Do you dream of steak tartare? Are the names ossenworst, kitfo, crudos, yookhwe, or larb lu, music to your ears? You are not alone. Globally, including in the United States, countless people swear by these and other raw meat dishes. The question is – are you putting yourself at risk?
According to 2011 CDC estimates, every year foodborne illnesses attack 1 in 6 Americans (or 48 million people), resulting in 128,000 hospitalizations, and 3,000 deaths. The spectrum of foodborne diseases evolves over time, because while improvements in food safety and public health measures may help conquer some diseases, others may appear or reappear as a result of various extraneous (social, cultural, or economic) factors. One such factor is the consumption of raw or under-cooked meat or meat-products, favored across many cultures.
Thanks to scientific research and advances in medicine and diagnostics, we now know that raw meat may carry disease-causing microbes (a.k.a. pathogens), due to unhygienic handling during production, improper storage (inadequate temperature control, cross-contamination from other food stuff stored alongside), or unsanitary preparatory practices prior to consumption. Pathogens commonly associated with raw meat are mostly bacteria, such as toxin-producing E. coli, Staphylococcus, Salmonella, Campylobacter, and Listeria (which in recent times has prompted recalls of cheese and fruits).
These apart, there are several types of parasites, small and large (Giardia, Toxoplasma, Taenia/Tapeworm, Trichinella, and so on) – that cause food-borne illness in humans. While parasitic diseases do not count within top five domestically acquired foodborne illnesses, they remain a significant public health problem, especially due to their chronic nature and diagnostic challenges.
Human trichinellosis (pronounced ‘TRICK-i-NELL-o-sis’) or trichinosis (‘TRICK-i-no-sis’) is one such parasitic disease caused by nematode roundworms called Trichinella (‘TRICK-i-NELL-a’). In the United States, trichinellosis has been tracked since the late 1940s, and made nationally notifiable since 1966; cases reported to the CDC are summarized and followed up as a part of trichinellosis surveillance. Recently, the CDC released the surveillance summaries for 2008-2012, listing 84 confirmed cases during this period, almost half of which came from five localized outbreaks.
Trichinellosis cases reported to the CDC have decreased greatly from over the years; from approximately 400 (with 10–15 trichinellosis-related deaths) annually during 1947-1951, the number has declined to a median of 15 cases reported per year during 2008–2012. Nonetheless, the latest figures represent an increase in incidence; the annual median was 8 during the previous period, 2002-2007. This is a cause for concern, because Trichinellosis cases are always related to consumption of raw or under-cooked meat.
Figure: Number of reported confirmed cases of trichinellosis, by year — National Notifiable Disease Surveillance System, United States, 1947–2012; figure source, CDC.
Raw meat and Trichinella, a unique relationship
Most parasites have encapsulated (surrounded by a protective, chitinous shell) cysts or parasite eggs as their infective forms, which are passed through feces, and get into food via fecal contamination. Trichinella, uniquely, is transmitted in the larval form – inside the muscle or meat. This parasite’s life cycle comprises two generations in the same host. Host invasion starts by ingestion of larva-burdened raw meat. (Note, this is the reason why Trichinella transmission in nature occurs by hunting, scavenging and/or cannibalism by carnivores, and human-to-human transmission is not known to occur.) The parasite larvae are released by action of gastric acids, reach and embed themselves within the mucosa (internal lining) of the host small intestines. Therein the larvae molt within two days, developing into sexually-active adult worms – who mate and the female delivers its larvae.
With the delivery of the newborn, second-generation larvae (which takes about a week), the adult worms are usually expelled from the intestines through feces, via the action of intestinal immune mechanisms. However, the nascent larvae migrate directly into blood vessels and lymphatics of the host, thereby reaching highly vascular (blood vessel-rich), oxygenated tissues, such as striated/skeletal muscles. Inside an infected muscle cell (referred to as a ‘nurse cell’), the newborn larvae grow into the infective stage in about two weeks, and can remain in that dormant (a.k.a. ‘hypobiotic’) state for about 20-40 years. Ingestion of these larvae as before by a new host initiates a new cycle.
Trichinella larvae in muscle cells; figure courtesy: CDC
Trichinella – tricky fella
Trichinella parasites demonstrate a few interesting evolutionary adaptations.
- During the dormancy of muscle larva, five species of the genus Trichinella, including the most common Trichinella spiralis, cause the nurse cell to secrete a thick collagen capsule outside the larva to create a protective niche; the capsule, as well as the nurse cell, may become calcified with time.
- Interestingly, these ‘encapsulated’ species restrict themselves to mammalian hosts, whereas three ‘non-encapsulated’ species – in which the nurse cell forms a very thin collagen capsule, not visible except with an electron microscope – are able to infect a broader variety of hosts.
- Trichinella tricks the nurse cells into thinking that there is less oxygen around (a condition called ‘hypoxia’), which causes these cells to secrete a substance that promotes growth of more blood vessels in the infected muscle (favoring nutrient supply to the nurse cell). However, the parasite larvae rely upon anaerobic metabolism, which allows them to survive even in absence of oxygen – as in dead/decaying carcasses.
- Some Trichinella species can successfully survive below freezing temperatures (-18˚C or lower) for an extended period of time.
- Interestingly, the host immune response generated during the intestinal phase (which results in later expulsion of the adult worms) partly influences the subsequent inflammatory immune response to larvae in nurse cells; the parasite is able to modulate the host immune response to favor a long-lasting muscle infection. In addition, the non-encapsulated species (such as the T. pseudospiralis, which infects mammals and birds) incite a lower intensity inflammatory response to the nurse cell than do the encapsulated ones.
Trichinella has an additional interesting feature. Recent studies have shown that parasitism-related genes in Trichinella spiralis are differentially regulated in the larval and adult stages of the worm, by means of a chemical modification (‘methylation’) of the DNA. This opens up exciting possibilities to study the mechanistic evolution of parasitism, and perhaps eventually to discover a genome-targeted drug against such parasites.
Ecology of infection and human influence
Human trichinellosis has been attributed to raw or under-cooked meat from a variety of sources: domestic and wild pigs, wild game animals – deer, elk, moose, bison, bear, wild felines (bobcat, cougar), wild canines (coyote, wolf, fox, dog), wild boars and warthogs, beaver, rabbit, alligator, and armadillo, as well as birds (such as quail, pheasant, duck, wild turkey, raven, and so on) – in addition to horse, beef, goat, and walrus. In fact, the range of natural hosts for Trichinella infection is extremely broad, encompassing mammals, birds, and reptiles. In the nature (‘sylvatic environment’), wildlife is the primary reservoir, with hunting/scavenging carnivores supported the parasitic life cycle. Experimental infection has been observed in frogs, insects and shrimp, but biological characteristics of the parasite interaction with these lower vertebrates and invertebrates make them unlikely to play any role in the natural transmission. However, there is well-documented evidence from around the world that human actions may influence the sylvatic cycle of Trichinella. Transmission to the domestic environment usually occurs as a result of human failure to undertake proper sequestration and management of domestic animals and wildlife.
For instance, risk of transmission to new hosts is enhanced due to inadequacies in wild game hunting practices – improper handling and/or careless disposal of dead animal prey in the field, as well as unhygienic handling and storage of the harvested raw meat. High human activity areas offer wild animals potential alternative food sources (such as domestic animals and garbage), facilitating the chances of sylvatic to domestic transmission. Presence of outdoor farms (containing pigs, dogs, horses, or crocodiles) and certain high-risk farming practices (feeding of food waste containing pork or wild game scraps; unsecured free-range pasturing which may cause a domestic animal to be exposed inadvertently to infected meats) contribute to the risk of transmission.
In the industrialized nations of North America and Europe, human trichinellosis from domestic pigs have nearly disappeared because of advancements in pig-farming facilities, measures undertaken to improve the health of farm-raised pigs, and employment of enhanced detection technologies in slaughterhouses, as well as systematic disease surveillance and increased consumer awareness of the dangers of raw and under-cooked meat. However, occasional infections continue to occur via consumption of meat from home-raised or organically farmed pigs, as well as non-pig meat (horse, bear, deer). More than half of the confirmed trichinellosis cases in the US during the current period (2008-2012) came from non-pork meats. In contrast, the developing nations of Central and South America, Europe and Asia continue to harbor a significant proportion of Trichinella biomass in wildlife and domestic animals, and important demographic factors (sociocultural/economic) continue to contribute to the burden of human trichinellosis.
NOTE: For more information, I refer the reader to these two exhaustive reviews – dated 2006 and 2009 – authored by Prof. Edoardo Pozio, an acclaimed parasitologist at the Istituto Superiore di Sanità, Rome.
Trichinellosis: disease, diagnosis, treatment, control
Since the life-cycle of the worm starts at host gut, the primary clinical symptoms of trichinellosis, appearing within two days of consumption of larva-laden raw meat, are gastrointestinal – nausea, diarrhea, vomiting and abdominal pain. Classical accompanying symptoms, that often occur within two weeks and may last up to eight weeks, are somewhat flu-like – with fever and chills, muscle and joint pain, headache, weakness or fatigue, itchy skin, and swelling of the face and/or eyes. These symptoms mostly occur as a result of the host immune system declaring war on the larval and/or adult parasite. However, in severe infections (especially in the at-risk population: people with weakened immune system, as in cases of HIV/AIDS, organ transplants, or cancer chemotherapy), the patient may have difficulty in coordinating movements, as well as heart and breathing problems, sometimes with a fatal outcome. It is known that the severity of disease is strongly correlated with the number of larvae consumed in the meat by the patient.
Patients with a history of consumption of raw meats are given an antibody test when exhibiting the symptoms of trichinellosis; the antibody is formed by the patient’s immune system in response to Trichinella larvae, and it reacts to antigens from this worm in laboratory tests. Serum levels of these antibodies depend upon the amount of larvae consumed; the values generally peak within 60-90 days after infection, and then decline. However, the antibody may remain detectable for 10+ years, which often poses a diagnostic challenge for physicians – in differentiating between a past and a recent infection, or more importantly, in attributing current symptoms to Trichinella (as opposed to some other infection, such as influenza, causing same symptoms).
Definitive diagnosis, as well as species identification and genotyping of the parasite, requires biopsies of skeletal muscles, which are done infrequently in human patients, but mostly in animal carcasses for the purpose of disease surveillance and outbreak investigations.
Mild to moderate symptoms may go away in a few months. Prompt treatment during the initial phase of the infection (first several days) with anti-parasitic drugs, albendazole, mebendazole, or related therapeutic agents – available on prescription – may kill the adult worms and prevent further release of larvae. However, initiation of treatment may be delayed due to the delayed appearance of symptoms and lack of a definitive diagnosis – which may necessitate a longer course of treatment, sometimes along with a steroid in more severe cases.
However, for this parasite, an ounce of prevention is most certainly worth more than a pound of cure. Cooking meat to safe temperatures prior to consumption is the recommended best practice. Proper handling of dead animal prey in the field, as well as adequate and hygienic practices for handling, storage and cooking of the harvested raw meat, are extremely important steps in preventing transmission of Trichinella and the occurrence of human trichinellosis.