Requirement for Completion
By: Marie Fe G. Yumul



Trichinellosis/ Trichinosis
The Causal Agents: Genus Trichinella
The genus Trichinella has undergone changes, because of the advent of reliable DNA probes that can be used to distinguish the various species of the genus. There are 8 recognized genotypes. Members of this genus are able to infect broad spectrum of mammalian hosts, making them one of the world’s most widely distributed group of nematode infections. Trichuris spp. are genetically related to Trichuris spp, and Capillaria spp; all belonging to the Family Trichurata. These roundworms constitute an unusual group of organism in the phylum nematoda, because they all live as an intracellular parasite one part of their lives. (Despomier,2004) T. spiralis (found worldwide in many carnivorous and omnivorous animals) - is the primary cause associated with domestic animals. - Has low tolerance to freezing, and has high reproductive potential in swine, laboratory rats, and laboratory mice. - Primary cause of domestic animal trichinosis although it also occurs in sylvatic hosts. T. pseudospiralis (mammals and birds worldwide) - has been documented in birds and does not form a capsule in the muscle. T. nativa (Arctic bears) - has been documented in cougar, walrus, whale, and bear flesh. T. nelsoni (African predators and scavengers) - seen in various large carnivores T. britovi (carnivores of Europe and western Asia). - seen frequently in wild boar, horses, and free ranging swine.

Life Cycle and Morphology:
T. spiralis (Owen, 1835) is a relatively small nematode with adult females 1.4 to 4 mm, adult males 1.4 to 1.8 mm and muscle larvae of approximately 1mm. The life cycle of the parasite begins with the enteral phase of infection when a person or an animal eats contaminated meat containing first stage muscle larvae. Digestive juices from the stomach (pepsin and hydrochloric acid) dissolve the capsule-like cyst and release the larvae which pass into the small intestine, where they invade the columnar epithelium (Katz, 1989). Shortly thereafter, the larvae molt four times, mature to adults that mate. Female worms can produce 500–1,500 newborn larvae (immature L1) during a life span, before expulsion by the host immune system. The migratory phase of infection begins when these newborn larvae are passed into tissue, enter lymphatics and then enter the general circulation at the thoracic duct. These larvae are widely distributed in tissue by the circulation and eventually make their way through the capillaries (tiny blood vessels) into the muscle fibers, which intiates the muscle phase of infection. Once in the muscle fibers, they encyst, undergo development, become infective within 15 days and remain for months to years.

Adult worms that developed in the small intestine following oral infection with muscle larvae A; the small worms are newborn larvae (immature L1), which are infective to muscle . Infective muscle larva in altered muscle cell surrounded by a collagen capsule (blue) B. Infective muscle larva, Azan staining of longitudinal section of excysted larvae. M: midgut, G: genital primordium, S: stichocyte. C

Center for Disease Control and Prevention

Trichinellosis is acquired by ingesting meat containing cysts (encysted larvae) of Trichinella. After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa where they develop into adult worms (female 2.2 mm in length, males 1.2 mm; life span in the small bowel: 4 weeks). After 1 week, the females release larvae that migrate to the striated muscles where they encyst . Trichinella pseudospiralis, however, does not encyst. Encystment is completed in 4 to 5 weeks and the encysted larvae may remain viable for several years. Ingestion of the encysted larvae perpetuates the cycle. Rats and rodents are primarily responsible for maintaining the endemicity of this infection. Carnivorous/omnivorous animals, such as pigs or bears, feed on infected rodents or meat from other animals. Different animal hosts are implicated in the life cycle of the different species of Trichinella. Humans are accidentally infected when eating improperly processed meat of these carnivorous animals (or eating food contaminated with such meat).


Discovery of Trichinella spiralis
It was February 2, 18985 when young Jim Paget, a first year medical student at London Hospital Medical School, joined an ongoing autopsy procedure at St. Bartholomew’s Hospital. The 51 year old Italian brick layer who died of tuberculosis that they were dissecting also had a

sandy diaphragm, a condition that dulled even the sharpest scalpel. When the surgeons went out of the necropsy room, Jim quickly took a small bit of muscle tissue from the diaphragm as he was more curious of its nature. He examined the muscle with the hand lens he always carried. He though he saw small worms coiled up inside each nodule and shared his preliminary observations to Dr. Thomas Wormald, and he informed his intention to run the specimen over the British Museum so that he could get a closer look the tissue under the microscope. Paget went into the Zoology Department at the museum and borrowed the microscope owned by the botanist, Robert Brown. He examined the tissue under the microscope and saw tiny refractile bodies that sure enough revealed the presence of coiled worms. Jim went home and reported his findings to his older brother as he always done every night. Richard Owen, an assistant curator at the Royal College of Surgeons, was known to Wormald, the surgeon took a second piece of the tissue from the diaphragm with him to Owen after reflecting on Paget’s cursory assessment as to its potential medical importance, Owen who had access to first-class microscopes back then saw the same critters as what Paget saw. But unlike Paget, Owen wrote his findings, drew pictures, and went to report to the Royal Society three weeks later, not giving credit to the original observations of Jim Paget. The rudiments if the life cycle of Trichinella spiralis were soon in ravelled by Rudolf Virchow et. al..(Campell, 2004)

The Discovery of the Life Cycle
The famous German Pathologist, Rudolph Virchow, with the help of his fellow Rudolph Leukart and Friedrich Zenker, deciphered the essentials of the life cycle of Trichinella spiralis in the mid 1850’s to the !870’s. Virchow took advantage of serendipity, an old dog and a fresh cadaver who’s muscle tissue was riddled with white flecks, just like what Richard Owen described in 1835. The experiment proceeded as Virchow fed the canine a large quantity of this infected human muscle tissue. Days later the dog died, he autopsied the dead dog and observed the enteral stage (adult worm) in the intestine, and concluded correctly that trichinella may cause disease in humans, as well. Most importantly, Virchow discovered that if the infected meat is first heated to 137oF for 10 min, the worms were no longer infective. He experimented vigorously and wrote extensively about the life of these worms. (Campell,2004)

Geographic Distribution
The parasites are found worldwide and most common in parts of Europe and in the United States. An average of 12 cases per year were reported in 1997-2000. In China, serologic population surveys have revealed prevalence rates between 0.66-12%. (Takahashi, 2000), (Liu, 2002). **A detailed information on the world wide distribution of Trichinella spp. In man and animals can be accessed through this link: Click Click Click 

Trichinella are nematode worms that are affecting different people from different countries worldwide. This genera cause diseases to both human and animal population and poses a threat to life. Infection by Trichinella spp. has been detected in domestic animals of all continents with the exception of Antartica, where there is no record of the parasite (Pozio and Murrel, 2006). The global distribution of trichinella together with different cultural eating habbits, represents the main factor favouring human infections in industrialised and nonindustrialized countries. (Pozio, 2007)

The Disease:
The diseases that Trichinella spp. cause are collectively referred to as trichinellosis. Currently, prevalence of trichinellosis is low within the United States, occurring mostly as scattered outbreaks, and the majority of human cases are due to Trichinella spiralis and T. murrelli. The domestic pig is the main reservoir host for T. spiralis. This species is significantly higher in prevalence in people living in certain parts of Europe, Asia, and Southeast Asia than in the United States. It is now considered endemic in Japan and China. A large outbreak of trichinellosis occurred in Lebanon in 1997, infecting over 200 people. Trichinella spiralis infection in humans has been reported from Korea for the first time. In contrast, trichinella infections in wildlife within the United States are now thought to be largely due to the T5 strain, tentatively designated T. murrelli.

Infective first stage larva of Trichinella spiralis in its Nurse cell in muscle tissue. The worm measures 1mm x 36 µm.

An outbreak of T. pseudospiralis in Thailand has been reported. This species can also infect birds of prey. Foci have also been described in Sweden, The Slovak Republic, and Tasmania (Australia). Trichinella paupae (provisional), apparently similar in biology to T. pseudospiralis, has been described in wild and domestic pigs in Papua New Guinea. Humans can also be infected with T. nativa and T. britovi. Reservoir hosts for T. nativa include sled dogs, walruses, and polar bears. T. britovi is the sylvatic form of trichinellosis throughout

most of Asia and Europe. There are numerous reports in the literature of infections with this parasite in fox, raccoon, dog, opossum, domestic and wild dogs, and cats.

Adult T. spiralis in situ. Small intestine of experimentally infected mouse. The worm is embedded within the cytoplasm of the columnar cells. T. nelsoni is restricted to mammals in Equatorial Africa, such as hyenas and the large predatory cats. Occasionally people acquire infection with T. nelsoni. Most animals in the wild, regardless of their geographic location, acquire trichinella by scavenging. The recently discovered T. zimbabwensis infects crocodiles and mammals in Africa, and is a non-encapsulate species. No human cases have been reported, so far. Puerto Rico and mainland Australia remain trichinellafree. T. pseudospiralis has been isolated from the Tasmanian Devil, but not from humans living in that part of Australia Trichinellosis is a foodborne disease caused by tiny parasitic worm, Trichinella spiralis. The worms spread when flesh from infected animals were ingested by other animals. Humans are infected by eating improperly cooked or raw meat. Soon after infection, symptoms may appear 4-45 days depending on the number of parasite ingested but it is usually 10 to 14 days. The symptoms usually start with pain and diarrhea, followed by fever, weakness, muscle soreness, pain and swelling around the eyes. Thirst, profuse sweating, chills, weakness and tiredness may develop. Chest pain may be experienced since the parasite may become imbedded in the diaphragm. The proper hygiene and handling in the preparation of our daily meals are important considerations to keep our food disease free and safe for consumption. One of the most widespread zoonotic pathogen in the world could possibly be present on our meals and that it should be of major concern to prevent these pathogens from affecting our health. In the Philippines, a research entitled, “Incidence and Epidemiology of Trichinella in Philippine Swine” is currently being conducted all over the land with the aim to determine the impact of local swine management in the incidence of Trichinella.


Cellular and Molecular Pathogenesis

Enteral Phase

The enteral (intestinal) phase includes larval stages 1 through 4, and the immature and reproductive adult stages. In humans, this phase can last up to 3 weeks or more. Developing worms damage columnar epithelium, depositing shed cuticula there. Later in the infection, at the onset of production of newborns, local inflammation, consisting of infiltration by eosinophils, neutrophils, and lymphocytes, intensifies in the local area. Villi flatten and become somewhat less absorbent, but not enough to result in malabsorption syndrome. When larvae penetrate into the lymphatic circulation or bloodstream, a bacteremia due to enteric flora may result, and cases of death due to sepsis have been reported. Loss of wheat germ agglutinin receptors along the entire small intestine occurs.26 The myenteric electric potential is interrupted during the enteral phase, and as the result, gut motility slows down.

Newborn larva of T. spiralis. 70 x 7 mm.

Newborn larva of T. spiralis entering muscle cell.

Parenteral Phase

The parenteral phase of infection induces most of the pathological consequences. It is dose dependent and is attributable directly to the migrating newborn larvae as they randomly penetrate cells (e.g., brain, liver, kidney, heart) in their search for striated skeletal muscle cells (Fig. 21.6). Cell death is the usual result of these events. The more penetration events there are, the more severe the resulting pathology. The result during heavy infection is a generalized edema. Proteinuria may ensue. Cardiomyopathies and central nervous system abnormalities are also common in those experiencing moderate to heavy infection. Clinical Signs The first symptoms of trichinellosis are gastrointestinal, usually occuring 1-2 weeks after a person consumes raw or undercooked meat from a Trichinella-infected animal. These symptoms include:
   

Nausea Diarrhea Vomiting Abdominal pain

Further symptoms (that correspond with the second phase of infection) usually occur about 2 weeks after eating contaminated meat, and can last up to 8 weeks:
   

Headaches Fevers Fatigue Chills

      

Cough Eye swelling Aching joints Muscle pains Itchy skin Diarrhea Constipation

Symptoms may range from very mild to severe and relate to the number of infectious worms consumed in the meat. Many mild cases of trichinellosis are never specifically diagnosed because they are assumed to be the flu or other common illnesses. Furthermore, many people with Trichinella infection do not experience any symptoms at all. If the infection is heavy, persons may have trouble coordinating movements, and have heart and breathing problems. Although rare, death can occur in severe cases. For mild to moderate infections, most symptoms go away within a few months. Diagnosis Definitive diagnosis depends upon finding the Nurse cell-parasite complex in muscle biopsy by microscopic examination or detection of Trichinella–specific DNA by PCR. PCR is very sensitive and specific for detecting small numbers of larvae in muscle tissue, but due to the infrequency of request and the costs associated with maintaining such a capability, PCR is usually prohibitive for most hospital laboratories. This will undoubtedly change in the near future, as more and more parasitic infections become diagnosed routinely by PCR-based methods. Muscle biopsy can be negative, even in the heaviest of infections, due to sampling errors. In addition, the larvae may be at an early stage of their development, making them inconspicuous, even to experienced pathologists. A rising, plateauing and falling level of circulating eosinophils throughout the infection period is not direct proof of infection, but armed with this information, the clinician could treat the patient as if the diagnosis of trichinella had been made. Bilateral periorbital edema, petechiae under the fingernails, and high fever, coupled with a history of eating raw or undercooked meats, is further indirect evidence for this infection. It is helpful to remember that wild mammals can also be sources of infection. Outbreaks of trichinellosis have been traced to hunters and the recipients of their kills. Muscle enzymes, such as creatine phosphokinase (CPK) and lactic dehydrogenase (LDH), are released into the circulation causing an increase in their serum levels. Serological tests begin to show positive results within two weeks. ELISA can detect antibodies in some patients as early as 12 days after infection.

Treatment: (Dugdale, 2010) Mebendazole or albendazole can be used to treat infections in the intestines. There is no specific treatment for trichinosis once the larvae have invaded the muscles. The cysts remain viable for years. Pain killers can help relieve muscle soreness. Complications
   

Encephalitis Heart failure Heart rhythm problems (arrhythmias) from heart inflammation (myocarditis) Pneumonia

Prevention/Control and Treatment:
Within the last 10 years, outbreaks of trichinellosis in the United States have been rare and sporadic in nature. Most have been associated with the ingestion of raw or undercooked meats from game animals and not from commercial sources. This represents a shift in the epidemiology of outbreaks compared to 20-30 years ago, when commercial pork sources of infection were much more common than today. Pigs raised on individual farms, as compared to commercial farm operations, are more likely to be fed uncooked garbage, and thus acquire the infection. This is because feeding unprocessed garbage containing meat scraps is against federally mandated regulations. In the past 10 years, small farms have, in the main, been bought up and replaced with larger so-called “factory” farms, in which upwards of 10,000 pigs can be managed with a minimum of labor. Enforcement of laws governing the running of large production facilities is a full time activity and has been key in reducing the spread of diseases infecting livestock and humans alike. As already mentioned, top carnivores such as bear, fox, cougar, and the like often become infected. Hunters sharing their kill with others are best warned to cook all meat thoroughly. Herbivores can harbor the infection as well, since most plant eaters occasionally ingest meat when the opportunity arises. Epidemics due to eating raw horsemeat have been reported from France, Italy, and Poland. Meat inspection is nonexistent in the United States with respect to trichinella. In Europe, the countries participating in the common market employ several strategies for examining meat for muscle larvae. Most serve to identify pools of meat samples from given regions. If they are consistently negative, then a trichinella-free designation is applied to that supply of meat. Nonetheless, rare outbreaks occur, despite this rigorous system of inspection. Trichinellosis due to Trichinella spiralis can be prevented by either cooking meat thoroughly at 58.5° C for 10 minutes or by freezing it at -20° C for three days. However, with other species of trichinella, the story is quite different, since they are mostly found in wild animals. For example, bears and raccoons have special proteins in their muscle cells that prevent ice crystals from forming during periods of hibernation, inadvertently permitting survival of the larvae at

temperatures below freezing. Hence, the only way to render those meats edible is to cook them thoroughly.

Thanks to the following sources that I compiled for the progress of this study.
REFERENCES: Edoardo Pozio. World distribution of Trichinella spp. infections in animals and humans (2007). Veterinary Parasitology 149 (2007) 3–21. Available online at Trichinosis/Trichinellosis Disease Fact Sheet. Division of Public Health, Bureau of Communicable Disease, Communicable Disease Epidemiology Section, Wisconsin Department of Health (2001). Available online at W.C. Campell. History of Trichinella. © 2004 Ma. Noreen Eng.(2011). Serological Survey for Trichinella Infection. Centers for Disease Control and Prevention. Parasites - Trichinellosis (also known as Trichinosis)

David C. Dugdale (2010). Trichinosis. A.D.A.M. Medical Encyclopedia.

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