Department of Orthopaedics Mycetoma

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DEPARTMENT OF

ORTHOPAEDICS
KMC,MANGALORE

MADURA FOOT
DR.VINAY PAWAR

MODERATORS
DR SURENDAR U KAMATH
DR HARSHVARDHAN

DATE: 29.1.08

WHY SHOULD WE KNOW IT..


It can be confused with chronic osteomyelitis
Actinomycosis itself can invade the bone
Endemic in INDIA(esp Tamil Nadu)

HISTORY
There have been references to this disease in Homers
Iliad
In ancient Indian texts it has been referred as
Padavalmika or foot anthill
In scientific era the syndrome was first described by Gill
in 1842
Its fungal etiology was established by Carter in 1868
Definition:
it is a chronic,painless,subcutaneous, infection usually
involving the feet, characterized by formation of localised
leasions in form of tumefactions and multiple draining
sinuses

Etiology
Madura foot or mycetoma (named because of the tumour-like mass
it forms) is a chronic granulomatous disease characterised by
localised infection of subcutaneous tissues and bone.
The infection can be caused by true fungi
(eumycetoma) in 40%, or filamentous bacteria
(actinomycetoma) in 60%.
Actinomycetoma may be due to Actinomadura
madurae, Actinomadura pelletieri, Streptomyces
somaliensis, Nocardia species

Pathophysiology:
The body parts affected most commonly are the foot or
lower leg, with infection of the dorsal aspect of the forefoot
being typical. The hand is the next most common location;
however, lesions can occur anywhere on the body. Lesions
on the chest and back frequently are caused by Nocardia
species, whereas lesions on the head and neck usually are
caused by Streptomyces somaliensis.
The causative organism enters through sites of local trauma
(eg, cut on the hand, foot splinter, local trauma related to
carrying soil-contaminated material). A neutrophilic response
initially occurs, which may be followed by a granulomatous
reaction. Spread occurs through skin facial planes and can
involve the bone. Hematogenous or lymphatic spread is
uncommon.

History:

The earliest sign is a painless subcutaneous swelling.


Some patients have a history of a penetrating injury at
that site.

Several years later, a painless subcutaneous nodule is


observed. After some years, massive swelling of the
area occurs, with induration, skin rupture, and sinus
tract formation.

As the infection spreads to contiguous body parts, old


sinuses close and new ones open.

Pain occurs in nearly 20% of patients and usually is due


to secondary bacterial infection or, less commonly,
bone invasion.

Constitutional symptoms and signs are rare.

Patients may complain of a deep itching sensation.

Physical:

Irrespective of the causal agent, the appearance of the


lesion is similar and consists of the following:
o

Initially, subcutaneous swelling is present.

In a later phase, a subcutaneous nodule develops.

Eventually, massive swelling with induration,


rupture of the skin, and formation of sinus tracts
occur.

In general, eumycetomas are more circumscribed and


progress slower than actinomycetomas.

Regional lymphadenopathy is unusual, but when it does


occur, it is due to one of the following:
o

Lymphatic spread of mycetoma to regional nodes


occurs in only 1-3% of patients.
Secondary bacterial infection or local
immunological reaction can cause enlargement of
regional lymph nodes.

Lymphatic obstruction and fibrosis can cause


lymphedema and erythema.

Pulmonary mycetoma has been found to develop and


progress more rapidly in individuals infected with HIV.

Lab Studies:

Staining
o

Hematoxylin-eosin staining of a biopsy sample


allows for detection of grains.
Process hematoxylin-eosin and May-GrnwaldGiemsa staining of a cytologic smear of a sample
obtained by fine-needle aspiration. Mycetoma
grains can be distinguished from artifacts and
other organisms by the intimate relationship
between the grain and neutrophils. The
appearance of the grains is determined as follows:
Actinomycetoma - Homogenously
eosinophilic with hematoxylin-eosin stain;
blue in the center with pink filaments in the
periphery with May-Grnwald-Giemsa stain
Eumycetoma - Brownish color with
hematoxylin-eosin stain; black with a green
tinge with May-Grnwald-Giemsa stain
The causal agent of each type of mycetoma can
be visualized better with the following:
Tissue Gram stain to detect fine, grampositive, branching filaments within the
actinomycetoma grain
Gomori methenamine silver or periodic acidSchiff stain to demonstrate the larger hyphae
of eumycetoma

Evaluation of the characteristics of the associated


granules suggests an initial differential diagnosis, as
follows:
o

White-to-yellow grains are indicative of P boydii (S


apiospermum), Nocardia species, or A madurae
infection.
Yellow-to-brown grains are indicative of S
somaliensis infection.
Black grains are indicative of Streptomyces
paraguayensis, Madurella species, or
Leptosphaeria species infection.
Red-to-pink grains are indicative of A pelletieri
infection.

Culture the grains obtained from a deep-seated wedge


biopsy or a sample obtained by puncture and fineneedle aspiration. The primary isolation media used
should be Lwenstein-Jensen for actinomycetoma or
blood agar for eumycetoma.

Serologic diagnosis is available in a few centers and


can be helpful with some patients for diagnosis or
follow-up care during medical treatment. Antibodies can
be determined by means of (1) immunodiffusion, (2)
counterimmunoelectrophoresis, (3) enzyme-linked
immunosorbent assay, or (4) Western blot.

Caution: Superficial samples of the draining sinuses are


inadequate for culture due to frequent contamination
with bacteria.

Imaging Studies:

Bone radiograph
o

Once mycetoma has invaded the bone, several


changes can be observed, as follows:
Cortical thinning is due to compression from
the outside by the mycetoma.
Cortical hypertrophy or periosteal proliferation
may present as a sunray appearance and a
Codman triangle.
Multiple lytic lesions or cavities may be large,
few in number, and with well-defined margins
in eumycetoma or small, numerous, and with
ill-defined margins in actinomycetoma.
Disuse osteoporosis may occur in late
mycetoma.
Bone involvement has been radiographically
classified, as follows:
Stage 0 - Soft-tissue swelling without bone
involvement
Stage I - Extrinsic pressure effects on the
intact bones in the vicinity of an expanding
granuloma
Stage II - Irritation of the bone surface without
intraosseous invasion
Stage III - Cortical erosion and central
cavitation
Stage IV - Longitudinal spreading along a
single ray
Stage V - Horizontal spread along a single
row
Stage VI - Multidirectional spread due to
uncontrolled infection

MRI helps with the differential diagnosis of the swelling


and can provide a better assessment of the degree of
bone and soft tissue involveme

dot in circle sign: 2.5mm signals of high intensity signals


in low intensity foci-highly specific for mycetoma
Ultrasonography: Single or multiple thick-walled cavities
with hyperreflective echoes and no acoustic enhancement
always are observed with mycetoma, whereas these
features are not demonstrated in nonmycetoma swellings.
o

In eumycetoma, the hyperreflective echoes are


sharp, corresponding to the grains in the lesion.
In actinomycetoma, the hyperreflective echoes are
fine and closely aggregated and commonly settle
at the bottom of the cavities.

CT scan provides a better detail of changes than those


observed with conventional radiographs.

Treatment
Actinomycetoma is a bacterial infection that can respond to
antibiotics if treatment is administered early in the course of the
disease. A combination of 2 drugs in 5-week cycles is used. If
needed, the cycles can be repeated once or twice. The following
agents have been used in combination: trimethoprimsulfamethoxazole (TMP-SMZ), dapsone
(diaminodiphenylsulfone), and streptomycin sulfate. Amikacin can
be substituted for streptomycin but usually is kept as a second-line
drug because of its cost. Rifampin has been used as a second-line
drug in resistant cases. In one case report, a patient required
salvage therapy with amikacin and imipenem for 6 months.

Eumycetoma may respond partially to antifungal agents,


although surgical therapy is preferred if the disease is
localized. Madurella mycetomatis may respond to
ketoconazole (200 mg bid). Other agents of eumycetoma
may respond intermittently to itraconazole (200 mg bid) or
amphotericin B. The minimum treatment duration is 10
months.
Deterrence/Prevention:

Educate patients to avoid activities that expose them to


agents of mycetoma. Instruct patients to avoid carrying
sticks and thorny branches that have had contact with
the soil.

Complications:

Complications result mainly from toxicity due to


prolonged administration of antimicrobial or antifungal
drugs.

Amputation may result from neglected chronic


infections.

Prognosis:

Prognosis is good with prompt diagnosis and treatment.


Although prognosis for survival is good, amputations or
ankylosis can lessen the quality of life.

In late stages, response to treatment is limited.

REFERANCES
1.`Orthopaedic infections by Robert Marier(pg 295)
2.`Text book of diagnostic microbiology by Lehman
3.`Text book of microbiology by Ananthnarayan(pg 618,402)
4.`Text book of clinical microbiology by Jawetz
5. J. Bone Joint Surg. Am., Sep 1970; 52: 1229 1234
, Jun 1978; 60: 546 - 548.
6. Abd El Bagi ME: New radiographic classification of bone
involvement in pedal mycetoma. AJR Am J Roentgenol 2003 Mar;
180(3): 665-8[Medline].

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