Trichinosis / PORK LINKED TO LIVER CIRRHOSIS

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Trichinosis

 

 

Authors:

K. Darwin Murrell, USDA/ARS Peoria, Illinois

George T. Woods, University of Illinois

LeRoy G. Biehl, University of Illinois

 

Reviewers:

Ray Gamble, USDA/ARS, Beltsville, Maryland

Peter M. Schantz, CDC, Atlanta, Georgia

 

 

Trichinosis has been a stigma to the consumption of pork for years. A recent

study indicates that a trichina-safe pork supply would increase consumer

confidence and pork consumption, and result in additional income to pork

producers. The National Pork Producers Council is studying trichinosis and

methods of providing trichina-safe pork to consumers. The Council has set a goal

of a trichina-safe pork supply by 1987.

 

Trichinosis is a disease of man and other animals caused by a tiny parasitic

worm, Trichinella spiralis. Humans may be

infected by eating the meat of infected domestic pigs or occasionally the meat

of wild bears, wild pigs, or walruses. A number of wild animals are known to be

infected. Over the last decade, between 100 and 150 human cases per year are

reported in the United States. One study indicated 73.2% of the human cases were

attributed to pork products.

 

The number of human cases of trichinosis has declined dramatically in the United

States in the last 40 years, but the infection rate remains the highest of any

developed country in the world. Recent surveys indicate the national infection

rate in swine is about 0.125% per year. The infection rate in swine in Germany

is 0.00003%, 0.0008% in Russia, and 0.0% in Denmark. With approximately 89

million hogs slaughtered each year in the United States, this means there are

about 110,000 infected hogs per year. If 360 meals are obtained from one hog

carcass, approximately 40,000,000 potential servings of infected pork are

produced each year in the United States. Some investigators estimate that there

are 100,000 to 300,000 human exposures per year in the United States but 99% of

resulting infections are subclinical. In Europe, a major factor in reducing the

incidence of swine trichinosis has been the adoption of specific trichina

inspection procedures at the slaughter houses.

 

Life Cycle

 

 

Swine and wild animals are the reservoirs of trichinosis. Swine are usually

infected by consuming viable trichinae larvae in pork scraps found in uncooked

garbage and by meat from infected carcasses of swine, rats, and other

carnivorous wildlife (Figs. 1, 2, and 3).

 

After the ingestion of infected meat, the larvae are digested free of the muscle

cyst, enter the small intestine, and within four to six days develop into

sexually mature adults. The adults give birth to larvae that migrate through the

intestinal wall into the circulatory system. When they come into contact with

skeletal muscle, the larvae invade the muscle and by 17-21 days after infection

become mature encysted larvae. Once again, the life cycle is complete, and the

trichinae are in the infective stage. Encysted larvae can survive in putrefying

meat for long periods. It has been estimated that 25-30% of the total number of

muscle larvae present in an infected pig carcass are in the hams and 20% are

present in the shoulder cuts. Apparently, swine naturally infected with

trichinosis do not show clinical

effects. In experimental infections with large numbers of larvae, however, rear

paralysis and systemic reactions have been reported.

 

 

Treatments

 

 

No routine treatment for infected swine before slaughter has been developed that

will clean the animals of trichina cysts. In human infections, thiabendazole and

other supportive treatments are used. Similar drugs have been used

experimentally in swine and have been found effective, primarily against the

adult worms in the intestine and less effective against muscle larvae.

 

 

Prevention and Control

 

 

Experimental vaccines are being studied in pigs but are not available. At this

time, management practices are the only tools available to producers to

eliminate trichinosis from their market animals. Producers should practice the

following trichina-preventive measures:

 

- Observe all garbage feeding regulations. If garbage is fed, feed only

well-cooked garbage, including household scraps (212o F. for 30 min.).

 

- Practice stringent rodent control. Rats may be important sources in some swine

herds.

 

- Avoid exposing dead pig or wild animal carcasses to live

hogs. Do not throw wild game carcasses or parts to hogs or domestic pets.

 

- Ensure that hog carcasses are properly buried, incinerated,

or sent to a rendering plant.

 

- As often as possible, construct effective barriers between hogs and wild

animals.

 

Pork and meat from all wild mammals should be thoroughly

cooked before human consumption. Official federal and state meat inspection

programs require that all processed pork products that may be eaten without

additional cooking be heated to at least 137o F. to assure destruction of any

trichinae larvae that may be present. A recent USDA study indicated an increased

chance of survival of trichinae in microwave cooking. Uneven cooking with cold

spots in the microwave oven may cause some areas of fresh pork not to reach 137o

F. and thus any live trichina would persist. This has brought on a wave of

anxiety about trichinosis by

the public. However, recent research indicates that pork can be prepared safely

in the microwave if an oven cooking bag is used in the cooking procedure. To

allow a margin of safety the USDA recommends fresh pork be cooked to 170o F.

 

Fresh pork less than 6 in. thick can be rendered safe if

frozen to 5o F. (-17o C.) for 20 days, -10o F. (-23o C.) for 10

days, or -20o F. (-29o C.) for 6 days. Dry curing, which is the interaction of

salt and drying for relatively long periods, will

devitalize trichina cysts, if proper time and temperature relationships are

established.

 

Hamburger ground in a grinder not properly cleaned following grinding raw pork,

or hamburger that has pork added illegally, may transmit the disease to humans

if it is insufficiently cooked.

 

 

Trichina-Safe Pork

 

 

As a part of the National Pork Producers Council's Trichina-Safe Pork in the

U.S. by 1987 program, samples would be collected from all swine at slaughter and

tested for trichinosis. Infected herds could then be traced back to the farm of

origin if a national swine identification program is enacted. The Trichina-Safe

Committee of the NPPC has recommended adoption of such a swine identification

program.

 

Since low-dose irradiation (30,000 rads) is sufficient to

inactivate encysted trichinae, feasibility of use of this pro-

cedure on pork carcasses after slaughter also is being studied.

 

Eradication and certification of trichina-safe pork will

open up new markets for the swine industry at home and abroad. A strong

educational campaign of producers and consumers is necessary to remove this

currently held stigma from pork.

 

REV 12/91 (7M)

 

 

Figure 1.Source:Zimmerman, W., and Zinter, D. H.S.M.H.A. Health Reports 86 (Oct.

1971): 937-945. (Adapted from and used with permission)

 

LIFE CYCLE OF TRICHINELLA SPIRALIS

 

1. INFECTED MEAT EATEN BY HOST

 

2. MEAT FIBERS AND CYST WALLS ARE DIGESTED WHICH...

 

3. RELEASE TRICHINAE... WHERE IN SMALL INTESTINE DEVELOP INTO...

 

4. SEXUALLY MATURE ADULTS... WHICH MATE

 

5. FEMALE GIVES BIRTH TO YOUNG TRICHINAE (1,000-1,500) IN MUCOSA

OF INTESTINE

 

6. YOUNG TRICHINAE TRAVEL BY WAY OF INTESTINAL LYMPHATICS TO

BLOOD CIRCULATION TO...

 

7. MUSCLES OF HOST WHERE THEY ENCYST

 

Figure 2.Sylvatic cycle, representing the transmission of trichi-

nosis in nature, independent of man.``Carnivores and scavengers'' include fox,

bear, rat, walrus, hyena, wildcats, and many others. In the case of human

infection, the source would be called game meat, rather than carrion, and the

infection would represent an offshoot of the cycle. Original diagram from W. C.

Campbell,``Epidemiology I. Modes of transmission.'' In Trichinella and

Trichinosis, edited by W. C. Campbell. (New York:Plenum Press, 1983): 425-444.

(Adapted from and used with permission)

 

Figure 3.Domestic cycle, the predominant source of human trichinosis.

(Illustration courtesy of Dr. K. D. Murrell)

 

 

% Figures are available in hard copy

 

____________

 

Cooperative Extension Work in Agriculture and Home Economics,

State of Indiana, Purdue University and U.S. Department of Agri-

culture Cooperating. H.A. Wadsworth, Director, West Lafayette,

IN. Issued in furtherance of the Acts of May 8 and June 30, 1914.

It is the policy of the Cooperative Extension Service of Purdue

University that all persons shall have equal opportunity and

access to our programs and facilities.

 

 

www.genome.iastate.edu/edu/PIH/103.html

 

 

 

 

 

 

 

Oh Daniel, ask and it shall be given...

" Find me an article or two linking current pig farming conditions to the

conditions described in this article and maybe i'll have something to worry

about. " - Young Daniel

 

Human Health Issues Associated with the Hog Industry

 

checc.sph.unc.edu/rooms/library/docs/hogs/hogs_hhealth.html

 

Pleasant dreams.

 

Ali Muhammad

 

 

 

 

 

 

I did write that the trichina worm was only one, right?

Common internal parasites in swine

 

 

Roundworms ( Ascarids ).

 

An adult female ascarid produces thousands of eggs daily. These pass out in the

feces and, under favorable conditions of adequate moisture and warm temperature,

become infective in 3 to 4 weeks or more. A protective shell resists adverse

environmental conditions, enabling the eggs to remain alive for 5 years or

longer. Consequently, infective eggs are abundant on hog lots, pastures and

other places contaminated by droppings of infected hogs. When pigs swallow

infective eggs, the larvae (young worms) emerge from the eggs in the intestinal

tract and migrate through the liver, lungs and other tissues. Migration of

roundworm larvae through the lungs may lead to pneumonia and coughing. These

larvae eventually return to the intestine where they mature and become prolific

egg layers. Roundworm infestation results in decreased feed efficiency, lowered

growth rates and condemnation of livers.

 

 

Nodular worms ( Oesophagostomum ).

 

Nodular worms also inhabit the intestinal tract causing intestinal damage and

unthriftiness in pigs. Eggs pass out in the feces and hatch on the ground. The

larvae develop over an extended period and are ingested by the pig. They burrow

into the intestinal wall and develop within nodules in the wall of the intestine

before re-entering the intestinal tract where they mature.

 

 

Intestinal threadworms (Strongyloides ).

 

Threadworms are another inhabitant of the intestinal tract. Their eggs pass out

in the feces and hatch within a few hours under favorable conditions. This

parasite can also multiply outside the animal host, can be transmitted from the

sow to the pig before birth (prenatal infection), can be transmitted through the

colostrum and is capable of penetrating unbroken skin. As a result, mature

threadworms have been detected in baby pigs as early as 4 days old. The

resulting yellowish diarrhea and possible death loss in baby pigs can be a

difficult problem. In fact, numerous deaths of baby pigs in Florida have been

caused by this internal parasite.

 

 

Whipworms ( Trichuris ).

 

Whipworms are common internal parasites of swine. Eggs passed with the feces

develop into infective larvae in the environment in about a month. The larvae

are ingested and penetrate the intestinal wall, damaging tissue, robbing the pig

of essential nutrients, and causing diarrhea. Pigs infected with whipworms are

also prone to other intestinal infections such as salmonellosis and swine

dysentery. Whipworm infestations can be particularly devastating in young pigs

(3 months old or less).

 

 

Kidney worms.

 

The kidney worm is one of the most damaging parasites. The mature kidney worm is

about 1 inch long and can be found in or around the kidney or along the tubes

leading from the kidney to the bladder. The adult female produces eggs that are

passed through the urine. Swine are infected by ingestion of the eggs. The young

larvae will migrate into the liver and cause considerable damage before

migrating on to the kidney where the larvae will mature. Unlike other parasites,

the life cycle of this parasite is quite long, a total of 15 months. The kidney

worm is a problem primarily in the southeastern USA.

 

 

Lungworms.

 

The adult lungworm produces eggs in the lungs which are coughed up, swallowed

and pass out in the feces. Earth worms ingest the eggs and become infected. Pigs

may root up and swallow earth worms containing the infective stage of the

parasite. Lung infection then occurs and considerable lung damage and pneumonia

can result.

 

Other internal parasites.

 

Several other parasites are also of importance in swine. These include coccidia,

thorny-headed worms, stomach worms and trichina (from raw or improperly cooked

garbage).

 

Pleasant dreams.

 

Ali Muhamma

 

 

 

 

 

 

 

PORK LINKED TO LIVER CIRRHOSIS

 

from Canadian Science News, January 1986

 

By

 

Carolyn Hoskins

 

FOR the first time, researchers have shown a possible link between

cirrhosis of the liver and dietary factors other than alcohol. The

recent findings of an Ottawa research team show that people who drink,

even in moderation, and consume pork are more likely to suffer the

potentially fatal liver disease than are people who consume other meat

or fatty diets.

 

Dr Amin A. Nanji, Head of Clinical Biochemistry at the Ottawa General

Hospital, and Samuel W French, Chairman of the Department of Pathology

at the University of Ottawa, investigated the relationship between

`per capita' consumption of total fat, beef, and pork in several

countries and the mortality rates for cirrhosis of the liver in these

same countries. They focused their studies on countries where alcohol

consumption was relatively low, such as Canada, the U.S., West Germany

and Australia. Dr Nanji says previous reports had shown a high rate of

deaths from cirrhosis in countries where alcohol consumption was very

high, but a " curious scatter " of deaths in countries where alcohol

consumption was low.

 

In other words, countries with low levels of alcohol consumption

showed a great variation in the incidence of cirrhosis deaths. Dr

Nanji concluded that some other factor besides alcohol must be at

work. Cirrhosis of the liver is a leading cause of death in North

America. In the early stages of this degenerative disease, the liver

becomes inflated by fat, a condition called `alcoholic fatty liver'.

This condition can be reversed.

 

In the later stages of cirrhosis, normal liver tissue is gradually

replaced by fibrous tissue, the liver structure becomes misshapen and

disorganized, and the liver cannot recover. Eventually the victim dies

from liver failure. When the Ottawa team examined the diets of the

countries in their study, they found no relationship between deaths

from cirrhosis and dietary fat or beef consumption. However, they did

find a striking correlation between pork consumption and cirrhosis

mortality for the same countries. When they examined the relationship

in terms of pork consumption multiplied by alcohol consumption, the

results were overwhelming.

 

The two scientists also compared similar data from Canada's ten

provinces. Again cirrhosis mortality was significantly associated with

pork, but not with alcohol consumption - presumably because Canadians

as a group are not heavy drinkers. When the researchers left

Newfoundland and Prince Edward Island, where more seafood is eaten,

there was an even stronger link between the fatal liver disease and

pork consumption.

 

Even more convincing to the researchers were comparisons of pork

consumption and its effect on cirrhosis death rates within a

population. Among the Canadian provinces where alcohol consumption

varies little between provinces (from 9.23 litres per person a year in

New Brunswick to 13.05 in Alberta) the death rates from cirrhosis were

directly related to `per capita' pork consumption, but not to alcohol

intake.

 

For example, although Albertans drink slightly more than people in

British Columbia, they suffer far less from cirrhosis deaths than do

people in B.C.,who have a higher pork intake. Dr Nanji says the

researchers don't know how pork might cause or enhance cirrhosis of

the liver. Nor should their study be taken to mean that alcohol does

not cause liver disease, he says. But other researchers have

speculated that some " facilitating factor " might explain why only some

alcoholics get cirrhosis. The Ottawa team may have found part of the

answer Dr Nanji says. Drs. Nanji and French hope to follow their

statistical study with a " case control study " in which they will

investigate meat consumption of individual alcoholic and cirrhotic

patients. They also plan to initiate rat feeding studies to

investigate the possible role of unsaturated and saturated fats in

chronic alcoholism.