What is Trichinosis?
Trichinosis (trichinellosis) – acute helminthiasis of humans and mammals, the important medico-social importance of which is due to the severity of clinical manifestations, often loss of ability to work, and in some cases fatal. Invasion is characterized by fever, muscle aches, swelling of the face, skin rashes, high eosinophilia, and in severe cases, damage to the myocardium, lungs, and central nervous system.
Causes of Trichinosis
The causative agent of trichinosis is Trichinella spiralis (Paget, 1835, Owen, 1835). In nature, there are other species – T. pseudospiralis, T. nativa, T. nelsoni. Their role is less studied, species independence is discussed.
Trichinella – small, almost filiform helminths (thrix – hair), covered with cross-striated cuticle. The body of T. spiralis is rounded, somewhat narrowed towards the front end. The length of a mature male is 1.2–2 mm with a width of 0.04–0.05 mm. The length of a mature female before fertilization is 1.5-1.8 mm; after fertilization, its length increases to 4.4 mm.
The digestive system begins with the mouth opening, which leads to the mouth capsule, on its ventral side there is a stylet with which the parasite is attached to the intestinal mucosa of the host. The esophagus – a narrow capillary tube – in the second third of the body passes into the intestine, ending with a short rectum.
The reproductive system is unpaired. In the male, it ends at the posterior end of the body with two copulative appendages. In females in the back of the body is the ovary, which passes into the oviduct. A large part of the body is occupied by a long and wide uterus, which ends with a sexual opening at the end of the anterior quarter of the body.
Trichinosis among animals is found in all latitudes of the globe, on all continents except Australia. Trichinosis is more prevalent in the northern hemisphere.
The range of trichinosis among humans corresponds to its distribution among animals. The greatest infestation of people is observed in the USA, Germany and Poland, where there are persistent stationary foci.
Trichinosis is registered in some regions of Russia (Magadan Region, Khabarovsk, Krasnoyarsk and Krasnodar Territory), in Belarus, the Baltic States, and Ukraine.
Trichinosis – natural focal invasion.
The existence of two types of trichinosis foci has been established: natural and synanthropic. Natural foci are primary in origin. Trichinella can parasitize in the body 57 species of wild and domestic animals, the basis of the circulation of the pathogen lies alimentary communication. In these outbreaks, parasites circulate among wild animals (wild boars, badgers, raccoon dogs, brown and polar bears, foxes, hens, minks, ferrets, etc.), marine mammals (whales, sea seals) due to predation or eating carrion. In synanthropic foci of trichinas circulate among domestic animals (pigs, cats, dogs), rodents (mice, rats) also due to eating each other or falling. In addition, synanthropic foci are replenished by hunting trophies – trichinosis wild animals.
There is a direct and inverse relationship between natural and synanthropic foci. Invasion from natural foci is entered into synanthropic in two ways: by a person who hunts invasive wild animals and feeds their remains to domestic animals, and wild synanthropic (rats, mice) that migrate in the spring to natural foci, and return back in the fall. As a result, mixed natural-synanthropic foci are created.
The dispersal of trichinosis invasion is promoted by birds of prey and birds that feed on carrion of the trichinosis animal through invasive droppings or their own carcass in case of death. According to G. G. Smirnov, A. A. Ginetsinskaya, and A. A. Dobrovolsky, larvae and adult insects — predatory carrion flies and carnivorous beetles — dead beetle beetles, ground beetle larvae that feed on wild animals, contribute to the dispersion of trichinosis invasion.
Infection of marine mammals occurs when they swallow Trichinella larvae that enter the water with remains of carrionous birds (polar owls, raven, etc.), as well as sea animals that feed on carrion (crustaceans) in which the larvae retain viability .
In the muscles of animals, the larvae remain invasive for years, and in the cadaveric material they die under the influence of very high or low temperatures (-40, -50 ° C) and can tolerate the conditions of the Arctic zone.
Domestic and wild animals affected by trichinosis are the source of human invasion. Most often it is pigs, wild boar, brown and polar bear, coypu, badger, fox, for some nationalities – dogs.
The mechanism of infection is oral. The susceptibility of people to trichinosis is very high. In order to get a serious illness, it is enough to eat 10-15 g of trichinosis meat. Infection usually occurs when eating raw or insufficiently boiled meat of animals affected by trichinosis, most often meat, lard, ham, bacon bacon, brisket, sausage made from infested pork, and wild animal affected trichinella (bear, wild boar, badger ).
The incidence of trichinosis usually has a group character. Members of the same family, persons participating in the same holiday feast, a hunting meal, who used the meat of the same trichinosis animal without prior sanitary-veterinary control, get sick.
Trichinella larvae die when the temperature inside the piece of meat reaches at least 80 ° C. Salting and smoking of meat on the encapsulated larvae does not work.
The seasonal nature of group outbreaks has been established. In synanthropic foci, they are in most cases associated with the autumn period – the period of slaughter of pigs and the preparation of meat products.
Outbreaks of trichinosis in natural foci are associated with the hunting season – the autumn-winter period. Due to existing poaching, they can occur at any time of the year.
The formation of foci of trichinosis contributes to the incorrect management of pig breeding: the free keeping of pigs, their vagrancy, access to the pigs rodents, cats, dogs.
Trichinella life cycle
Trichinella are viviparous worms. An important biological feature is also the fact that the same organism becomes first definitive and then intermediate host. Trichinella have the most different owners, except man. They parasitize many mammals – pigs, boars, bears, wolves, foxes, badgers, dogs, cats, as well as rodents, insectivorous and marine mammals.
In the mature stage, the helminths are parasitic in the wall of the small intestine, and in the larval stage, in striated muscles, except for the heart muscle.
A person becomes ill with trichinosis when eating infected with encapsulated larvae of pork or meat of wild animals. In the process of digestion, the larvae are released from the capsules and within an hour are introduced into the mucous membrane, reaching the submucosal layer of the small intestine.
In a day they turn into males and females. Mature individuals with the help of the head stylet are attached to the intestinal mucosa, where they are then copulated.
In the body of different animals, the female trichinella parasitizes from 10 to 56 days, giving birth to 200 to 2000 live larvae. During the entire period of parasitization in the human intestine (no more than 42-56 days), one female gives birth to an average of 1500 larvae. The larvae penetrate through the mucous membrane of the intestine into the lymphatic, then the blood vessels and blood flow through the host organism. On the 5-8th day, the larvae fall into the skeletal striated musculature. With the help of hyaluronidase secreted by them, they penetrate into the sarcolemma of the muscle fiber, where their further development occurs, already in the body, which has become an intermediate host for the pathogen. 18-20 days after infection, the larva in the muscles extends to 0.8 mm, reaches the invasive stage and begins to coil.
Due to the response of the surrounding tissue around the larva, a connective tissue capsule is formed within 35-40 days. The average size of capsules in humans is 0.35 x 0.24 mm, they vary in different animals and vary in length from 0.25 to 0, 80 mm in length, and in width from 0.15 to 0.33 mm. The capsule plays a protective role, its wall is permeated with blood vessels, through which the larva receives nutrients and oxygen and releases metabolic products.
After 6-14-18 months, the muscle larva capsule is gradually impregnated with calcium salts and the calcification process begins, which ends on average 2 years after infection. However, in calcified capsules, the larvae can remain viable for 25 years or more. The distribution of larvae in the muscles is not the same. In the muscle of the heart and the smooth muscles of other organs, the larvae are not localized. Usually they accumulate in muscles rich in blood vessels: tongue, diaphragm, deltoid, forearm, gastrocnemius, intercostal, masticatory, abdominal muscles. In this way, the biological cycle of trichinella in the organism of one host ends. The encapsulated larva can continue its further development to a mature individual only if it is swallowed, eaten with raw muscle tissue by another host. In the intestines of the new host, it is released from the capsule and repeats the new development cycle.
Pathogenesis during Trichinosis
The pathogenesis of trichinosis is complex, representing a complex of pathological reactions, the trigger mechanism of which is the pathogen.
As you know, the entire biological cycle of Trichinella passes in the body of one host, in this case, a person in which the successive stages of helminth growth have different localization: an invasive larva in the lumen, and then in the mucous membrane of the small intestine; a growing and then an adult in the tissue of the small intestine; migratory larva – in the bloodstream and lymph; muscle larva – in striated muscles. As a result, the products of metabolism and partial decay, especially of larval and growing individuals, enter directly into the tissues. They are parasitic antigens with high sensitizing activity.
The allergic nature of trichinosis lies at the heart of its pathogenesis. N. N. Ozeretskovskaya distinguishes three phases of the development of the pathological process: enzymatic-toxic (1-2 weeks after infection), allergic (from the end of the second, 3-4 weeks after infection) and immunopathological.
The enzymatic-toxic phase is associated with the penetration of invasive Trichinella larvae into the intestinal mucosa and the formation of adult helminths, under the influence of enzymes and metabolites of which an inflammatory reaction develops in the intestine.
The second – the allergic phase of trichinosis – is characterized by the occurrence of common allergic manifestations in the form of fever, myalgia, edema, skin rashes, conjunctivitis, catarrhal pulmonary syndrome, etc. By the end of the first week, mature adult trichinella begin to regenerate young larvae that migrate through lymph and blood to lymph striated muscles. The suppressed host defense reaction due to the immunosuppressive action of adult parasites does not interfere with the active circulation of the larvae.
However, by the end of the second – in the third week of the disease, the level of specific antibodies in the serum of the invaded increases and a violent allergic reaction develops.
Rapid allergic inflammation in the small intestine contributes to the death of adult trichinella, the formation of granulomas around the trichinella larvae in the muscles, from which fibrous capsules subsequently form, preventing the entry of parasite antigens into the host organism.
The severity of immunological reactions depends on the dose of antigen and immunoreactivity of the host organism, on the degree of adaptation of the parasite to the host. An increase in the dose of infection leads to an increase in the intensity of intestinal and muscle invasion, which in turn leads to an increase in the severity of the disease and inhibition of immunological processes. This is accompanied by systemic damage to organs and tissues as a result of the sensitization of the body not only by the products of helminth metabolism, but also by the decay products of damaged or destroyed host tissues. This phase is manifested by fever, muscle pain, swelling, conjunctivitis, and respiratory disorders.
The immunopathological phase of trichinosis, usually associated with intense infection, is characterized by the appearance of allergic systemic vasculitis and severe organ lesions.
Nodular infiltrates occur in the myocardium, brain, lungs, liver, and other organs. Trichinosis is complicated by severe allergic diffuse focal myocarditis, meningoencephalitis, focal pneumonia and other equally severe organ lesions, which can be combined with each other, accompanied by high fever, severe muscle pain, skin rashes, and the spread of edema.
By the 5-6th week after infection, the inflammatory process in the parenchymal organs is replaced by dystrophic disorders, which recover slowly over a period of 6-12 months.
Treatment of patients with all forms of trichinosis, except for erased, is carried out in a hospital, since the progression of the disease and severe adverse reactions to specific treatment are possible. Treatment of patients with erased and mild forms of trichinosis, as well as patients who came under observation in the period of convalescence after a moderate illness, is carried out with anti-inflammatory non-steroid drugs. Specific treatment – mebendazole (vermox) is carried out by patients with moderate trichinosis and seriously ill. Vermoxum is prescribed for adults at 0.3 g per day (for children at a dose of 5 mg per 1 kg of body weight) in 3 divided doses after meals for 7-10 days, depending on the severity of the disease. To prevent adverse allergic reactions in response to the death of parasites, specific treatment is carried out against the background of anti-inflammatory therapy with brufen or voltaren. Glucocorticoids are prescribed together with specific drugs for severe illness with organ lesions – prednisone at a dose of 30 to 80 mg per day or 6-10 mg of dexamethasone per day for the period of chemotherapy with a rapid reduction in the dose of the drug after 5-7 days of its use.
The forced position of the patient and his immobility require care with a change in his position in bed, after removal from a serious condition – massage, passive, and then active gymnastics.
Prevention of Trichinosis
The fight against trichinosis is carried out by comprehensive medical, veterinary and hunting organizations with mandatory mutual information between them.
The most important task for the prevention of trichinosis is to prevent the introduction of invasion from the main reservoir – natural foci. The basic rule of the epizootological principle is that carcasses of inedible animals and birds, the remains of edible predatory animals, are hunted, as well as domestic animals that died from trichinosis, should be buried to a depth of at least 1 meter after preliminary treatment with kerosene.
An important role in the system of preventive measures is provided by the stall maintenance of pigs and the obligatory trichinoscopy during their slaughter.
According to the veterinary legislation in force in our country, meat of pigs, wild boars and bears is subjected to compulsory trichinoscopy. Meat products are subjected to trichinoscopy regardless of the processing technology, i.e. corned beef, smoked pork, and in some cases sausages. If at least one trichinella is found in 24 muscle sections, the meat is destroyed by burning or sent for technical disposal, the external fat is overheated for 20 minutes. at a temperature of 100 ° C, and the internal can be used without heat treatment.
The meat and meat products received in the sale in stores and markets undergo trichinoscopy and are not dangerous. As a rule, diseases of trichinosis arise due to the use of pig meat, slaughtered at home, wild boars, bears, hunted and not tested in the laboratory.
In settlements, slaughterhouses and biothermal pits should be equipped for the disposal of slaughter waste and carcasses of animals, trapping and extermination of stray dogs and cats should be organized, and deratization measures should be carried out. It is forbidden to slaughter animals without veterinary and sanitary control, as well as the sale of pork, meat of wild animals without the stigma of vetsanekspertiza.
Personal prevention of trichinosis consists in eating only the meat of pigs and wild animals examined for trichinosis. You can’t buy the meat of these animals or meat products in random markets in the absence of a certificate of veterinary expertise. If there is a suspicion for a full guarantee, the meat should be subjected to prolonged heat treatment (at least 2.5 hours) with a thickness of a piece of meat not more than 8 cm.
Existing methods of salting and smoking of meat do not guarantee the destruction of muscle Trichinella in the deep layers.
Extensive sanitary and educational work (especially in existing centers, recently rehabilitated) should consist in familiarizing the population with the ways of infection, the danger of the disease, and measures of social and personal prevention.