ABSTRACT To study the clinical features and natural history of disseminated histoplasmosis(DH) in India.
We retrospectively analyzed the data obtained from the in-patient medical records of adults (age > 13 years) diagnosed to have DH during the period from January 1989 to December 1999. DH was diagnosed when histologically compatible intracellular organisms were present or Histoplasma capsulatum was obtained in culture from the extrapulmonary sites.
Nineteen patients (18 male and 1 female) were diagnosed to have DH. Diabetes mellitus and HIV infection were the most common co-morbid conditions. Weight loss, fever and oropharyngeal ulcers were the commonest symptoms. Physical signs included hepatosplenomegaly, oropharyngeal ulcers and lymphadenopathy. The diagnosis was confirmed by histopathology and/or culture from the following sites: bone marrow, adrenal gland, lymph node, oropharyngeal ulcers, rectal mucosa and skin. Two patients were treated with Amphotericin B, 6 with various azoles and 3 had Amphotericin B followed by various azoles. Among the eleven treated, 7 were cured, 2 improved, 1 had a relapse and 1 patient died.
DH is not uncommon in India and should be considered in the diagnosis of patients with prolonged fever, weight loss, oropharyngeal ulcers, hepatosplenomegaly, lymphadenopathy and adrenal enlargement. Correct diagnosis and treatment leads to a favourable outcome.
- [show abstract] [hide abstract]
ABSTRACT: Oral histoplasmosis in a 30-year-old male with no history of travel outside India is described. An ulcerating lesion was located on the hard palate. A chest X-ray was normal. Based on physical examination, regional lymph nodes, liver and spleen were not involved. The diagnosis was established by demonstrating yeast-like budding cells in a biopsy of the lesion and by isolating Histoplasma capsulatum in pure culture. The identity of the isolate was confirmed by a chemiluminescent DNA-probe assay and the exoantigen test. A review of the Indian literature from 1968 to 1992 revealed the occurrence of 25 authentic cases of histoplasmosis in India. In 19 cases, lesions were confined to the oral cavity confirming prior observation that histoplasmosis in Indian patients tends to occur primarily in extrapulmonary sites, particularly the oral cavity.Journal of medical and veterinary mycology: bi-monthly publication of the International Society for Human and Animal Mycology 02/1994; 32(2):93-103.
- The Indian journal of medical research 08/1975; 63(7):1020-8. · 2.06 Impact Factor
Article: A unique case of histoplasmosis.Journal of the Indian Medical Association 04/1954; 23(6):257-8.
© JA PI • V OL. 53 • MA RCH 2005www.japi.org185
S Subramanian*, OC Abraham**, Priscilla Rupali*, A Zachariah**,
Mary S Mathews#, D Mathai**
Objective : To study the clinical features and natural history of disseminated histoplasmosis(DH) in India.
Methods : We retrospectively analyzed the data obtained from the in-patient medical records of adults (age
>13 years) diagnosed to have DH during the period from January 1989 to December 1999. DH was diagnosed
when histologically compatible intracellular organisms were present or Histoplasma capsulatum was obtained
in culture from the extrapulmonary sites.
Results : Nineteen patients (18 male and 1 female) were diagnosed to have DH. Diabetes mellitus and HIV
infection were the most common co-morbid conditions. Weight loss, fever and oropharyngeal ulcers were the
commonest symptoms. Physical signs included hepatosplenomegaly, oropharyngeal ulcers and
lymphadenopathy. The diagnosis was confirmed by histopathology and/ or culture from the following sites:
bone marrow, adrenal gland, lymph node, oropharyngeal ulcers, rectal mucosa and skin. Two patients were
treated with Amphotericin B, 6 with various azoles and 3 had Amphotericin B followed by various azoles.
Among the eleven treated, 7 were cured, 2 improved, 1 had a relapse and 1 patient died.
Conclusion : DH is not uncommon in India and should be considered in the diagnosis of patients with
prolonged fever, weight loss, oropharyngeal ulcers, hepatosplenomegaly, lymphadenopathy and adrenal
enlargement. Correct diagnosis and treatment leads to a favourable outcome. ©
intracellular dimorphic fungus, Histoplasma capsulatum.
Samuel Darling, in 1905, first identified this pathogen
in the visceral tissues and bone marrow of an adult male
presumed to have died of miliary tuberculosis.1 The
organism exists in the mould (mycelial) form at soil
temperatures and switches to the yeast form at normal
human body temperatures (37oC) and resides within
macrophages. The quality of the surface soil (upper 15
cm) that supports growth of organism is usually found
in the vicinities of chicken houses, roosting places of
birds and bat caves that abound in decaying guano. The
mycelial form of H. capsulatum has two conidia - the
macroconidia and the microconidia. The latter are
smaller infective forms, which are 2-5 micrometer in
diameter, and are oval and smooth. During outdoor
activities such as spading of soil, deconstruction of
chicken coops, spelunking etc., aerosolized
isseminated histoplasmosis (DH) is a relentlessly
progressive granulomatous disease caused by the
*Lecturer; **Professor in the Department of General Medicine
Unit 1 and #Professor of Clinical Microbiology, Christian
Medical College, Ida Scudder Road, PB No. 3, Vellore, Tamil
Nadu, India. Pin : 632004.
Received : 2.6.2004; Revised : 16.11.2004; Accepted : 2.12.2004
microconidia are inhaled, settle in the alveoli and are
then ingested by the alveolar macrophages. The
microconidia convert to the yeast form and replicate
within the macrophages, and then spread to the regional
lymph nodes, and throughout the reticulo-endothelial
system. The transition from the mycelial to the yeast form
is heat sensitive and is crucial for the development of
the infection. The infected macrophages induce
cytokines in order to enlist more macrophages and
monocytes to fight the organism, and these coalesce
together to form granulomas. This activation of the T-
cell mediated immune response is usually complete
within two weeks and failure of this result in the
progressive spread of infection to other organs.
Histoplasmosis may present clinically in different
forms - asymptomatic infection; an acute or chronic
pulmonary infection; mediastinal fibrosis or
granulomas; and disseminated histoplasmosis. The
development of progressive DH indicates impaired cell
mediated immune responses. The acute form of DH is
seen mostly in the immunocompromised host, and is
characterized by an abrupt onset of symptoms (fever,
malaise, hepatosplenomegaly, lymphadenopathy,
anemia, leucopenia and thrombocytopenia), lack of
granulomatous inflammatory response and high case-
fatality rates. The chronic form of DH is characterized
186www.japi.org© JA PI • V OL. 53 • MA RCH 2005
by an indolent course, focal lesions and an effective cell
mediated immune response. The subacute DH pursues
a subacute, but relentless course and focal lesions in
various visceral organs.
In India, histoplasmosis seems to be prevalent in the
Gangetic delta.2 Panja and Sen reported the first case of
DH from Calcutta in 19543 and since then individual
cases have been reported from various states, mostly from
West Bengal. Among the forms of histoplasmosis
reported from India, DH is the rarest. We have
summarized here a 10-year experience of patients with
DH diagnosed in our institution, and have reviewed the
relevant literature to provide an overview of the current
management of DH.
MATERIALS A ND METHODS
During the 10 years from January 1989 to December
1999, we retrospectively analyzed data obtained from
the in-patient medical records of adult patients aged >13
years diagnosed to have DH and hospitalised in
Christian Medical College Hospital, Vellore, a tertiary
care, teaching medical center with hospital capacity of
1750 beds. Patient demographics, socioeconomic status,
domiciliary status (urban or rural), associated co-
morbidities, clinical features at presentation, laboratory
and imaging results, treatment and outcome of patients
with DH were documented.
Inclusion criteria: A dults (age >13 years) were
included as cases if: (a) histology revealed granulomas
and tissue smears revealed histologically compatible,
capsulated intracellular yeast like organism, and/ or (b)
the fungal culture revealed growth of H. capsulatum from
tissue specimen obtained from extra-pulmonary sites
(skin, mucosa, bone marrow, liver, spleen, lymph node
and adrenal glands). We excluded those patients who
showed granulomas on histology without identifiable
organism on smear or cultures. Patients with a diagnosis
of pulmonary histoplasmosis (acute and chronic) were
Clinical course of the illness and outcome of the
therapy were monitored. Patient was considered
clinically cured when all clinical signs abated along with
normalization of laboratory parameters and regression
of initial lesions seen on imaging such as chest x-ray, CT
scan and ultrasound.
Nineteen patients fulfilled the inclusion criteria. The
domiciliary status of patients (statewise) was as follows:
West Bengal 7, Andhra Pradesh 4, Bihar 2 and 1 each
from Assam, Orissa, Uttar Pradesh, Tamil Nadu, and
Kerala. One patient was from the neighboring country
Bangladesh that borders West Bengal. Mean age was
42.8 years (range 13-71 years). Eighteen patients were
The patients were followed up from six to 37 months
(mean of 19 months). The most common underlying
illnesses were diabetes mellitus (5 patients) and HIV
infection (4 patients). CD4 cell counts were not done for
these patients. There were two renal transplant recipients
and two patients were undergoing treatment for
tuberculosis. Chronic obstructive airway disease and
lymphoma were seen in one patient each. The remainder
four patients did not have any significant co-morbid
Symptoms of significant weight loss (> 10% body
weight) were seen in 89% and fever in 73%. Less
commonly occurring symptoms included fatigue,
diarrhoea, cough, abdominal pain, dysphagia and skin
nodules. On examination, non-tender erythematous
skin papules and nodules in the extremities, trunk and
face were seen in two of our patients and the other signs
were lymphadenopathy (31%), oropharyngeal ulcers,
and hepatosplenomegaly in a third of our patients (37%
and 31%) and hepatomegaly in a sixth (15%). One had
isolated splenomegaly [Table 1].
Common laboratory abnormalities were anemia [Hb
< 8gm%] in 8 (42%), thrombocytopenia [platelets
<1,00,000/ mm3] in 7 (37 %), elevated ESR [> 50mm/ hr]
and hypoalbuminemia [< 3.5 g%] in 7 (36%) and elevated
alkaline phosphatase [ >125 U/ l] in 5. Imaging revealed
adrenomegaly in 8(42%). Chest x-ray was normal in all
Histopathological confirmation of diagnosis was
made from bone marrow (BM) aspirates or biopsy in
seven of eleven patients in whom BM evaluation was
done. Diagnosis was established by fine needle
aspiration cytology (FNAC) of adrenal glands in five,
lymph node and palate biopsies (four each), rectum (two),
skin and liver tissue (one each). In some patients more
than one procedure was done to make a diagnosis and
hence H. capsulatum was isolated from more than one
site. These tissues subsequently grew H. capsulatum in 3
( 16%) patients. The media used were Sabouraud’s
dextrose agar, biphasic medium or Brain Heart infusion
Eleven patients opted for treatment (duration ranged
Table 1 : Frequency of occurrence of clinical symptoms
and signs in the patients with disseminated
Clinical feature Number
Fever > 1010F
Erythematous papules and nodules
© JA PI • V OL. 53 • MA RCH 2005www.japi.org187
from 6 to 37 months) with conventional Amphotericin B
and azoles (amphotericin B alone 2, azoles 6,
amphotericin B followed by azoles 3).The azoles used
were Itraconazole 400 mg OD for 6 months followed by
200 mg OD, Fluconazole 400 mg OD, Ketoconazole
200mg BD till resolution of clinical and radiological
abnormalities. Seven of these eleven patients had a
clinical cure. In two patients, symptoms and signs
improved with regression of initial lesions on imaging,
and are currently being followed up. In one, relapse
occurred after the patient discontinued the treatment
within six months and death occurred in one, during
hospital stay. Among the seven patients who did not
receive treatment, six died, one patient was discharged
from hospital at request and one could not be followed
This article documents the largest number of patients
with DH reported from a single center in southern India.
Numerous case series have reported histoplasmosis from
all over India, the largest series being from Delhi, a
compilation of thirty-seven patients from all over India.4,5
There are sporadic reports from Andhra Pradesh and
Bihar as well. We found that 60% of our patients were
from South India and 40% were from West Bengal. This
seems to indicate that histoplasmosis has no particular
predilection to East India as was hitherto believed.
immunocompetent and immunocompromised
individuals with the disseminated forms being more
common in the latter group. The risk factors for acquiring
been reported in
the infection include, occupations involving disruption
of soil rich in bird and bat guano like, agriculture, outdoor
construction and rehabilitation of buildings inhabited
by birds.6 In HIV infected patients, the prevalence of
histoplasmosis varies from 5% to 32%, depending on
the endemicity of H. capsulatum in these areas.7 Annual
incidence of symptomatic histoplasmosis is 2.6% when
the mean CD4 count< 50 / cumm.8 HIV co-infection was
seen in one fifth of our patients and it is note worthy that
all of them died. In HIV infected patients, history of
exposure to chicken coops, CD4 counts <100 cells/ µL
and positive baseline serology for complement fixing
antibodies for histoplasma antigen or residence in
endemic areas have been identified as possible risk
factors for developing DH.8 DH is common in the setting
of advanced AIDS. Early diagnosis and treatment is likely
to impact survival among HIV infected patients in
regions where histoplasmosis is endemic and
antiretroviral therapy is not available. The other causes
for immunosuppression in our patients included
diabetes mellitus, renal transplantation and lymphoma.
The duration of symptoms prior to presentation to
the hospital was 3 - 6 months. The most common
symptoms seen in our series were significant weight loss,
and prolonged fever as reported in other studies .The
prominent symptoms of anorexia and malaise were of
comparable frequency as seen with other reports.9
Occurrence of hepatosplenomegaly in a half, and
lymphadenopathy in a third of our case series seems to
be consistent with the clinical picture reported from other
A third of our patients had mucocutaneous lesions,
which were predominantly oropharyngeal, involving
Table 2 : Laboratory investigations and imaging in the
patients with DH
Hemoglobin < 8 gm/ dL
Platelet count < 1,00,000/ cmm
Albumin < 3 gm/ dL
ESR (> 50mm/ hr)
Alkaline phosphatase > 125 IU.
Adrenal gland enlargement
Table 3 : Diagnosis of Histoplasma capsulatum
Bone marrow aspirate
and trephine biopsy
Adrenal gland FNAC
Lymph node biopsy
Postmortem (liver) biopsy
*One patient may have more than one site for tissue diagnosis.
Table 4 : Outcome of patients treated with antifungals
Treated (n=11)Untreated (n=8)
Cured = 7
Improved and on treatment = 2
Died = 1
Relapse = 1
Discharged at request = 1
Died = 6
Lost to follow-up = 1
Fig. 1 :
188www.japi.org© JA PI • V OL. 53 • MA RCH 2005
larynx, tonsils, tongue, buccal mucosa, lip and palate.
These ulcers were deeply indurated painless and
indolent with distinct heaped up margins.
Gastrointestinal histoplasmosis leads to ulceration,
nodules, hemorrhage, obstructive lesions or intestinal
perforations.11 Two patients had ulcerative lesions in
the rectum, ileum and esophagus seen on endoscopy
and multiple intestinal hemorrhages seen in another.
A nother notable feature was the presence of
adrenomegaly in half of our patients. Despite a high
proportion (80%) of adrenal gland affectation detected
via imaging studies and autopsy findings, clinical
manifestation of adrenal insufficiency is uncommon,
and occurs in only about 7-20%.12 The adrenal gland
affectation may be silent or may present as unilateral or
bilateral adrenal masses.13 This granulomatous
inflammation, within the adrenals is due to a large
number of macrophages amidst high concentration of
steroid hormones that promotes growth of the organism.14
Low normal ranges of plasma cortisol were seen. The
adrenal function recovers following cure with antifungal
therapy unlike that seen with treatment of tuberculosis,
where lifelong cortisol replacement is needed.
Occasionally, with initiation of antifungal therapy acute
adrenal insufficiency may be precipitated, possibly
through a mechanism similar to Jarish-Herxheimer
reaction.4 Symmers et al in 1972 described a distinct
clinical syndrome “Asian Histoplasmosis” with two
salient features i.e., mucosal ulceration at
mucocutaneous junctions or body orifices and a
propensity to acute adrenocortical insufficiency.15
Hematological abnormalities such as anemia,
thrombocytopenia and an elevated ESR are common and
have been reported in the disseminated forms due to
involvement of the bone marrow.16 Elevated
transaminase and alkaline phosphatase levels suggest
a diffuse hepatic involvement. Recent reports suggest
that elevated lactate dehydrogenase levels (≥ 500 U/ L),
along with alkaline phosphatase ≤ 300 U/ L and WBC
<4500/ cmm could help to distinguish DH from
Mycobacterium avium complex infections in febrile
patients with AIDS.17
On histopathology, granulomas may be caseating or
non-caseating in the self-limited forms of histoplasmosis.
However, in the progressive forms of histoplasmosis, a
massive influx of macrophages with scattering of
lymphocytes and ill-formed granulomas may be seen.
Mycelial forms are absent in tissues and this
differentiates it from other moulds causing
granulomatous inflammation. Granulomas commonly
occur due to other chronic mycobacterial and fungal
infections and hence it becomes imperative to use
appropriate staining and culture techniques to identify
this organism especially in the immunocompromised
patients. In our study, organism was grown from 15%
(bone marrow, palatal mucosa and lymph in node one
each). Mycobacterium tuberculosis coexisted with
histoplasmosis in two patients and was excluded by
negative cultures for mycobacteria in others.
Antifungal agents reduce mortality to < 25% in those
patients with disseminated histoplasmosis.18 Mortality
without treatment can be as high as 80-100%.19 Treatment
is indicated for all patients with progressive
disseminated histoplasmosis. In our series, treatment
could be initiated only in 11 of the 19 patients. Fever
abatement and weight gain occurred within 4 weeks.
Cure was obtained in seven, clinical improvement in
two and death occurred in one. Relapse was seen in
one, in whom the therapy was discontinued after 6
months. Among the eight patients in whom treatment
could not be initiated, six died.
Liposomal Amphotericin B is more effective and less
toxic in the treatment of DH as compared to conventional
Amphotericin B20 and produces more rapid clearance of
fungemia (though clinical response rates are similar)
when compared to Itraconazole21 in patients with AIDS.
In studies that mostly included immunocompetent hosts
and specifically excluded those with AIDS, clinical
response rates are 68-92% with conventional
Amphotericin B, 85-100% with Itraconazole, 74-86%
with oral Fluconazole and 56-70% with Ketoconazole.22
Even though the response rates are impressive with
Fluconazole and Ketoconazole the relapse rate is as high
as 30%.23 In AIDS the relapse rate is 80%; hence lifelong
maintenance therapy Itraconazole 200 mg daily is
recommended to prevent relapses.24 In our series also,
only six patients opted for Amphotericin B and the rest
were given azoles. Among the seven cured, six had
received Amphotericin B.
Our study has limitations. The data we have
chronicled may not represent true national prevalence
or endemicity, as our center draws patients from southern
and eastern regions. Being a tertiary care referral center,
it may not be truly representative of the entire nation but
highlights the high mortality owing to delayed diagnosis
particularly in endemic areas. Practicing physicians and
the patient population in endemic areas need to be
informed regarding the risks of acquiring infection.
In conclusion, DH has been reported sporadically
from all regions of the nation. A high index of suspicion
is needed to make diagnosis sooner especially in
immunocompetent hosts who are resident in endemic
areas. Clinical features and laboratory features are
identical to the commonly seen granulomatous
infections such as disseminated tuberculosis.
Oropharyngeal ulcers and adrenal gland enlargement
with prolonged fever provide specific clues suggesting
DH and diagnosis needs to be established via smears
and/ or cultures of tissues obtained from these affected
tissues as early diagnosis and antifungal treatment
results in remission or cure, usually with no sequelae. In
those severely immunocompromised especially those
© JA PI • V OL. 53 • MA RCH 2005www.japi.org189
with HIV/ AIDS in view of the high mortality and
frequent relapse, lifelong maintenance treatment is
1.Deepe Jr GS. Histoplasma capsulatum. In: Mandell GL,
Benett JE, Dolin R (eds) Mandell, Douglas and Bennett’s
Principles and Practice of Infectious Diseases. Philadelphia:
Churchill Livingstone, 2000;2:2718-2732.
Sanyal M, Thammayya A. Histoplasma capsulatum in the
soil of Gangetic Plain in India. Indian J Med Res 1975;63:1020-
Panja G, Sen S . A unique case of histoplasmosis. J Ind Med
Randhawa HS, Khan ZU. Histoplasmosis in India: Current
Status. Indian J Chest Dis Allied Sci 1994;36:193-213.
Padhye AA, Pathak AA, Katkar VJ, Hazare VK, Kaufman
L. Oral histoplasmosis in India: a case report and an overview
of cases reported during 1968-92. J Med Vet Mycology
Hajjeh RA, Pappas PG, Henderson H, et al. Multicenter case-
control study of risk factors for histoplasmosis in Human
Immunodeficiency virus- infected persons. Clin Infect Dis
Mc Kinsey DS, Gupta MR, Riddler SA, Driks MR, Smith DL,
et al. Long term Amphotericin B therapy for disseminated
histoplasmosis in patients with acquired immunodeficiency
syndrome. Ann Med 1989;111:655-659.
McKinsey D S, Speigel R A, Hutwagner L, Stanford J, Driks
M R, et al. Prospective Study of Histoplasmosis in patients
infected with Human Immunodeficiency virus: Incidence,
risk factors and pathophysiology. Clin Infect Dis 1997;1195-
Goodwin RA Jr , Lloyd JE, Des Prez RM. Histoplasmosis in
normal hosts. Medicine (Baltimore) 1981;60:231-266.
10. Radhakrishnan S, Vanchilingam S, Subramaniam S,
Venkataraman IT. Acute disseminated histoplasmosis with
unusual features. An autopsy report. J Assoc Physicians India
11.Lamps LW; Molina CP, West AB, Hagitt RC, Scot MA. The
pathologic spectrum of gastrointestinal and hepatic
histoplasmosis. Am J Clin Pathol 2000;113.;64-72.
12. Goodwin RA, Shapiro JL, Thurman GH, et al. Disseminated
histoplasmosis: Clinical and pathologic correlations. Medicine
13. Gohar S, Sule A, Gaitonde S, Mittal G, Ejaz P, et al. Adrenal
histoplasmosis. J Assoc Physicians India 2001;49:916-7.
14. Angeli A, Masera RG, Gatti G. Mycoses and adrenocortical
function. New pathogenetic aspects of adrenal hypofunction.
Recenti Prog Med 1991;82:652-60.
15. Symmers WS. Histoplasmosis in southern and south-eastern
Asia. A syndrome associated with a peculiar tissue form of
Histoplasma : A study of 48 cases. Ann Soc Belg Med Trop
16. Kurtin PJ, McKinsey D S, Gupta M R, Driks M. Histoplasmosis
in patients with A cquired Immunodeficiency Syndrome-
Hematologic and Bone marrow manifestations. Am J Clin
17. Graviss EA, Vanden Heuvel EA, Lacke CE, Spindel SA, White
AC Jr, Hamill RJ. Clinical prediction model for differentiation
of disseminated Histoplasma
Mycobacterium avium complex infections in febrile patients
with AIDS. J Acquir Immune Defic Syndr 2000;24:30-6.
18. Furcolow ML. Comparison of treated and untreated severe
histoplasmosis. JAMA 1963;183:121-7.
19. Rubin H, Furcolow ML, Yates JL, et al. The course and
prognosis of Histoplasmosis. Am J Med 1959;27:278-88.
20. Johnson P, Wheat L J, Cloud G, Thomas C, Dismukes W,
Goldman M, et al. A Multicenter randomized trial comparing
A mphotericin B(A mB) and liposomal A mphotericin B
(A mBisome, LamB) as induction therapy of disseminated
histoplasmosis in AIDS patients [abstract 232].Presented at
the 7th Conference on retroviruses and Opportunistic
Infections. San Francisco CA, January 31,2000.
21. Wheat LJ, Cloud G, Johnson PC, Connolly P, Goldman M, Le
Monte A , Fuller DE, Davis TE, Hafner R. A IDS Clinical
Trials Group; Mycoses Study Group of NIAID. Clearance of
fungal burden during treatment of disseminated
histoplasmosis with liposomal amphotericin B versus
itraconazole. Antimicrob Agents Chemother 2001;45:2354-7.
22. Wheat LJ, Kauffman CA. Histoplasmosis. Infect Dis Clin N
23. Wheat J, MaWhinney S, Hafner R, et al. Treatment of
histoplasmosis with fluconazole in patients with acquired
immunodeficiency syndrome. Am J Med 1997;103:223-32.
24. Wheat J, Hafner R, Wulfson M, et al. Prevention of relapse of
histoplasmosis with itraconazole in patients with the
acquired immunodeficiency syndrome. Ann Intern Med
Second Indo-US Workshop on Diabetic Foot Complications, April 22 and 23, 2005.
? Demonstration of Surgical procedures
? Learn the latest surgical techniques in diabetic foot.
Venue : Hotel Taj Connemara, Chennai.
Registration : Before 15th March : Rs. 1500/ -
After 16th March : Rs. 2500/ -
Demand draft on favour of "DRC Indo US Workshop" payable at Chennai.
Contact : Dr. V Viswanathan, Joint Director, #4, Main Raod, Royapuram, Chennai 600 013.
E-mail : email@example.com; Fax : 91-44-25954919