Letters to Editor

An anecdotal case of cysticercus of axillary lymph node in a patient with metastatic breast carcinoma Dear Editor, Cysticercosis is a common parasitic infestation caused by Cysticercus cellulosae, a larval stage of intestinal cestode, Taenia solium. The infection is common in many parts of the world including China, Russia, Philippines, Indonesia, Mexico and India. The parasite has a predilection for subcutaneous tissue, brain, striated muscle, heart, liver, lungs and eyes.[1] Only four cases of submandibular, mesenteric and cervical lymph node involvement by cysticercus have been reported so far.[2‑4] We report the first case of cysticercus of axillary lymph node in a patient harboring metastatic breast carcinoma. A 54‑year‑old female patient of Indian origin, presented with a lump in upper outer quadrant of the left breast. On examination, the lump was non mobile and firm to hard. Overlying skin, nipple and areola were unremarkable. Following fine‑needle aspiration from the lump, that showed a carcinoma, left modified radical mastectomy was done. Grossly, the tumor measured 3.5 cm × 2.8 cm and was firm and grey white on cut section. Histopathological examination confirmed an invasive ductal carcinoma. Four out of 18 axillary lymph nodes had tumor metastasis [Figure 1a]. Incidentally, in largest of the uninvolved lymph nodes, a parasitic cyst was noted [Figure 1b]. The parasite showed characteristic morphology of cysticercus having three layers: An outer cuticle, middle cellular and an inner reticular layer along with invaginated scolices [Figure 2]. Following this, patient’s clinical

a

history, physical examination, and radiological investigations failed to reveal any focus of cysticercus in other more common sites such as subcutaneous tissue, muscle, brain, eyes or elsewhere. The life cycle of T. solium occurs between human (definitive host where the parasite reaches the adult stage, the tapeworm, in the gut) and pig (intermediate host, where the parasite develops the larval stage, the cysticercus). Humans acquire the infection consuming raw or undercooked pork containing the larvae. The tapeworm develops in the gut and the eggs are shed by human feces in the environment. The eggs can be ingested by free‑ranging and backyard pigs feeding on human feces. The embryo exits from the egg in the pig gut and migrates to muscles and other sites where it develops into infective larval stage, the cysticercus, waiting the human consumption of the pork. However, humans can also act as an intermediate host when ingest eggs contaminating vegetables and fomites, or alternatively by self‑infection in a tapeworm carrier. Thus, vegetarians and other people, who do not eat pork can also acquire cysticercosis. The intestinal infestation with the tapeworm, i.e. carrier stage is generally asymptomatic and may go unnoticed. Cysticercosis in more than 80% of the cases is asymptomatic. The severity of the clinical picture is related to the localization and number of cysticerci; neurocysticercosis being the most serious clinical picture, whereas muscle localization can be asymptomatic.[5] Cysticercosis can be diagnosed by imaging methods (ultrasonography/computed tomography/magnetic

b

Figure 1: (a) Lymph node with subcapsular tumor emboli from breast carcinoma (H and E, ×200); (b) Photomicrograph showing intranodal paracytic cyst (H and E, ×200) Tropical Parasitology

Figure 2: Cysticercus with all the three layers (H and E, ×200) 133

Jul 2014 | Volume 4 | Issue 2 |

Letter to Editor

resonance imaging), serodiagnosis (enzyme linked immunosorbent assays, co‑agglutination tests), fundus examination of eye and by pathological examination of aspirates and tissue biopsies.[6]

Riti Aggarwal, Seema Rao, Brij B Agarwal1

REFERENCES

Tapeworm carriers must be treated with praziquantel (PZQ) as such persons are the immediate common source of infection in both humans and pigs. No treatment is recommended for asymptomatic, nonviable cysticercal lesions in subcutaneous tissue, and muscle. However, surgical excision is preferred for solitary symptomatic lesion. For neurocysticercosis, symptomatic therapy is the mainstay for treatment and includes analgesics, corticosteroids to control inflammation and antiepileptic drugs to control seizures. Anti‑parasitic agents, either albendazole or PZQ are effective in killing live cysticerci; however, many patients develop an exacerbation of neurologic symptoms, attributed to intense local inflammation due to the death of the larvae. Therefore, it is recommended to give anti‑parasitic treatment under hospital conditions and prime the patient with steroids before starting cysticidal drugs.[7]

1. Prasad KN, Prasad A, Verma A, Singh AK. Human cysticercosis and Indian scenario: A review. J Biosci 2008;33:571‑82. 2. Sodhi PK, Ratan SK. Submandibular lymph node enlargement due to cysticercosis infestation. Scand J Infect Dis 2004;36:227‑9. 3. Mohan H, Bal A, Aulakh R. Multiple cysticerci as an unusual cause of mesenteric lymph node enlargement: A case report. J Med Case Rep 2008;2:196. 4. Elhence P, Bansal R, Sharma S, Bharat V. Cysticercosis presenting as cervical lymphadenopathy: A rare presentation in two cases with review of literature. Niger J Clin Pract 2012;15:361‑3. 5. Bothale KA, Mahore SD, Maimoon SA. A rare case of disseminated cysticercosis. Trop Parasitol 2012;2:138‑41. 6. García HH, Gonzalez AE, Evans CA, Gilman RH, Cysticercosis Working Group in Peru. Taenia solium cysticercosis. Lancet 2003;362:547‑56. 7. Nash TE, Garcia HH. Diagnosis and treatment of neurocysticercosis. Nat Rev Neurol 2011;7:584‑94.

Nodal filariasis is a fairly common phenomenon; however, nodal cysticercosis is rarely reported, with only four such documented cases in literature so far. This is the first reported case of cysticercus in axillary lymph node in a patient with breast carcinoma. This case highlights that all enlarged lymph nodes in a known case of malignancy may not necessarily imply metastasis. Infrequently, one may find an unusual finding, like a parasite.

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Website: www.tropicalparasitology.org DOI: 10.4103/2229-5070.138545

DOA: 10-01-2014 DOP: ***

for diagnosis of visceral leishmaniasis. However, it is a painful procedure, needs expertise and difficult to interpret in low parasitemic conditions. Currently, immunochromatographic test (ICT) coating rk39 recombinant kinesin antigen has become more popular for the diagnosis of Kala‑azar.[2] It shows high sensitivity and specificity for the diagnosis of Kala‑azar, however has limited role in the disease prognosis.[2] Plasma lipid profile alterations such as hypocholesteraemia, increased triglyceridemia are previously reported in few cases of visceral leishmaniasis.[3‑5] However none of them had correlated the above parameters as a diagnostic and prognostic adjunct with that of the established clinical and hematological parameters. Here, we would like to point out these metabolic alterations in nine visceral leismaniasis patients, which might give a clue for the best markers as the diagnostic and prognostic indicator for visceral leishmaniasis cases.

Lipid derangement as diagnostic and prognostic indicator for visceral leishmaniasis patients Sir, Visceral leishmaniasis popularly known as Kala‑azar, is caused by an intracellular protozoa Leishmania donovani (LD). Fever, hepatosplenomegaly and weight loss are the common presenting features of the disease. Anemia, leukopenia, thrombocytopenia and hyperglobulinemia with alteration of albumin: globulin (A:G) ratio are some of the most common laboratory finding observed in this condition. In India, more than 50% of Kala‑azar cases are reported form Bihar.[1] Bone marrow aspiration is the gold standard Jul 2014 | Volume 4 | Issue 2 |

Departments of Pathology, and 1General Surgery, Sir Ganga Ram Hospital, New Delhi, India. E‑mail: [email protected]

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An anecdotal case of cysticercus of axillary lymph node in a patient with metastatic breast carcinoma.

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