Elsevier

Parasitology International

Volume 59, Issue 3, September 2010, Pages 487-489
Parasitology International

Case Report
A case of giardiasis expressing severe systemic symptoms and marked hypereosinophilia

https://doi.org/10.1016/j.parint.2010.06.006Get rights and content

Abstract

An 88-year-old Japanese woman was referred to our hospital due to a one-month history of face edema, aphagia, shortness of breath, and skin rush over almost her entire skin. She had no abdominal symptoms. Her peripheral blood count showed a white blood cell (WBC) count of 27.1 × 109/L with 82.1% eosinophils. Serum non-specific Immunoglobulin E was within a normal range. Soluble interleukin-2 receptor was elevated to 4200 U/mL. At first, her eosinophil count was so high that we suspected she had an eosinophilic leukemia or hypereosinophilic syndrome. After admission, cysts of Giardia duodenalis (G. duodenalis) were detected in the patient's feces by microscopic analysis, then she was diagnosed with giardiasis, and 750 mg per day of metronidazole was administered for seven days. Her WBC count decreased to 6.0 × 109/L with 10% eosinophils, and her systemic symptoms improved. At that time her serum IL-5 was within a normal range. A few months later, the patient again complained of skin rush, and G. duodenalis was once again found in her feces. Her serum IL-5 was elevated to 751 pg/mL. Metronidazole was administered for two weeks, and her eosinophil count decreased. G. duodenalis is a protozoan parasite, and it is one of the most common waterborne transmission gastrointestinal parasites in the world. G. duodenalis rarely causes hypereosinophilia. To our knowledge, this is the first case report of giardiasis with extreme hypereosinophilia and severe systemic symptoms.

Introduction

Giardia duodenalis (synonymous with G. lamblia and G. intestinalis) is a flagellated protozoan parasite, and it is one of the most common waterborne transmission gastrointestinal parasites in the world [1]. In Japan, all physicians have to report cases of G. duodenalis infection under the Infectious Disease Control Law, which was enacted in April 1999. Since then, about 100 cases of G. duodenalis infection have been reported per year [2], with more than half occurring in travelers returning from areas where it is endemic [3]. Water is the major source for the endemic or epidemic spread of giardiasis [4].

The clinical spectrum of giardiasis's symptoms varies from asymptomatic to serious; two-thirds of those infected remain asymptomatic [5]. Patients with chronic giardiasis exhibit loose stool, steatorrhea, and profound weight loss. Occasionally, hypersensitivity phenomena such as rush, urticaria, aphtous ulceration, and reactive arthritis synovitis [5], [6] are seen in giardiasis, although these manifestations are very rare.

The host's immune cells act in concert with G. duodenalis during infection [7]. The immune responses in human or experimental hosts infected with G. duodenalis have not been fully elucidated [8], [9], [10].

During the acute phase of G. duodenalis infection, T-cell-dependent mechanisms are essential. G. duodenalis do not usually invade the host's intestine, but G. duodenalis infection causes a diffuse shortening of the epithelial microvilli. This enterocytic injury is mediated by activated host T lymphocytes. Pathophysiological activation of lymphocytes is secondary to G. duodenalis-induced disruption of epithelial tight junctions, which in turn increases intestinal permeability [11].

A study focusing on the antigenicity of G. duodenalis revealed that somatic extracts from G. muris were poorly immunogenic to mice [12], but the G. duodenalis' excreted/secreted (E/S) proteins, which contain a cysteine protease, induced immune responses in BALB/c mice, so high titers of specific IgG1, IgG2, and IgE antibodies were detected after immunization with native E/S proteins [9]. Furthermore, to avoid the hosts' immune reaction, G. duodenalis continuously changes its surface antigen coat [13]. Antigenic variation is associated with a unique family of surface antigens, named VSP (variant surface protein). In the experimental murine host, the humoral immune response is directed predominantly against VSP, but in human patients the antibodies against invariant antigens are also produced during G. duodenalis infection [8], [14].

We describe here a case of giardiasis presenting with severe hypereosinophilia and systemic symptoms without gastrointestinal symptoms.

Section snippets

Case report

An 88-year-old Japanese woman was referred to our hospital due to a one-month history of face edema, aphagia, shortness of breath, and skin rush on her neck and back, and she also had hypereosinophilia. She had no abdominal symptoms or particularly relevant past medical history. On physical examination, edema of the face and neck was observed, and edema of the eyelids was especially severe. Rushes with scratching scars were observed over almost her entire skin. Her peripheral blood count showed

Discussion

We describe here an extremely rare case of giardiasis presenting with hypereosinophilia and systemic symptoms. The patient's eosinophil count was so high that we suspected she had an eosinophilic leukemia or hypereosinophilic syndrome. However, cysts of G. duodenalis were found in her feces; upon administration of metronidazole, her symptoms improved and her eosinophil count returned to normal. Some questions were raised regarding the route of infection and hypereosinophilia without elevation

Acknowledgement

We would like to thank all of our colleagues.

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