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What's your interpretation?
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Non refereed
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Toxoplasmosis: Silently
declining
Dave Pyburn,
DVM
National Trichinae
Coordinator and Acting Program Manager, NVAP; USDA, APHIS, VS, 210 Walnut
St, Room 891, Des Moines, IA 50309; Tel: 515-284-4122; Fax: 515-284-4191.
Cite as: Pyburn
D. Toxoplasmosis: Silently declining. J Swine Health Prod. 2004;12(2):98-99.
The charts show serological test results from USDA's National Animal Health
Monitoring System National Swine Surveys. Seroprevalence in 1990 is included
for sows but not finishers. Can you speculate on what organism this is and
why the level of seroprevalence is steadily falling in both sows and finishers?
Toxoplasma gondii, a protozoan para-
site capable of infecting all mam- mals and birds, is the causative agent
of one of the most common parasitic global
zoonoses.1 Even though T gondii infections in
humans are often asymptomatic, the organism still causes an estimated 112,500
cases of foodborne illness in the United States annually, and together with
two other
pathogens, accounts for 75% of the foodborne-illness deaths attributable to
known agents.2
On the basis of national serologic data collected during the 1994 National
Health and Nutritional Examination Survey, approximately 40% of the adult
population of the United States has had
toxoplasmosis, the disease caused by the parasite
T gondii.2 If a woman is infected with
T gondii for the first time during pregnancy,
spontaneous abortion or infection of the fetus may
occur. Infant mortality may be as high as 12%, and 30% of infected infants suffer
severe birth defects, including mental
retardation.3 The Centers for Disease Control and
Prevention estimates that the incidence of congenital infections with
T gondii in the United States ranges from 400 to
4000 cases per year. They also estimate that the annual economic impact of
toxoplasmosis in humans is $7.7 billion($US).4
Toxoplasmosis may be reactivated in immunosuppressed people, resulting in
severe illness and death. Toxoplasmic encephalitis (in which the parasite multiplies in
the brain) is the second most common opportunistic infection of the central
nervous system related to acquired
immunodeficiency syndrome (AIDS). The cost of
treating toxoplasmosis in AIDS patients in the United States ranges between $23
and $106 million each year ($US).3
The natural route of T gondii
transmission to humans is from animals and
contaminated soil and water by way of ingestion.
People, other mammals, and birds are usually infected with
T gondii in one of three ways: by eating tissue cysts in undercooked
meat; by swallowing oocysts (eggs) from cat feces during gardening or other activities
involving soil contact; or by ingesting food and water contaminated with oocysts.
Cats, and possibly other Felidae, are the only hosts that can shed the
environmentally resistant oocysts of T
gondii. Animals develop immunity to additional infection
as tissue cysts form after infection. These cysts remain alive for the lifetime of the
animal, and, in undercooked or uncooked meat, they are infective for animals and
humans. Sheep, goats, pigs, chickens, and wild
game all may have infective T gondii
tissue cysts in edible portions of
meat.5
When T gondii is considered as a
foodborne pathogen, pork is often singled out as
the most likely carrier food. This perception stems from past studies, which
indicate that the seroprevalence of antibodies against
T gondii is high in swine relative to other food-producing
animals.6 The results of the 2000 USDA National
Animal Health Monitoring System's National Swine Survey, the most recent
comprehensive study of the US pork industry, found
a seroprevalence rate of 6.00% for sows and 0.90% for finisher pigs (Table 1) (Dr
E. Bush, Veterinary Epidemiologist and Swine Specialist with the USDA Center for
Animal Health Monitoring, 2002, personal communication). These are both
significantly lower than in previous studies of the
pork industry (Table 1). In 1995, the USDA's National Animal Health Monitoring
System National Swine Survey found rates of 15.00% in sows and 3.20% in
finishers (Table 1).7 In 1990, the same study
tested only sows and found a seroprevalence rate of 20.00% (Table 1) (Dr E. Bush,
2002, personal communication).
Others still assert that handling raw pork or eating undercooked pork is a major
way that people in the United States become infected with
T gondii. The Centers for Disease Control and Prevention
estimates that 50% of T gondii infections are due
to foodborne transmission of the
organism.2 Of the food-producing animals, it is
believed that swine are more commonly infected and thus more often the foodborne
source of the organism.7 Risk factors that
have been identified for swine infection with T
gondii include lot size, water source, swine contact with cats and cat feces, failure
to clean the facility between groups of animals, and a lack of barn-specific boots.
The seroprevalence of antibodies against T
gondii in US swine has decreased in the last decade, indicating that the infection rate
of T gondii in US swine has decreased. This decrease may be due to
increased biosecurity in the industry and
production practices that separate swine from cats
and cat feces.
As a veterinarian, the most effective way you can assist your clients in
preventing swine infection with this organism is
to advise them on biosecurity and proper rodent control programs.
T gondii oocysts are very hardy and may be tracked into facilities
on boots, shoes, and clothing. Footwear should be barn specific, ie, when
people enter the barn, they put on boots that are worn only within that barn. This will
help to avoid bringing T gondii oocysts into
the barn. You should also inform your clients that cats do not act as a safe or
effective means of rodent control on a farm.
Assist your producers with implementing a complete on-farm rodent control program
that includes addressing rodent harborage, rodent feed and water, rodent exclusion
measures, and rodent population reduction and elimination procedures.
References
1. Tenter AM, Heckeroth AR, Weiss LM. Toxoplasma
gondii: from animals to humans. Int J
Parasitol. 2000;30:1217-1258.
2. Mead PS, Slutsker L, Dietz V, McCaig LF,
Bresee JS, Shapiro C, Griffin PM, Tauxe RV.
Food-related illness and death in the United States.
Emerg Infect Dis. 1999;5:607-625.
*3. Roberts T, Weiss M, Southard L. Issues in
pork safety: Costs, controls, and incentives. Agric
Outlook. 1993;201:28-32.
4. Jones JL, Kruszon-Moran D, Wilson M, McQuillan G, Navin T, McAuley JB.
Toxoplasma gondii infection in the United States:
Seroprevalence and risk factors. Am J
Epidemiol. 2001;154:357-365.
5. Dubey JP, Beattie CP. Toxoplasmosis of
Animals and Man. Boca Raton, Florida: CRC
Press. 1988;220.
*6. Davies P. Foodborne pathogens and pork production: What is our Achilles' heel?
Proc AASP.
New Orleans, Louisiana. 1999;275-285.
7. Hill D, Dubey JP. Toxoplasma gondii:
transmission, diagnosis and prevention. Clin Microbiol
Inf Dis. 2002;8:634-640.
* Non-refereed references.
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