Granulomatous Infection

Ovid: Oncology and Basic Science

Editors: Tornetta, Paul; Einhorn, Thomas A.; Damron, Timothy A.
Title: Oncology and Basic Science, 7th Edition
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IV – Basic Science > 27 – Infectious Disorders of Bone and Joint
> 27.2 – Granulomatous Infection

Granulomatous Infection
Granuloma is defined as a microscopic-sized aggregation
of histiocytes and hypertrophied fibroblasts termed epithelioid cells,
centrally located and rimmed by a chronic inflammatory infiltrate of
lymphocytes and plasma cells (Fig. 27.2-1). The
entire focus can be surrounded by a ring of fibrosis. Multinucleated
giant cells, with a characteristic positioning of the nuclei at the
periphery of the cell (foreign body or Langhans giant cells), are
frequently present (Table 27.2-1). Over time
the granuloma may be replaced by scarring and even calcification. In
tuberculosis, the central area may undergo caseous (cheese-like)
  • Conditions associated with granulomatous histology (see Fig. 27.2-1) include:
    • Infection by mycobacteria, fungi, or parasites
    • Foreign materials
    • Eosinophilic granuloma
    • Sarcoidosis
      The response in bone is indolent, with slowly enlarging
      lytic defects in bone with smooth walls accommodating confluent,
      usually caseating granulomas.
  • Eosinophilic granuloma (Langerhans cell
    histiocytosis or Langerhans cell granulomatosis) only infrequently has
    clear-cut granulomatous histology (see Table 27.2-1).
    This disorder can progress with rapid local osteolysis (unique among
    granulomatous bone processes, which are usually indolent).
Mycobacterial Osteomyelitis
  • Tuberculosis (TB) will be discussed in detail as the prototype disorder in this section.
  • Tubercle bacillus induces an acute
    inflammatory response on entry into host tissue that usually controls
    the infection, walling it off to form a primary complex; if infecting
    dose overwhelms the response, the infection persists and spreads;
    during the early stages, bacilli may move into the circulation and
    metastasize to central nervous system, bones, or liver.
  • PMNs, on ingesting the bacilli, may necrose and become engulfed by macrophages and mononuclear cells.
  • Macrophages adopt epithelioid morphology
    on accepting the lipids of the bacilli, or may aggregate to form
    Langhans giant cells, whose task is to digest and remove the bacilli;
    these cells may also be overcome by the bacillus, also necrosing and
    inducing further phagocytic activity. Necrosis of epithelioid and
    Langhans cells becomes confluent (caseating).
  • After 1 week, lymphocytes form a ring around the periphery of the lesion, forming a 1- to 2-mm nodule known as the tubercle.
  • During the second week caseation starts to occur, induced by the protein fraction of the tubercle bacilli.
  • Over time, the PMN response is replaced
    by chronic inflammatory round cell infiltration accompanied by a
    fibroblastic proliferation that is variable in degree around the
    tubercle (chronic inflammatory focus).
  • This immune response usually will control
    the infection, in essence walling it off, where it can lie dormant for
    a lifetime, potentially becoming active as old age and impaired immune
    response occur.



    Figure 27.2-1 Granuloma (TB).
    (A) Granuloma formation is present. At this power, cellular detail is
    not visible, but there are four granulomas present, each within a ring
    of fibrosis. The center of the granuloma may manifest caseous necrosis;
    these granulomas are in the earliest stages of central necrosis. There
    are multinucleated giant cells of the Langhans or foreign body type
    frequently found in the granuloma. (B,C) Caseating granuloma (TB). (B) Here, granulomas are seen replacing normal marrow elements within bone. (C)
    Necrotic material is seen on the left, and the intermediate margin
    shows epithelioid cells centrally, with inflammatory cells
    (lymphocytes, plasma cells on the right, and a Langhans giant cell).
    Langhans cells have peripherally placed nuclei and are the cells to
    study carefully for the presence of acid-fast bacilli or fungi. (D,E) Granulomatous osteomyelitis (foreign body).
    Strictly speaking, a granuloma is a microscopic structure formed by two
    or more histiocytes or macrophages. They tend to have a nodular or
    circumscribed appearance and can be non-necrotizing or necrotizing. (D)
    In this photomicrograph, well-formed non-necrotizing (noncaseating)
    granulomas of histiocytes and multinucleated giant cells are evident,
    surrounded by fibrous connective tissue. Granulomas on hematoxylin and
    eosin stain are not specific, and their evaluation requires an
    evaluation of special stains and examination under polarized light
    (birefringent foreign particles are highlighted in this manner). (E) Higher-power view of D
    brings out the details of a single foreign body granuloma. Note the
    multinucleated giant cell and the surrounding plump mononuclear cells
    (histiocytes/macrophages). The vacuolated cytoplasm of the
    multinucleated giant cells underscores the brisk metabolic activity of
    these phagocytic cells. (F–H) Granulomatous (fungal, mycotic) osteomyelitis secondary to Cryptococcus infection. (F)
    This field shows a mixed inflammatory infiltrate with a few small
    discrete noncaseating granulomas composed of histiocytes and a few
    giant cells. Note the pale blue spherical structures within the
    cytoplasm of some of the histiocytes. Special stains (e.g., GMS and PAS
    stains) are useful for identification of the organism. (G) Higher-power view of F
    brings out the details of the histiocytes and multinucleated giant
    cells. A few gray-blue intracellular spherical bodies suspicious for
    fungi are noted. (H) Same view as in G
    with PAS stain (one fungal organism positive), which brings out a
    dark-pink spherical structure that is morphologically consistent with
    the yeast form of Cryptococcus species (this species has a capsule rich in mucin, which is readily stained by PAS).
  • Musculoskeletal lesions form by metastasis from 3 months to 3 years after the primary infection.
  • Children: Spine involvement begins in the vertebral body, usually anteriorly, then extends to adjacent disc and vertebral body.
  • Adults: Onset is beneath the periosteum
    under the anterior longitudinal ligament and may spread up and down the
    spine, bypassing some vertebrae to lodge at more than one level; disc
    space narrowing, vertebral body destruction, collapse with kyphosis,
    and eventual fusion may occur after 1 to 2 years.
  • Unlike bacteria, TB does not produce
    proteolytic enzymes that aggressively destroy cartilage, affording more
    time to make the diagnosis before the joint is destroyed in tuberculous
  • Bacillus lodges in synovium and proliferates, opposed by the immune process in sequence as outlined above.
    • The inflamed synovium enlarges to fill all recesses


      of the joint, spreading over the cartilage from the periphery as a
      pannus, mechanically eliminating nutrition of the cartilage from the

      Table 27.2-1 Langhans Versus Langerhans Cells
        Langhans Cells Langerhans Cells
      Appearance Giant cells with nuclei distributed around the periphery Histiocytes with typical coffee-bean cleaved nuclei (NOT giant cells)
      Associated conditions Tuberculosis, foreign body granulomas Langerhans cell histiocytosis or Langerhans cell granulomatosis or eosinophilic granuloma (older terminology)
    • Central joint space is preserved for months.
  • Cold abscess
    • A marked exudative reaction consists of serum, PMNs, caseous material, bone debris, and tubercle bacilli.
    • This collection migrates under the
      influence of gravity and may present along the spine and pelvis, in the
      groins, or about involved joints.
    • It may present through the skin as a
      sinus or ulcer, which may then become secondarily infected, obscuring
      the diagnostic picture.
  • Regional osteopenia
    • The inflammatory process induces an
      active hyperemia with osteoclastic deletion of bone, resulting in
      marked regional osteopenia.
  • Kissing sequestrate
    • The inflammatory synovial mass invades weakened subchondral bone from the periphery.
    • Rarely, sequestration of the opposing
      joint surfaces can occur as a result of this bone destruction, leading
      to the radiographic picture of “kissing sequestrate.”
  • Causative organisms include Mycobacterium tuberculosis (TB), Mycobacterium leprae, and environmental mycobacteria.
  • Organisms grow on enriched medium slowly so that colonies appear at 2 to 4 weeks.
    • Acid-fast stain may reveal classic “red snappers.”
  • One third of global population is infected with TB; most frequent cause of death and disability worldwide.
  • U.S. statistics
    • 10 million are infected; 90% of new activated cases come from this pool.
    • In non-Hispanic whites, median age at diagnosis is 61; among minority groups it is 39.
    • Americans >65 represent 6.5% of population but account for 26% of reported cases.
    • 20% of new cases of TB have extrapulmonary disease.
    • 33% of patients with TB and HIV have extrapulmonary disease.
    • 1% to 3% of patients with TB develop musculoskeletal manifestations.
Clinical Presentation
  • Classic: Patient becomes insidiously ill and develops chronic local musculoskeletal pain, fever, and weight loss.
  • Initial presentation may include:
    • Cold abscess: juxta-articular or paraspinal soft tissue mass without inflammation
    • Spinal involvement: may be truncal
      rigidity, muscle spasm, and neurological signs and deficit; spinal
      deformity (gibbus) is a late finding
    • TB arthritis: more common than TB osteomyelitis
    • Dactylitis: Small joints of the hands and
      feet are infrequently involved except in infancy, when digits may be
      involved with swelling.
    • Osseous disease: occurs by metastatic
      spread from an initial focus, usually the lungs, with involvement most
      often of spine (lower thoracic most frequent, with multiple vertebral
      bodies in 50% of cases), followed by pelvis in 12%, hip and femur 10%,
      knee and tibia 10%, hand, and any other joint
  • Important clinical points
    • Diagnosis can be difficult in the elderly, whose presentation may initially be only nonspecific constitutional symptoms.
    • If you suspect musculoskeletal TB, check the lungs, kidneys, and gastrointestinal tract.
Radiologic Features
  • No pathognomonic features
  • Joints
    • Osteopenia and soft tissue swelling with
      minimal periosteal reaction early, then marginal deletion of
      subchondral bone on both sides of the joint with late loss of central
      joint space (Fig. 27.2-2)


      Figure 27.2-2 (A)
      TB of the knee. When TB first lodges in the synovium of a joint, it
      creates many tubercles (usually small, without caseation) and induces
      marked synovial proliferation. The suprapatellar pouch in this knee is
      filled with inflamed synovium with histology as in Figure 27.2-1. There is significant osteopenia. (BD) TB of the hip. (B)
      Once the infection is established, the inflamed synovium invades the
      joint space from the margins, growing as a pannus as in rheumatoid
      arthritis, destroying the underlying cartilage by interfering with the
      diffusion of nutrients to the cartilage. The joint surface is usually
      preserved centrally until the process becomes much more advanced.
      Synovial pathology involves both sides of the joint. TB must be in the
      differential diagnosis for any periarticular disorder involving more
      than one bone around a joint area or marginal erosions. (C) Photomicrograph of the edge of a joint showing the pannus growing from the right onto the underlying articular cartilage. (D) This higher-power view shows complete destruction of the cartilage by the pannus.
    • P.513

    • Subchondral cysts
    • Enlargement of epiphysis
    • Subchondral erosions may cross epiphysis in one third of children affected.
  • Spine
    • Rarefaction of vertebral endplates
    • Increasing loss of disc height
    • Focal bony destruction with disc involved and late vertebral body collapse (Fig. 27.2-3)
    • Paravertebral soft tissue mass often present
    • Needle biopsy in HIV/TB patients must rule out other diseases such as Kaposi sarcoma.
Mycotic Osteomyelitis
  • Occurs mostly in immunocompromised
    patients or as opportunistic infections in individuals exposed to the
    specific contaminated environment (workers)
  • Fungal infection mimics TB, so always culture for fungi if granulomatous pathology is found (see Fig. 27.2-1).
  • Radiographic differential includes myeloma and metastasis (due to frequent multifocality).
  • Relevant features of the fungal infections of the musculoskeletal system are outlined in Table 27.2-2.
  • A systemic granulomatous disorder of unknown cause; no known organism
    Figure 27.2-3
    Gross specimen of TB of the spine. There is marked destruction of the
    bony architecture, with extension of the granulomatous process
    extending posterior to compress the cord. This degree of destruction
    can produce spinal deformity and paraplegia.
  • Differential diagnosis in any clinical situation manifesting granulomatous histology
Clinical Presentation
  • Typical patient is an adult, more commonly African-American, age 20 to 40 years, with fever, fatigue, malaise, and weight loss.
  • Affects lungs (90%), lymph nodes, skin, skeleton
    • Skeletal distribution: hand (“sausage fingers”), wrist, foot, skull, vertebral bodies, long bones, synovium
    • Typical musculoskeletal presentation: swollen, mildly painful fingers
Radiologic Features
  • No large destructive lesions as seen more commonly with TB
  • Mixed lysis and sclerosis is typical.
  • Hands/feet: punched-out cortical lesions,
    with trabecular resorption (honeycomb lytic pattern) and linear
    end-osteal sclerosis (acro-osteolysis; Fig. 27.2-4)
Laboratory Findings
  • Elevated angiotensin-converting enzyme (ACE) derived from epithelioid cells
  • Hypercalcemia arising from overproduction of 1-25-(OH)-D3, driven by activated pulmonary macrophages
  • Cultures negative
Pathologic Findings
  • Mimics TB but without caseation (see Fig. 27.2-4)
  • Giant cells show nonspecific cytoplasmic inclusions.
    • Asteroid body: a central core of degenerating organelles encompassed by rays of collagen
    • Schaumann bodies: large, concentrically laminated concretions of a protein matrix impregnated with calcium and iron salts
  • Symptoms are usually self-limited. If severe, prolonged treatment with corticosteroids may be attempted.
  • Immunosuppressive agents, such as methotrexate, azathioprine, and cyclophosphamide can be used.
  • Rarely, some individuals with irreversible organ failure require organ transplantation.
Rare Forms of Osteomyelitis
These conditions, whose relevant information is outlined in Table 27.2-3, include:
  • Brucellosis
  • Cat-scratch disease
  • Microangiopathic osteomyelitis
    • Syphilis
    • Lyme disease
  • Fibrosing osteomyelitis (fibrocystic)
    • Ecchinococcosis



Table 27.2-2 Fungal Forms of Osteomyelitis
Organism Entry Skeletal Manifestations Pathology Diagnosis Treatment
Blastomycoses dermatidis Inhalation of conidia; they convert to yeast form in lungs and then disseminate systemically Primary presentation in 10% with septic arthritis or osteomyelitis Neutrophils ingest but cannot destroy organism; pus plus noncaseating granulomas termed pyogranulomas Yeast forms: 8 to 15 mm, multinucleated (8 to 12), thick double-contoured cell walls; single broad-based budding Amphotericin B; ketoconazole; surgery according to stage of disease
Histoplasmosis capsulatum; Midwestern and south-central U.S. Inhalation of conidia from infected soil and bird droppings, same sequence as for B. dermatidis African variant with skeletal infection 50% (H. capsulatum diboisii,
large yeast, 10 to 15 mm); 50% incidence of skeletal lesion (skull,
ribs, long bones, spine); eccentric, punched-out area of lysis
Suppurative areas mixed with
epithelioid giant cell pyogranulomas; African histology contains large
giant cells containing many yeast forms
Yeast forms 3- to 4-mm, spherical to oval, uninucleate, thin-walled, narrow-based budding Primary: ketoconazole or itraconazole
Secondary: amphotericin B for systemic, severe infection
Coccidioides immitis; arid regions of southwest U.S., Mexico, and Argentina Same sequence as for B. dermatidis
Infection—direct link to exposure
40%: symptomatic disease, usually lung
90% resolve
10% lung sequelae
1% have dissemination; of these one third have multisystem disease
Arthritis, tenosynovitis, osteomyelitis
unifocal in 60%, wide distribution; vertebral lesions often multiple,
may spare the disc and extend to posterior elements and ribs. Joint
lesions are unifocal in >90%; knee and ankle predominate.
In joints, primary response is
neutrophils and macrophages, changing at 1 week to granulomatous
inflammation to developing spherules; new endospores elicit a
neutrophil response, initiating a new cycle.
In lungs conidia enlarge,
become spherules 10 to 15 mm with thick double-contoured walls and many
endospores, which then rupture.
Oral ketoconazole, itraconazole, or amphotericin B systemic with or without intra-articular
Cryptococcus neoformans; world-wide distribution Soil fungus disseminated by excreta of pigeons produces asymptomatic lung infection in the immunocompetent host. In immunodeficient may
disseminate to central nervous system, skin, and bone. Bone lesions 5%
to 10%: distribution—pelvis, femur, spine, tibia, and scapula, causing
chronic pain and swelling in some; some are asymptomatic
Inflammatory response varies
with usual lymphocytes and plasma cells, with or without large
neutrophils and giant cells; granulomas absent usually.
Pleomorphic encapsulated yeast form, 2 to 20 mm, reproduces by budding. In the absence of AIDS for disseminated disease, amphotericin B and flucytosine; surgery rarely used
Sporothrix schenckii; tropical America Direct inoculation into the skin of hands or feet; rare inhalation Typical in gardeners handling
roses and sphagnum moss; local painless mobile nodule becomes red and
soft and ulcerates; secondary lesions follow lymphatics; ulcers present
for years; regional lymph nodes enlarge; local spread to bone/joint
mimicking TB
Pyogranulomas Dimorphic fungus: hyphal form
in vitro at <37 degrees; in vivo, 2- to 6-mm oval to cigar-shaped
yeast forms with unequal budding
Cutaneous treatment: saturated potassium iodide, 50 mg/day for 6 weeks
Surgery plus amphotericin B for bone and joint manifestations
Candidiasis Systemic dissemination: neonates/immunocompromised patients
Cutaneous and mucous membrane portals
Hematogenous spread to bone
and joint with a radiologic picture mimicking TB; clinical setting
immunocompromised patients, neonates, rare case reports of candidal
total joint infection
Mimics TB; combination of immune impairment and broad-spectrum antibiotics creates opportunity for pathogenicity. >150 candida species exist, normally inhabit mucous membranes or damaged skin Amphotericin B
Rarely surgery


Figure 27.2-4 Boeck’s sarcoid. (A) Radiograph shows a small lytic lesion with sclerotic borders in the proximal phalanx of the great toe. (B) A small tubercle in sarcoid, with each of the cellular elements of a granuloma demonstrated.





Table 27.2-3 Rare Forms of Osteomyelitis
Organism Entry Clinical Manifestations Pathology/Skeletal Involvement Diagnosis Treatment
Brucella (gram-negative coccobacilli) Gastrointestinal: Goat’s milk, B. melitensis
Cow’s milk, B. abortus
Exposure to infected cattle, B. abortus
Swine, B. suis
Dogs, B. canis
Acute (malignant) form:
overwhelming infection with fever, chills, collapse,
reticuloendothelial system [RES] activation (lymphadenopathy,
hepatosplenomegaly), delirium, coma, early death
Recurrent (undulant fever): B. melitensis presents with flu-like symptoms with relapses.
Chronic (intermittent): B. abortus (rare) presents with malaise, mild fever, weakness.
20% to 60% with septic arthritis, osteomyelitis, tenosynovitis, bursitis
Sacroiliitis is most common location; TB-like spinal presentation in elderly.
Radiographs mimic TB spinal and peripheral.
Microscopy: B. melitensis and suis—necrotizing granulomas mimic TB.
B. abortus—non-necrotizing granulomas mimic sarcoid.
Culture of blood, marrow, and infected tissue
Serologic testing: serum agglutination or ELISA
Difficult to stain and identify in infected tissue
Tetracycline with rifampin; or tetracycline with minocycline; or ciprofloxacin
Surgery as indicated clinically
Cat-scratch disease (Bartonella henselae) Skin puncture Initial papule at inoculation
site in 3 to 10 days, then regional lymphadenopathy (months to years),
then systemic spread to RES and bone. Initial mild flu-like symptoms.
Nodes may suppurate and drain through skin. Rare rash, conjunctivitis.
Bone involvement near skin lesions, mixed lysis/sclerosis.
granulomas with rare giant cells, undergo necrosis with coalescence to
form confluent microabscesses. Neutrophils common in early lesions.
Raised white blood cell count,
erythrocyte sedimentation rate, eosinophilia (10% to 20%), positive
skin test (90%), IFA Ab titer >1:64; positive culture; polymerase
chain reaction (PCR) of DNA
No specific antibiotic therapy has proven useful.
No treatment is indicated in normal host; self-limited condition.
Symptomatic relief (no effect on duration of symptoms) with 5-day course of azithromycin.
In immunocompromised host choices include trimethoprim– sulfamethoxazole; gentamicin; ciprofloxacin; rifampin.
Syphilis (Treponoma pallidum, a spirochete) 1. Direct: Mucosal surface entry is followed by 3 stages:
a. Primary: incubation 10 to 90 days, then chancre + regional lymph node enlargement (50%)
b. Secondary: 6 to 24 weeks, systemic infection to every system (“the great imitator”), followed by latency, early phase (4 years) retaining infectiousness (25%) followed by late noninfectious latent syphilis
c. Tertiary: years to decades, presents with gummas in any system
2. Indirect: Congenital: intrauterine transmission from mother to child
Direct syphilis
presents in the benign tertiary (gummatous) stage in the skeleton (50%)
with bone pain (+/-) and local swelling without local signs of
Indirect syphilis may be: Early in first 2 years; infectious, resembles severe secondary syphilis in adult; Late, after 2 years; noninfectious; Residual stigmata:
Hutchinson’s teeth (centrally notched, widely spaced upper central
incisors); “mulberry molars” (6-year molars with multiple cusps);
abnormal facies (frontal bossing, saddle nose, poorly developed
maxilla); saber shins (anterior tibial bowing).
There are numerous other rare manifestations.
Skull, tibia (anterior
aspect), clavicle are preferred sites of osteomyelitis. Inflammation is
a periostitis with microangiitis, gummatous change, and granulomas,
with possible spread to overlying skin and medullary space. Moth-eaten
changes + sclerosis represent destruction induced by gummas (mimics
chronic suppurative osteomyelitis).
Septic arthritis of syphilis:
painful, symmetric swelling of knee, elbow, ankle, shoulder, and wrist,
with normal range of motion; spread is contiguous from osteomyelitis.
Early congenital syphilis:
symmetrical widespread osteochondritis and perichondritis affecting the
most rapidly growing area (ends of cartilage model bones) progressing
during first 6 months, then subsiding. Periostitis continues and
becomes apparent between the ages of 5 and 20.
Serologic tests: rapid plasm
reagin (RPR) test: reflects disease activity VDRL slide flocculation
test: reflects the exact titer of serum regain antibody.
Specific anti-treponemal antibody.: FTA-ABS is the standard test; T. pallidum
hemagglutination tests (MHA-TP and TPHA) are convenient but less
sensitive than the FTA-ABS test for detection of primary syphilis.
the MHA-TP and FTA-ABS tests are very specific and have high positive
predictive value when used for confirmation of positive reaginic tests.
Lyme borreliosis; zoonosis transmitted by ticks, disease affecting skin, central nervous system, the heart, and joints Causative organism: spirochete Borrelia burgdorferi
– Northern hemisphere distribution
– Reservoirs of spirochete are intermediate and small mammals, and birds.
– Ticks transmit the organism to man; species is Ixodes, and geni include dammini, pacificus, and scapularis in North America
3 clinical stages: – Not all stages need appear, and they may overlap.
Stage I: erythema migrans with centrifugal spread, 3 days to 16 weeks after tick bite, flu-like symptoms
Stage II:
weeks to months later, central nervous system, cardiac, skin, and joint
symptoms appear. Other manifestations include lymphadenopathy,
inflammatory eye disorders, hepatomegaly, testicular swelling, and
Stage III: Chronic organ involvement affects joints (arthritis), skin, central nervous system, heart, muscles, and bone marrow.
In various organ systems the
lesions are a chronic inflammatory infiltrate consisting of
lymphocytes, plasma cells, and histiocytes. There is a microangiitis
with perivascular cuffing by mononuclear cells resulting in an
endarteritis obliterans, similar to syphilis. In joints the response is
similar to rheumatoid arthritis histologically with a pannus invading
the joint.
The organism resides extracellularly but may attach to and invade some cells (fibroblasts and endothelial cells).
B. burgdorferi activates inflammatory cytokines affecting joints (interleukin-1 and tumor necrosis factor alpha [TNF-α]).
Possible immunogenetic predilection for Lyme disease in those with HLA-DR4 genotype.
Organism is difficult to
culture. Identification is by silver stains and immunohistological
techniques. Polymerase chain reaction testing is not yet validated.
Culture and biopsy identification is thus difficult.
Serologic testing: enzyme-linked immunosorbent assay (ELISA), indirect immunofluorescence assay (IFA), and Western blot.
Stage I: less than half have detectable antibodies, mostly IgM.
Stage II: 70% to 90% have antibodies, mostly IgG.
Confirm with Western blot, and repeat if negative.
For systemic disease: doxycycline, cefuroxime axetil, or erythromycin.
For arthritis, repeat 30-day courses of doxycycline, amoxicillin, plus probenecid.
Ecchinococcosis (hydatid cyst); parasitic infestation by a tapeworm Ecchinococcosis species include granulosis (most common cause of unilocular hydatid cyst); vogeli (canine tapeworms); multilocularis (causes multilocular cysts)
of canines in which herbivores (sheep, deer, cattle) serve as
intermediate host. Man inadvertently ingests tapeworm eggs from
contaminated food or water.
Asymptomatic until cyst
enlargement affects organ of involvement: liver, lungs, muscles, bones,
kidneys, central nervous system, and spleen. There is a slow
enlargement of the cyst with possible vague pressure effects; mass then
can impinge, obstruct, or rupture.
In bone: The cysts can be
an incidental finding; mass effect: vague pain; pathologic fracture;
vertebral body: nerve or cord compression.
Intraosseous lesion: large, multiloculated, distorted fluid-filled cyst, lined by gelatinous tissue, usually sterile.
marrow response: Local marrow necrosis Mixed inflammatory infiltrate
with eosinophils, and giant cells, hemosiderin deposits, and
cholesterol crystals
ELISA or Western blot serology
(>80% sensitive and specific for liver infection); radiology,
ultrasound, computed tomography, and magnetic resonance imaging allow
imaging of the cysts.
Surgical resection is the primary treatment.
management is indicated in patients with primary liver and lung cysts
that are inoperable, or those who have multiple cysts. Benzimidazoles
are used and the response rates are not encouraging (30% cure, 30% to
50% improvement with reduction in cyst size, and 20% to 40% no change).


Suggested Reading
AM, Damsker B, Green S, et al. The clinicopathological spectrum of
non-tuberculous mycobacterial osteoarticular infections. J Bone Joint Surg [Am] 1985;67(6):925–929.
Rasool MN. Osseous manifestations of tuberculosis in children. J Pediatr Orthop 2001;21(6):749–755.
Sponseller PD, Malech HL, McCarthy EF, Jr, et al. Skeletal involvement in children who have chronic granulomatous disease. J Bone Joint Surg [Am] 1991;73(1):37–51.
Tuli SM. General principles of osteoarticular tuberculosis. Clin Orthop Rel Res 2002;398:11–19.
Zlitni M, Ezzaouia K, Lebib H, et al. Hydatid cyst of bone: diagnosis and treatment. World J Surg 2001;25(1):75–82.

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