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Year : 2013  |  Volume : 56  |  Issue : 3  |  Page : 285-287
Glomerulopathy in a patient with sarcocystis infestation

1 Department of Anatomical and Clinical Pathology, St Luke's-Roosevelt Hospital Center, New York, USA
2 Department of General Pathology, Christian Medical College, Vellore, Tamil Nadu, India
3 Department of Neurological Sciences, Christian Medical College, Vellore, Tamil Nadu, India
4 Department of Internal Medicine, Christian Medical College, Vellore, Tamil Nadu, India

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Date of Web Publication24-Oct-2013


To date, sarcocystis has been considered an asymptomatic infection in humans. Even though cases with glomerulonephritis have been reported in animals with sarcocystis, there have been no reports of a similar occurrence in humans. We report a case of acute proliferative glomerulonephritis and leukocytoclastic vasculitis in a patient with sarcocystis infestation.

Keywords: Glomerulonephritis, leukocytoclastic vasculitis, sarcocystis

How to cite this article:
Balakrishna JP, Chacko G, Manipadam MT, RamyaI. Glomerulopathy in a patient with sarcocystis infestation . Indian J Pathol Microbiol 2013;56:285-7

How to cite this URL:
Balakrishna JP, Chacko G, Manipadam MT, RamyaI. Glomerulopathy in a patient with sarcocystis infestation . Indian J Pathol Microbiol [serial online] 2013 [cited 2020 Jun 1];56:285-7. Available from: http://www.ijpmonline.org/text.asp?2013/56/3/285/120400

   Introduction Top

Sarcocystosis , caused by Sarcocystis hominis and Sarcocystis sui hominis presents usually as an asymptomatic infestation in humans. The patient presented with features of glomerulonephritis and leukocytoclastic vasculitis (LCV) and was found to have sarcocystis infestation in skeletal muscle biopsy.

   Case Report Top

A 47-year-old man presented with a 1-month history of fever, skin lesions on both feet, and progressive renal failure. He had nephrotic range proteinuria. The urine analysis showed specific gravity: 1.020, blood: 3+, pH: 6.0, protein: 3+, leukocytes: negative, and RBC: 22-25. Renal function tests were abnormal with creatinine 1.8 mg% (normal range: 0.5-1.4) and urea 115 mg% (normal range: 15-40). Serum sodium was 122 mmol/l and potassium 6.0 mmol/l. Twenty-four-hour urine protein was 7.4 g with a urine volume of 680 ml.

The clinical impression was that of an Immunoglobulin A nephropathy or vasculitis. Serum vasculitic work-up including complement components and cANCA and pANCA was negative, dsDNA was normal, ANA was negative, and ASO titre was not elevated.

Renal biopsy revealed glomerular mesangial matrix expansion, mesangial hypercellularity, endocapillary cell proliferation, and exudation of neutrophils with karyorrhectic debris and segmental parietal cell proliferation. Two out of nine glomeruli showed circumferential cellular crescents [Figure 1]. There was interstitial edema with interstitial infiltrates of mononuclear inflammatory cells and neutrophils. Many of the tubules contained necrotic debris. Extraglomerular vessels showed no evidence of vasculitis. Immunofluorescence studies showed granular C3(1+) on glomerular capillaries. A diagnosis of acute proliferative glomerulonephritis with focal cellular crescents was made.
Figure 1: Proliferative glomerulonephritis (H and E, ×400)

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Skin biopsy from the lesions over leg showed LCV [Figure 2] and direct immunofluorescence studies showed smudgy granular fluorescence rimming some of the small-caliber dermal blood vessels for IgA and C3. There was no reactivity for Immunoglobulin G and Immunoglobulin M.

He was started on methyl prednisolone based on the diagnosis of LCV and acute proliferative glomerulonephritis.
Figure 2: (a) LCV in skin biopsy (H and E, ×100), (b) LCV in skin biopsy (H and E, ×400)

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Figure 3: (a) Encysted Sarcocystis in skeletal muscle (H and E, ×50), (b) Encysted Sarcocystis in skeletal muscle (H and E, ×100), (c) Encysted sarcocysti s in skeletal muscle (H and E, ×400)

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A muscle and nerve biopsy was also performed as part of the investigation for vasculitis. The muscle biopsy taken from vastus lateralis muscle showed several basophilic encysted parasitic forms containing long and tear-drop-shaped sporozoites of sarcocystis with no inflammation around the cysts [Figure 3]. Several atrophic fibers were present. There was no evidence of vasculitis. The sural nerve biopsy showed no evidence of vasculitis.

The patient was started on a course of co-trimoxazole and albendazole. He improved symptomatically and renal function was restored to normal with this treatment and other supportive measures. He was discharged after a period of hospital stay.

   Discussion Top

Sarcocystis is a protozoan parasite for which humans serve as both intermediate and definitive hosts. Humans may become infected by two species, S. hominis and S. sui hominis. [1] Intermediate hosts are the most affected by Sarcocystis in terms of disease. Twenty to forty days after ingestion of sporocysts and subsequent migration of sporozoites through body vessels, acute lesions such as edema, hemorrhage, and necrosis develop. [2] Lesions are associated with maturation of meronts within the endothelial and subendothelial cells. Symptomatic disease in humans is very rare; cysts are detected as incidental findings at autopsy or a biopsy containing muscle, performed for other diagnostic purposes. There is no inflammatory reaction around the cysts. [3]

This present case is unusual because Sarcocystis is considered to be an asymptomatic infection in humans, although there is one report of necrotizing vasculitis in humans with Sarcocystis in the initial stages of infestation. [2]

Systemic vasculitis has however been reported with other parasitic infections such as toxoplasmosis, trichinosis, strongyloidosis, amoebiasis, and leishmaniasis. [4]

The present case had skin lesions over both feet with evidence of LCV in a skin biopsy. This is in contrast to the skin lesions that are described in various parasitic infections like Schistosoma, Leishmania, Trypanosoma, Scabies, Dirofilaria, Onchocerca, Entamoeba, Acanthamoeba, Microsporidia, and many of the intestinal helminthes which are usually due to direct involvement of the skin at the site of entry of the organism rather than a generalized immune response. [5],[6]

There has been a single case report of Henoch - Schonlein pupura associated with Toxocara canis infection. [7] In the present case, although there were IgA deposits in the dermal vessels, the renal biopsy showed only C3 deposits, and no IgA on the glomerular capillary walls. The acute proliferative glomerulonephritis in this case remained unexplained. We postulate that the infestation with Sarocystis could have resulted in systemic manifestations. Glomerulopathy is known to occur with parasites such as Plasmodium, Schistosoma, Leishmania, Trypansoma, Filaria, Babesia, Toxoplasma, Trichinella, and Opisthorchis. The type of glomerulopathy is varied and ranges from mild and transient glomerulonephritis to persistent glomerulonephritis. [8],[9],[10] The histological changes noted include focal or diffuse mesangial proliferative glomerulonephritis, endocapillary proliferative glomerulonephritis, membranous, and membranoproliferative glomerulonephritis. Glomerulonephritis with eosinophilic infiltration has also been reported. [10] Interestingly, Sarcocystis has been reported to cause glomerulonephritis in animals. [7]

The occurrence of vasculitis and other manifestations like glomerulonephritis is suggested as a result of rupture of the cysts at irregular intervals with resultant release of antigens into the circulation, thus forming antigen and antibody complexes that in turn get deposited in vessel walls or glomerular capillary basement membrane and causing damage. [2]

To our knowledge, there have been no reports of glomerulopathy and vasculitis occurring alongside Sarcocystis in muscle in humans. It is unclear whether the two were coincidental or whether the systemic manifestations were the result of the infestation. Even though the parasitic encystation and occurrence of glomerulonephritis in this patient could be coincidental, as there was no other definite cause for the glomerulonephritis and vasculitis evidenced by the results of laboratory investigations and as there are other published reports of associations, it is likely more than coincidental and a causative mechanism needs to be considered.The parasite is rarely seen in routine practice that limits the availability of clinical information. This case is presented to illustrate its morphology, given its rarity, and stress the need for proper evaluation for parasitic infections in patients with unexplained glomerular disease.

   References Top

1.Fayer R.Sarcocystisspp. in human infections. ClinMicrobiol Rev 2004;17:894-902.  Back to cited text no. 1
2.McLeod R, Hirabayashi RN, Rothman W, Renington JS. Necrotizing vasculitis and sarcocystis: A cause-and-effect relationship? South Med J1980;73:1380-3.  Back to cited text no. 2
3.Mehrotra R, Bisht D, Singh PA, Gupta SC, Gupta RK. Diagnosis of human sarcocystis infection from biopsies of skeletal muscle. Pathology 1996;28:281-2.  Back to cited text no. 3
4.Lhote F. Systemic vasculitis during parasitosis. Presse Med 2004;33:1389-401.  Back to cited text no. 4
5.Mackey SL,Wagner KF. Dermatologic manifestations of parasitic diseases.Infect Dis Clin North Am1994;8:713-43.  Back to cited text no. 5
6.Meinking TL, Burkhart CN, Burkhart CG. Changing paradigms in parasitic infections: Common dermatological helminthic infections and cutaneous myiasis. ClinDermatol 2003;21:407-16.  Back to cited text no. 6
7.Van Velthuysen ML,Florquin S.Glomerulopathy associated with parasitic infections.ClinMicrobiol Rev 2000;13:55-66.  Back to cited text no. 7
8.Ginsburg BE, Wasserman J,Huldt G,Burgstrand A. Case of glomerulonephritis associated with acute toxoplasmosis. Br Med J 1974;3:664-5.  Back to cited text no. 8
9.Sitprija V, Boonpucknavig V. Renal involvement in parasitic diseases. In: Thisher CG, Brenner MB, editors. Renal Pathology with Clinical and Functional Correlations. 2 nd ed. Philadelphia: JB Lippincott; 1994. p. 626-55.  Back to cited text no. 9
10.Date A, Gunasekharan V, Kirubakaran MG,ShastryJC. Acute eosinophilic glomerulonephritis with Bancroftinfilariasis. Postgrad Med J 1979;55:905-7.  Back to cited text no. 10

Correspondence Address:
Geeta Chacko
Department of Neurological Sciences,Christian Medical College, Vellore - 632 004, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.120400

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  [Figure 1], [Figure 2], [Figure 3]

This article has been cited by
1 Human Infections with Sarcocystis Species
Ronald Fayer,Douglas H. Esposito,Jitender P. Dubey
Clinical Microbiology Reviews. 2015; 28(2): 295
[Pubmed] | [DOI]


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