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British Journal of Radiology (2005) 78, 158-160
© 2005 British Institute of Radiology
doi: 10.1259/bjr/33263789

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Case report

Visceral leishmaniasis: diagnosis by ultrasound-guided fine needle aspiration of an axillary node

M Reus, MD, PhD1, B García, MD, PhD2, V Vázquez, MD1, D Morales, MD1, M Fuster, MD1 and J Sola, MD3

Departments of 1 Radiology, 2 Internal Medicine and 3 Cytology, Hospital Universitario "Virgen de la Arrixaca", 30120 El Palmar (Murcia), Spain


    Abstract
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
A 77-year-old woman presented with fever up to 39°C and acute pain in the left upper quadrant and renal fossa. Full blood count and biochemical screen revealed a haemoglobin (Hb) of 9.8 g dl–1, an increased erythrocyte sedimentation rate and an elevated lactate dehydrogenase, all other parameters were normal. Thoracic and abdominal CT demonstrated two enlarged lymph nodes in the left axilla, and splenic infarcts. Ultrasound-guided fine needle aspiration of one of the axillary lymph nodes revealed macrophages filled with leishmanias.


    Introduction
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
Visceral leishmaniasis (VL), known also as Kala-azar, is a chronic infectious disease caused by a protozoan parasite of the genus leishmania; it is transmitted by fly bite [1]. It is endemic in the Indian subcontinent, East Africa, South America, South Texas and in the Mediterranean region. Commonly, patients with VL present with fever, abdominal pain, splenomegaly, hepatomegaly, cachexia, and pancytopenia [2]. We present a case of VL with multiple splenic infarcts, left axillary lymphadenopathy, without pancytopenia, diagnosed by means of ultrasound-guided (US-guided) fine needle aspiration cytology of the axillary lymph nodes.


    Case report
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
A 77-year-old woman presented with an 11 day history of shivering, fever up to 39°C, and pain in the left upper quadrant and renal fossa. Despite treatment with cefixime, 400 mg day–1, and ciproxine, 500 mg/12 hourly, the patient remained unwell. On physical examination, she had pale skin and mucus membranes and painless splenomegaly. Her full blood count showed a haemoglobin (Hb) of 9.8 g dl–1, with an increased erythrocyte sedimentation rate and an elevated lactate dehydrogenase. All other laboratory studies were normal.

An abdominal ultrasound demonstrated splenomegaly, and an upper pole triangular hypoechoic area. Thoracic CT (Figure 1Go) showed two enlarged lymph nodes with maximum transverse diameters of 1.5 cm in the left axilla. Abdominal CT (Figure 2Go) demonstrated a hypodense triangular segment in the spleen suggestive of ischaemic infarction. A diagnosis of lymphoma was suspected. Aspiration using US-guidance was performed on the axillary lymphadenopathy (Figure 3Go). This revealed macrophages filled with leishmanias (Figure 4Go), confirmed using an antileishmania antibody immunofluorescence test. Treatment was initiated with intravenous liposomal amphotericin B, 150 mg day–1, for 10 days. On review at 2 months the patient remained asymptomatic.



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Figure 1. Contrast enhanced thoracic CT showing in the left axillary an enlarged lymph node (arrow).

 


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Figure 2. Contrast enhanced abdominal CT scan of the left upper quadrant demonstrated a wedge-shaped area of decreased attenuation in the surface of the spleen (arrow).

 


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Figure 3. Ultrasound-guided aspiration showing the tip of the needle (arrowhead) inside lymphatic nodule (arrow).

 


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Figure 4. Macrophages containing intracellular leishmanias (black arrow) found in the axyllare lymphadenopathy aspirate (haematoxylin-eosin x 400).

 

    Discussion
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 Abstract
 Introduction
 Case report
 Discussion
 References
 
VL (Kala-azar) is a protozoal infection common in underdeveloped countries; there are an estimated 500 000 new cases every year and there were 41 000 recorded deaths in the year 2000 [2].

Leishmania infantum is the main cause of VL in the Mediterranean region [24]. Infected animals – mainly dogs – are the carriers of the disease in the Mediterranean [5]. An insect bite is the vector of transmission. People from unaffected areas, may contract the disease [6, 7] after visiting endemic areas. Cases of leishmaniasis in overseas travellers and US Gulf War veterans has prompted growing interest in this disease [3, 8]. Factors increasing the risk of clinical development of the disease include malnutrition, immunosuppression, and most importantly, HIV infection [2].

Delay and difficulty in diagnosis are common especially in the early stage of the disease, due to non-specific symptomatology and difficulty in demonstrating intracellular protozoa in tissue aspirates [9]. Intracellular leishmania can be identified from aspirates of spleen, bone marrow, lymph node, or liver [2].

The CT findings of hepatosplenomegaly, and abdominal lymphadenopathy secondary to visceral leishmaniasis has been previously reported [9, 10].

Patients with advanced Kala-azar die without treatment: pentavalent antimony is the main therapeutic agent, but resistance has been reported and there are complications associated with treatment; particularly in cases of associated HIV infection. Liposomal amphotericin B is highly effective against Visceral leishmaniasis [11], even in immunosuppressed patients, but it is expensive [1, 3].

Our case is of interest as presenting with multiple splenic infarcts in VL has not previously been reported [12, 13]. The absence of pancytopenia was also atypical. US-guided aspiration of the axillary lymph nodes was chosen as it is minimally invasive and has a lower risk than aspiration of bone marrow or spleen. Although splenic aspiration is reported to have a sensitivity of 98% [2] in VL.

In conclusion, we suggest that US-guided aspiration of a peripheral lymph node should be considered as a technique to obtain a tissue sample in a patient with suspected VL and peripheral lymphodenopathy, in order to avoid the complications of spleen puncture.


    Acknowledgments
 
The authors thank Lee Boyes, Richard Barbosa, Dolores Abellán and Sally Toft for their review of the English in this manuscript.

Received for publication January 21, 2004. Revision received October 4, 2004. Accepted for publication October 26, 2004.


    References
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 Abstract
 Introduction
 Case report
 Discussion
 References
 

  1. Desjeux P. Human leishmaniases: epidemiology and public health aspect. World Health Stat Q 1992;45:267–75.[Medline]
  2. Guerin PJ, Olliaro P, Sundar S, et al. Visceral leishamniasis: current status of control, diagnosis, and treatment, and a proposed research and development agenda. Lancet lnfect Dis 2002;2:494–501.
  3. Herwaldt BL. Leishmaniasis. Lancet 1999;354:1191–9.[CrossRef][Medline]
  4. Berman JD. Human leishmaniasis: clinical, diagnostic, and chemotherapeutic developments in the last 10 years. Clin Infes Dis 1997;16:251–5.
  5. Murray HW. Kala-azar—progress against a neglected disease. N Engl J Med 2002;347:1793–4.[Free Full Text]
  6. Granert C, Elinder G, Ost A, Henter JI. Kala-azar in a one year-old Swedish child. Diagnostic difficulties because of active hemophagocytosis. Acta Paediatr 1993;82:794–6.[Medline]
  7. Büyükasik Y, Ileri NS, Haznedaroglu IC, Demiroglu H, Dündar S. Fever hepatosplenomegaly, pancytopenia in a patient living in the Mediterreanean region. Postgrad Med J 1998;74:237–41.[Abstract/Free Full Text]
  8. Pantsan MW, Coleman TA. Images in clinical medicine. Kala-azar. N Engl J Med 2003;349:e13.
  9. Cohen D, Fields S. CT findings in visceral leishmaniasis mimichking lymphoma. Comput Med Imaging Graph 1988;12:325–7.[CrossRef][Medline]
  10. Deutch SJ, Sandles MA, Alpern MB. Abdominal lymphadenopathy in benign disease: CT detection. Radiology 1987;163:335–8.[Abstract/Free Full Text]
  11. Gaeta GB, Maisto A, Di Caprio D, et al. Efficacy of amphotericin B colloidal dispersion in the treatment of Mediterranean visceral leishmaniasis in immunocompetent adult patients. Scand J Infect Dis 2000;32:675–7.[CrossRef][Medline]
  12. Nores M, Phillips EH, Morngestern L, Hiatt JR. The clinical spectrum of splenic infarction. Am Surg 1998;64:182–8.[Medline]
  13. Jaroch MT, Broughan TA, Hermann RE. The natural history of splenic infarction. Surgery 1986;100:743–9.[Medline]




This Article
Right arrow Abstract Freely available
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Right arrow Articles by Sola, J


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