, and supersensitive antibodies are
present in trichinous animals and may be detected by
various tests.
 Antiadult and antilarval antibodies are found in the
gamma globulin fraction of the serum. There is no
absolute correlation between the degree of eosinophilia
and the antibody content of the blood serum.
Trichinella spiralis
TRICHINELLIASIS
IMMUNITY
Natural Immunity
 Depends upon the species, age and nutrition of the host.
Acquired immunity
 The presence of immature and adult trichinae in the
intestinal mucosa, and of unencysted and encysted larvae
in the tissue, produces an immunity in the host which may
be demonstrated by the production of precipitative,
complement-fixing, and sensitizing antibodies, by passive
protective tests, and by resistance to reinfection.
 Immunity may be acquired by natural oral infection with
living larvae or by parental inoculation of dead or living
worms and larvae or their products.
Trichinella spiralis
TRICHINELLIASIS
IMMUNITY
Passive Immunity
 Some degree of protection is conferred by passive
immunization
Mechanism of immunity
 The mechanism of immunity has aroused considerable
speculation.Resistance to
superinfection has been
considered to be due to circulating antibodies
supplemented by the action of leucocytes and cells of the
reticuloendothelial system
 Chandler has postulated the existence of a strong local
intestinal immunity on the part of the cells of the intestinal
mucosa and a weaker of parenteral immunity