Epidemiology, diagnosis, treatment, and control of trichinellosis

Abstract

Throughout much of the world, Trichinella spp. are found to be the causative agents of human trichinellosis, a disease that not only is a public health hazard by affecting human patients but also represents an economic problem in porcine animal production and food safety. Due to the predominantly zoonotic importance of infection, the main efforts in many countries have focused on the control of Trichinella or the elimination of Trichinella from the food chain. The most important source of human infection worldwide is the domestic pig, but, e.g., in Europe, meats of horses and wild boars have played a significant role during outbreaks within the past 3 decades. Infection of humans occurs with the ingestion of Trichinella larvae that are encysted in muscle tissue of domestic or wild animal meat. Early clinical diagnosis of trichinellosis is rather difficult because pathognomonic signs or symptoms are lacking. Subsequent chronic forms of the disease are not easy to diagnose, irrespective of parameters including clinical findings, laboratory findings (nonspecific laboratory parameters such as eosinophilia, muscle enzymes, and serology), and epidemiological investigations. New regulations laying down rules for official controls for Trichinella in meat in order to improve food safety for consumers have recently been released in Europe. The evidence that the disease can be monitored and to some extent controlled with a rigorous reporting and testing system in place should be motivation to expand appropriate programs worldwide.

FIG. 1.

Trichinella sp. life cycle. (A) Main sources of Trichinella sp. infections for humans (including pigs, horses, wild boars, dogs, walruses, foxes, and bears). (B) Trichinella sp. cycle in the host body. In the enteral phase, muscle tissues are digested in the stomach, and larvae are released (1); larvae penetrate the intestinal mucosa of the small intestine and reach the adult stage within 48 h p.i., and male and female mate (2); female worm releases newborn larvae in the lymphatic vessels (from the fifth day p.i. onwards; the length of newborn production, from 1 week to several weeks, is under the influence of host immunity) (3). In the parenteral phase, the newborn larvae reach the striated muscle and actively penetrate in the muscle cell (4); the larva grow to the infective stage in the nurse cell (the former muscle cell) (5); and, after a period of time (weeks, months, or years), a calcification process occurs (6). (Modified from www.iss.it/site/Trichinella/index.asp with permission of the publisher.)

FIG. 2.

World map showing the distribution areas of Trichinella spiralis (Tsp), Trichinella pseudospiralis from north America (TpsN), T. pseudospiralis from Europe and Asia (TpsP), T. pseudospiralis from Tasmania (TpsA), Trichinella papuae (Tpa), and Trichinella zimbabwensis (Tzi). (Modified from www.iss.it/site/Trichinella/index.asp with permission of the publisher.)

FIG. 3.

World map showing the distribution areas of Trichinella nativa (Tna), Trichinella britovi (Tb), Trichinella murrelli (Tm), Trichinella nelsoni (Tne), Trichinella genotype T6 (T6), Trichinella genotype T8 (T8), and Trichinella genotype T9 (T9). In some regions, the distribution areas of these encapsulated species and genotypes overlap between them. (Modified from www.iss.it/site/Trichinella/index.asp with permission of the publisher.)

FIG. 4.

Histological section (hematoxylin-eosin staining) of a muscle biopsy from a patient involved in a trichinellosis outbreak (100). (A) Cellular infiltrates; (B) collagen capsule of a “nurse cell”; (C) intersected muscle larva. (Photograph courtesy of Dietrich-Bonhoeffer-Klinikum, Neubrandenburg, Germany.)