| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
According to criteria defined by the Centers for Disease Control and Prevention, the diagnosis of trichinellosis is made by a positive serologic test result or a Trichinella-positive muscle biopsy specimen in a patient exhibiting one or more clinical symptoms compatible with trichinellosis, such as eosinophilia, fever, myalgia, or periorbital edema.3 However, the identification of new species in conjunction with its high prevalence in wild game could complicate the clinical picture of trichinellosis given that symptomology is not necessarily congruent among Trichinella species.5,6 Similarly, a review by Dupouy-Camet and others7 proposed a more stringent algorithm for determining the probability of acute trichinellosis in humans ranging from "very unlikely" to "confirmed" based solely upon clinical grounds and without parasitologic data. Using that algorithm, we report a case classified as a "confirmed trichinellosis" in the absence of a positive biopsy specimen, and present further clinical evidence of neurologic involvement.
Upon arrival in Omaha, the patient was still unconscious. With the initial suspicion of an early intracranial abscess or cerebritis, the patient was switched to intravenous ceftriaxone and metronidazole with no resolution of the symptoms. Magnetic resonance imaging (MRI) of the brain only showed non-specific white matter changes.
Three days after admission to the Nebraska Medical Center in Omaha, the patient was awake but remained disoriented and aphasic. She developed periorbital edema with petechia and conjunctivitis on the left side (Figure 1
). A re-evaluation of her peripheral blood count showed 16.4 x 103 white blood cells/mm3 with 22% eosinophils, and elevated creatine kinase levels at 467 U/L (normal < 145 U/L). We were informed by a relative that the patient and her husband would occasionally supplement their diets with wild game obtained by hunting. An ELISA for IgG antibodies to conserved immunodominant Trichinella antigens was performed (ARUP Laboratories, Salt Lake City, UT) and a positive result was obtained (> 1.0 optical density [OD] units at a serum titer of 1:64; positive > 0.3 OD units) using rabbit and human sera as positive and negative controls, respectively.
|
The patient was sent to a rehabilitation facility where she remained for an additional 24 days during which time her neurologic condition and ocular symptoms abated. The patient was unable to recall recent ingestion of fresh pork or wild game, but confirmed that her husband hunted regularly. After discharge, the patient became unavailable for follow-up; thus, convalesce-stage titers could not be obtained. The husband refused to be evaluated and the household was not shared by other relatives; consequently, they were not tested for trichinellosis.
Central nervous system inflammatory infiltration and damage may result from the secretion of toxic parasite antigens, larval migration and vascular obstruction, or eosinophil infiltration, although to date none of these hypotheses have ever been validated. It has been reported that myocardial injury and/or infarction often accompanies neurotrichinellosis, as assessed by electrocardiographic data.14,17 However, this is likely related to the severity of infection and resulting ischemia rather than any causal relationship between the foci.
After ingestion of contaminated meat and maturation of adult worms in the small bowel (enteral phase), larvae are released into the blood stream (parenteral phase) and travel to muscles and potentially other organs such as the brain. These phases are clinically associated with nausea and transient diarrhea during the first week of infection, and with myalgia, periorbital edema, conjunctivitis and neurologic symptoms during weeks 2–8 after infection, by which time the patient usually seroconverts.13 Symptoms of neurologic involvement appear early after the infection, and may include headache, tinnitus, vertigo, deafness, aphasia, seizures, and apathy.5,14 Concomitant peripheral eosinophilia is common with Trichinella-associated encephalopathy; however, in some cases, it may not be prominent until one week later. Nonetheless, hypereosinophilia as reported herein (> 3,700 cells/mm3) is significantly higher in patients with neurologic dysfunction than in those not exhibiting neurologic signs, and is directly associated with the intensity of infection.14 In addition to the other symptoms, the unconscious state of the patient at the time of admission and her obtunded and disoriented condition after regaining consciousness were consistent with neurologic involvement.
The patient did not recall ingestion of fresh game or pork prior to the incidence. However, evidence is clear that some forms of Trichinella found in sylvatic hosts can withstand freezing for long periods of time and remain infectious for up to a year or longer after freezing. Thus, the consumption of fresh infected meat is no longer requisite for acquiring an infection. In the United States, freeze-resistant genotypes of Trichinella have been identified in game meat from New Hampshire,18 Idaho,19 Pennsylvania,20 and Montana.21 One report indicated Trichinella infection from ingesting improperly processed cougar meat that had been frozen.19 A higher incidence of trichinellosis has been reported in Alaska,3 where the inhabitants consume a greater proportion of wild animal meat (particularly bear meat) in their diets, and where freeze-resistant species of Trichinella are normally found.
Other parasitic infections that may cause abnormal mental status and eosinophilia include toxocariasis, angiostrongyloidiasis, and baylisascariasis.22,23 Although we did not specifically test for these conditions, the absence of pets at home or contact with raccoons, the lack of eosinophils in the CSF, and the lack of ocular larva migrans on examination argue against these possibilities. Moderate eosinophilic pleocytosis is quite common24 in toxocariasis patients with CNS involvement, where 80% of patients exhibit eosinophilia 
10% in CSF.25 Likewise, Angiostrongylus cantonensis can cause eosinophilic meningitis and peripheral eosinophilia, although this infection is predominantly found in southeast Asia and the Pacific Islands. Nonetheless, no eosinophils were seen in the CSF of our patient. In contrast, CNS involvement by Baylisascaris is most often fatal. Those who survive are generally left in a persistent vegetative state, or with severe residual side effects.26
Although the United States does not require inspection of pork products for Trichinella, the number of cases of trichinellosis has been progressively decreasing from approximately 400 cases and 15 deaths per year in the 1940s to approximately 12 cases per year (range = 11–23) and no deaths during the last survey spanning 1997–2001.3 During this period, 76% of the patients had at least one common sign or symptom of trichinellosis: 54% eosinophilia, 46% fever, 64% myalgia, and 31% periorbital edema. Globally, outbreaks of the disease still occur in regions where the guidelines for meat inspection are lacking or poorly regulated. However, cases of neurotrichinellosis have been poorly documented because of a combination of low incidence and misdiagnosis, given the polymorphic manifestations of the disease. Nonetheless, diagnosis of neurotrichinellosis should be considered in patients with hypereosinophilia, elevation of muscle enzyme levels, and neurologic abnormalities in the setting of wild game consumption. Given the rapid onslaught of physical symptoms, unused portions of meat should be sought to confirm the source and species of the causative agent of the disease. However, as was the case herein, biopsy specimens may not always be positive, possibly because of a shortened time interval between the appearance of symptoms and the biopsy, and infected meat may not be available for parasite identification. In these cases, it is important to rely upon a paradigm such as that defined by Dubouy-Camet and others7 for final diagnosis. In this case, the rapid resolution of the symptoms after treatment with an antiparasitic drug is further evidence of a correct diagnosis.
Received March 13, 2007. Accepted for publication April 18, 2007.
* Address correspondence to Miguel G. Madariaga, Division of Infectious Diseases, University of Nebraska Medical Center, 985400 Nebraska Medical Center, Omaha, NE 68198. E-mail: mmadariaga{at}unmc.edu 
Authors’ addresses: Miguel G. Madariaga, Division of Infectious Diseases, University of Nebraska Medical Center, 985400 Nebraska Medical Center, Omaha, NE 68198, Telephone: 402-559-8650, Fax: 402-559-6005, E-mail: mmadariaga{at}unmc.edu. Edward R. Cachay, Division of Infectious Diseases, University of California, School of Medicine, San Diego, CA 92103. Dante S. Zarlenga, Bovine Functional Genomics Laboratory and Animal Parasitic Diseases Laboratory, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD 20705.
This article has been cited by other articles:
|
|
 |
|
  C. Graeff-Teixeira, A. C. A. da Silva, and K. Yoshimura Update on Eosinophilic Meningoencephalitis and Its Clinical Relevance Clin. Microbiol. Rev., April 1, 2009; 22(2): 322 - 348. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
