infectious disease of skin appendages muscles bone

1. INFECTIONS OF THE SKIN AND ITS
APPENDAGES, MUSCLE, BONES, AND
JOINTS
Skin lesions
OVERVIEW OF SKIN INFECTIONS
Skin infections are best classified according to the
nature of the lesion (e.g., macule, papule, vesicle, or
pustule), the layer involved (Figure), and the
microbial etiology. Certain of these infections, for
example uncomplicated impetigo, can be treated in
the primary setting without resort to special studies
such as Gram’s stains and cultures. The clinician
should be alert to the possibility of rare but serious
lesions such as the membranous ulcers of cutaneous
diphtheria or the malignant pustule of anthrax; of
sexually transmitted diseases; and of the possibility
that skin lesions signify underlying diseases.
NON-BULLOUS IMPETIGO

2. Impetigo is a common superficial infection of the
epidermis usually encountered in children, typically
on the face and extremities. In the past most cases of
impetigo have been attributed to Streptococcus
pyogenes (group A streptococcus). Group A
streptococcal strains causing impetigo are, in
general, of different M serotypes than those causing
pharyngitis. In recent years S. aureus has emerged as
the more common etiology at least in some
localities. Group A streptococci and S. aureus are
often encountered together, and asymptomatic
carriage of either or both of these bacteria
predisposes to impetigo. Some data suggest a
prominent role for anaerobic bacteria. Group B
streptococci can cause impetigo in newborn infants,
and streptococci belonging to Lancefield groups C
and G rarely cause this condition. Predisposing
factors include warm, humid climates, poor personal
hygiene, poverty, and minor skin trauma
Impetigo typically involves exposed areas of the
skin, especially the face but also the extremities. The
initial lesions are small vesicles, which quickly
become pustules and then rupture leaving a purulent
discharge on the skin that dries to form honey-

3. colored or golden-brown “stuck-on” crust. The
lesions are painless but are often pruritic, prompting
scratching which in turn spreads the infection to new
areas. Mild lymphadenopathy is common, but high
fever or other systemic symptoms should prompt a
search for another diagnosis. The disease infects the
most superficial layers of the epidermis. Impetigo is
nearly always a self-limited disease that heals
without scarring. However, it is a common cause of
acute post-streptococcal glomerulonephritis, which
is life threatening. Figure 1
Young sporangia of a Mucor spp. fungus. Mucor is a
common indoor mold, and is among the fungi that
cause the group of infections known as
zygomycosis. The infection typically involves the
rhino-facial-cranial area, lungs, GI tract, skin, or less
commonly other organ systems.
Figure 2
This patient presented with a case of a periorbital
fungal infection known as mucormycosis, or
phycomycosis. CDC

4. ECTHYMA
Ecthyma resembles non-bullous impetigo in that it is
usually caused by group A streptococci and/or
staphylococci and begins as vesicles that become
pustules which then rupture, leaving an exudates on
the surface of the skin. In ecthyma, however, the
process does not remain confined to the stratum
corneum but rather extends through the epidermis.
The result is typically a “punched-out” ulcer with
raised violaceous margins. The ulcer is covered with
a greenish yellow crust. The lesions are most
commonly located on the lower extremities.
Ecthyma occurs most frequently in young children
and in the elderly. Unusual causes of ecthyma
include cutaneous diphtheria, gonococcal infection,
mucormycosis (figure 1-2), molluscum contagiosum
(figure 3), and herpes simplex virus infection.
This form of “uncomplicated ecthyma” must be
distinguished from ecthyma resulting from systemic
infection (ecthyma gangrenosum).

5. Figure 3 Histopathology of molluscum
contagiosum, skin. CDC/Dr. Edwin P. Ewing, Jr.
Figure 4
This patient presented with these gluteal lesions that
proved to be impetigo, but was first thought to be
syphilis. Impetigo is usually caused by Group A
Streptococcus sp. or Staphylococcus aureus bacteria.
Note how the maculopapular lesions resemble
syphilis, which is caused by the Gram-negative
Treponema pallidum spirochete. CDC
BULLOUS IMPETIGO AND THE
STAPHYLOCOCCAL SCALDED SKIN
SYNDROME
Bullous impetigo is a serious form of the disease that
usually occurs in newborn infants and young
children, is manifested by large, flaccid bullae, and
is caused by strains of S. aureus capable of making
exfoliative toxins. More extensive skin involvement

6. caused by the same staphylococcal strains is known
as the staphylococcal scalded skin syndrome or,
when it affects neonates, pemphigus neonatorum
(Ritter’s disease).
Bullous impetigo is attributed to S. aureus strains
belonging to phage group II capable of producing
two extracellular exfoliative toxins (known as A and
B) that separate the stratum corneum from the rest of
the epidermis. The more common and milder form
of the disease―representing about 10% of all cases
of impetigo―differs from non-bullous impetigo in
that the vesicles enlarge into flaccid bullae before
rupturing (figure 4). The exposed skin surface is at
first moist and red, resembling a small burn. A thin,
light-brown, “varnish-like” crust then develops. The
more severe form, which usually affects younger
children, is known as the staphylococcal scalded
skin syndrome. Widespread, flaccid bullae rupture
causing exfoliation of the skin that resembles an
extensive third-degree burn. This form of the disease
can occur in epidemic form in nurseries, where it is
known as pemphigus neonatorum or Ritter’s disease.
Fever and other systemic symptoms are usually
absent in the more localized forms of the disease but
are invariably present in patients with the

7. staphylococcal scalded skin syndrome.
Staphylococcal scalded skin syndrome in adults is
rare, and is usually associated with
immunosuppression. Localized bullous impetigo is
self-limited, but the staphylococcal scalded skin
syndrome carries a significant mortality rate.
FOLLICULITIS
Folliculitis, by which is meant pyoderma involving
the hair follicles and apocrine glands, affects nearly
everyone at one time or another but is usually self-
limited. Occasionally, folliculitis evolves into larger
lesions known as furuncles and carbuncles.
S. aureus is the usual cause of folliculitis in non-
immunocompromised patients, the infection
probably arising from prior nasal colonization by
this bacterium. Pseudomonas aeruginosa (usually of
serogroup 0:11) has emerged as an important cause
of extensive folliculitis after exposure to
contaminated hot tubs, whirlpools, heated swimming
pools, or after diving suit dressing. Ps. aeruginosa
can also cause extensive folliculitis in
immunosuppressed patients. Other gram-negative

8. bacilli typically cause folliculitis in patients who
have undergone prolonged antibiotic therapy for
acne or rosacea, but some recent data suggest that
gram-negative folliculitis also occurs in persons
without this predisposition. Fungal etiologies of
folliculitis include Candida albicans (especially in
hospitalized patients who have received
corticosteroids and antibiotics) and Malassezia
furfur (in patients with diabetes mellitus,
granulocytopenia, or who have received
corticosteroids). A condition known as eosinophilic
folliculitis, of unknown origin, usually occurs in
patients with advanced HIV disease.
The characteristic unit lesion is a 2 to 5 mm
erythematous papule that often contains a small
pustule at its apex. The lesions are often multiple
and tend to be pruritic. When multiple deep lesions
appear on the bearded area of the face, the condition
is known as sycosis barbae.
Folliculitis is usually self-limited, but can lead to the
formation of furuncles or boils. Extensive folliculitis
due to Pseudomonas aeruginosa often includes otitis
externa as a manifestation. Rarely, folliculitis due to

9. Pseudomonas aeruginosa can progress to ecthyma
gangrenosum. The lesions of sycosis barbae tend to
be deeper and more chronic than those of other
forms of folliculitis.
Figure 5
Cutaneous abscess located on the hip, which had
begun to spontaneously drain, releasing its purulent
contents. The abscess was caused by methicillin-
resistant Staphylococcus aureus bacteria, referred to
by the acronym MRSA. CDC
Figure 6
Cutaneous abscess located on the thigh, caused by
methicillin-resistant Staphylococcus aureus bacteria.
A clinician had lanced the lesion in order to allow
the pus contained therein, to be released. CDC
FURUNCLES, CARBUNCLES, AND SKIN
ABSCESSES
The familiar furuncle or “boil” is thought to arise
from folliculitis. The term furunculosis refers to

10. multiple boils or to frequent recurrences. Carbuncles
are more extensive and difficult-to-treat lesions that
often require surgical intervention. Skin abscesses,
although similar to carbuncles histologically, are
usually deeper infections that do not originate in hair
follicles.
S. aureus is the usual cause of both furuncles and
carbuncles, and is also the sole or predominant
pathogen in about 50% of skin abscesses (figure 5-
6). Predisposing factors to recurrent furuncles
(furunculosis) include obesity, corticosteroid
therapy, disorders of neutrophil function, and
possibly diabetes mellitus. Immunoglobulin levels
are usually normal in patients with furunculosis (low
IgM levels have been demonstrated in some patients
but this is of uncertain significance and, in contrast
to IgG deficiency, replacement therapy is
impractical). Most patients with recurrent furuncles
have no obvious predisposing factors other than
being nasal carriers of S. aureus nasal carriers.
Outbreaks of furunculosis have been described in
families, athletic teams, and in village residents who
took steam baths together. Skin abscesses can result
from minor trauma, injecting drug use (the practice
of subcutaneous and intramuscular injection is

11. known as “skin popping”), or bacteremia.
Congenital immunodeficiency syndromes such as
the hyperimmunoglobulin E-recurrent infection
syndrome (Job’s syndrome) are sometimes present
in patients with recurrent skin abscesses. Rarely,
skin abscesses are self-inflicted (factitious abscess),
in which case Gram’s stain and culture may reveal
“mouth flora” bacteria.
Furuncles commonly present as tender, firm, round
subcutaneous nodules. The typical lesion is 1 to 2
cm in diameter, or about the size of a marble. The
overlying skin is often erythematous, but fever and
other systemic signs of illness are seldom present.
Common sites for furuncles include the face, neck,
axillae, and buttocks, but any area of the body that
contains hair follicles can be affected.
Carbuncles differ from furuncles in that they are
larger, deeper, and irregular lesions that are usually
associated with fever and malaise. Indeed, some
patients with carbuncles are acutely ill, meeting
criteria for the sepsis syndrome. Common sites for
carbuncles include the nape of the neck, the back,
and the thighs.

12. Skin abscesses present with local pain, swelling, and
erythema. Systemic toxicity is usually absent unless
cellulitis is present or unless the abscess originated
from bacteremia secondary to a deep infection
elsewhere. A majority of skin abscesses are located
over the extremities, although any part of the body
can be involved.
Furuncles often break down and drain
spontaneously, following which complete healing
occurs. Carbuncles, if untreated, tend to become
chronic. Both lesions, but especially carbuncles, can
give rise to bacteremia, which can result in
metastatic lesions such as endocarditis or
osteomyelitis. Furuncles or carbuncles located in the
“dangerous area” of the face―that is, the nose and
medial aspects of the cheeks―can spread to the
brain causing cavernous sinus thrombosis. Most skin
abscesses, if untreated, will eventually “point” drain
spontaneously but serious complications can result
from bacteremia.
HIDRADENITIS SUPPURATIVA

13. Hidradenitis suppurativa is a chronic disease of the
apocrine glands of the axillae (hidradenitis
suppurativa axillaris), inguinal region (hidradenitis
suppurativa inguinalis), and perianal skin. The
lesions become secondarily infected, leading to
abscesses, fistulas, and scarring. Surgery rather than
antimicrobial therapy is the usual cure for severe
cases.
Although the basic cause is unknown, the
mechanism of disease appears to be plugging of
apocrine gland ducts by keratin. Pressure within the
ducts causes them to dilate and rupture into the
surrounding tissues. The initial inflammatory lesions
are sterile, but bacterial superinfection quickly
occurs. Pathogens that have been isolated include S.
aureus, streptococci (including S. anginosus),
aerobic gram-negative rods (such as E. coli, Proteus
mirabilis, and Pseudomonas aeruginosa), and
anaerobic bacteria.
Early lesions consist of irregular reddish purple
nodules, typically located in the axillae, groin, or
perianal area. These lesions gradually enlarge and
become fluctuant. Drainage results in sinus tracts. A
foul odor to the drainage signifies anaerobic

14. infection.
In many patients the lesions remain, resolve or
remain generally stable. Spontaneous resolution,
however, is rare. In some patients, however, the
disease progresses relentlessly resulting in extensive
inflammation, undermining of the skin with sinus
tracts, chronic drainage, and scarring. Complications
tend to be more severe in the perineal and perianal
forms of the disease and include fistulas and
squamous cell carcinomas.
Figure 7
Facial erysipelas manifested as severe malar and
periorbital erythema and swelling. Note the purulent
discharge from the eye.
Erysipelas is a dermatologic condition, which
involves the inoculation of the skin and
subcutaneous tissue with streptococcal bacteria
causing edema and bright red erythema of the
affected areas. It is sometimes referred to as
cellulitis.
CDC/Dr. Thomas F. Sellers/Emory University

15. Figure 8
Facial erysipelas manifested as severe malar and
nasal erythema and swelling CDC/Dr. Thomas F.
Sellers/Emory University
ERYSIPELAS (SUPERFICIAL CELLULITIS)
“Cellulitis” refers to spreading infection in the
subcutaneous tissue. Erysipelas (figure 7 and 8) is a
superficial form of cellulitis in which the involved
skin assumes a fiery bright red color (hence the
alternative name, “St. Anthony’s fire”).
Group A streptococci (S. pyogenes) cause most cases
of erysipelas. Group B streptococci cause some
cases of erysipelas in newborn infants, and
streptococci belonging to groups C and G have
caused streptococci in adults. In one study, more
than 96% of cases of erysipelas were attributed to
streptococci on the basis of extensive studies that
included cultures of punch biopsy specimens.

16. Rarely, S. aureus causes erysipelas.
Two factors notoriously predispose to erysipelas:
breaks in the skin and lymphatic obstruction.
Examples of the former include minor skin
infections including athlete’s foot (tinea pedis), local
trauma or abrasions, eczema, and cutaneous ulcers.
Patients with lymphedema secondary to congenital
anomalies of the lymphatic system, surgery (e.g.,
radical mastectomy) or disease (e.g., filariasis
or―quite commonly―previous episodes of
cellulitis) are markedly predisposed to erysipelas.
About 50% of persons with severe lymphedema
develop erysipelas, compared with about 1 in 1000
persons in the general population. Other
predisposing factors include the nephrotic syndrome,
diabetes mellitus, alcoholism, and venous stasis of
any etiology.
Erysipelas usually presents as a rapidly progressive
infection accompanied by fever and other signs of
systemic toxicity. The involved skin is usually bright
red, indurated, and edematous. There is sharp
demarcation between involved and uninvolved skin.
When the extremities are involved there is

17. frequently one or more bright red “lymphangitic
streaks” that connect the involved skin to one or
more tender regional lymph nodes. Erysipelas most
commonly occurs on the lower extremities. The
upper extremities are involved especially in patients
who have undergone radical mastectomy. The face is
involved in about 20% of cases, most often affecting
the nose and cheeks.
CELLULITIS (OTHER THAN ERYSIPELAS)
Cellulitis other than erysipelas is a deeper infection
of the subcutaneous tissue usually caused by
streptococci, staphylococci, or both. However, the
etiologic spectrum is diverse. Cellulitis usually
results from introduction of a pathogen into the skin
by way of a wound or pre-existing skin lesion.
Examples of the former include cuts and punctures;
examples of the latter include ulcers (such as stasis
ulcers or decubiti), eczema, or furuncles.
Predisposing factors include tinea pedis, peripheral
vascular disease, peripheral edema including
lymphedema, prior history of cellulitis, and diabetes
mellitus. S. pyogenes (group A streptococci) and S.
aureus are the usual etiologies, but careful studies
have established that cellulitis is often a mixed

18. infection involving both of these microorganisms. A
large and growing number of microorganisms have
been associated with cellulitis, including the
following with therapeutic implications:
Aeromonas hydrophila cellulitis begins in
wounds exposed to fresh water, and can progress
rapidly with marked systemic toxicity.
Vibrio vulnificus and other marine vibrios cause
cellulitis in wounds exposed to salt water or
brackish water, and progress to necrosis of skin
and subcutaneous tissue. This pathogen also
causes sepsis in patients with liver disease
following ingestion of raw seafood.
Cryptococcus neoformans causes cellulitis in
immunosuppressed patients.
Haemophilus influenzae was an important cause
of cellulitis in children, often involving the face,
prior to the introduction of the conjugated
vaccine.
Aerobic gram-negative rods (e.g., E. coli,
Proteus species) sometimes cause cellulitis in
immunocompromised persons or persons with
diabetes mellitus.

19. Streptococcus pneumoniae can cause severe
cellulitis in immunocompromised persons and
persons suffering from alcoholism.
Non-group-A β-hemolytic streptococci (e.g.,
groups B, C, or G) cause cellulitis in neonates,
in frail elderly persons, and in persons with
lymphedema of the lower extremities.
Erysipelothrix rhusiopathiae causes erysipeloid
(“fish-handler’s disease”) which typically
presents as a painful, violaceous, expanding
lesion on an upper extremity on which an
abrasion has been exposed to freshwater fish,
shellfish, meat, hides, or poultry. “Seal finger,” a
cellulitis of unknown origin incurred while
caring for seals, resembles erysipeloid but seems
to respond best to tetracyclines.
Cellulitis presents with classic signs of
inflammation―redness, pain, warmth, and
swelling¬―accompanied by fever, malaise, and
other symptoms of toxicity. The line of demarcation
between involved and uninvolved skin is often not
as clear as is the case with erysipelas. Lymphangitic
streaks are usually not present, but there may be
tender regional lymphadenopathy. Depending to

20. some extent on the pathogen, there may be abscess
formation or extension into fat or fascial layers.
MEMBRANOUS ULCERS INCLUDING
CUTANEOUS DIPHTHERIA
Cutaneous ulcers such as those associated with
venous or arterial insufficiency in the lower
extremities are relatively common. Occasionally,
such an ulcer manifests at its base a layer of necrotic
debris resembling a membrane. Analysis of the
associated purulent drainage, which is often
abundant, usually discloses a mixture of various
aerobic and anaerobic bacteria. Rarely, such ulcers
are caused by cutaneous diphtheria, which is now
the most common form of diphtheria reported in the
U.S. and which serves as a reservoir for transmission
of the disease. A majority of confirmed cases in the
U.S. in recent years have been imported from other
countries, but vulnerable populations include
homeless persons, Native Americans, and certain
populations in the Southeastern states and the Pacific
Northwest. Primary cutaneous diphtheria presents as

21. an indolent, non-healing, “punched-out” skin ulcer
with a dirty-gray or gray-brown membrane at its
base. Wound diphtheria involves secondary infection
of a preexisting wound, all or part of which becomes
covered by a membrane. Suspicion of cutaneous
diphtheria should prompt attempts to make a
definitive diagnosis by culture and to demonstrate
the presence of the toxin by special methods. All
cases of suspected or confirmed diphtheria should be
reported promptly to the local health department.
PYOMYOSITIS
Pyomyositis, an acute pus-forming infection of
skeletal muscle, was in the past usually called
“tropical pyomyositis” to denote its geographic
association. Recent reports indicate that pyomyositis
is becoming more common in the U.S. and other
developed countries. These reports also emphasize
an association with HIV disease and with injecting
drug use, but some patients have no obvious
predisposing condition. S. aureus causes about 95%
of cases in tropical areas and about two-thirds of
cases in the United States. Streptococci (most often

22. group A streptococci but also groups B, C, and G, S.
pneumoniae, and S. anginosus) are as a group the
second most common cause in the United States. A
history of recent blunt trauma or unusual exertion is
obtained in up to one-half of patients with
pyomyositis, suggesting that local muscle injury
created a “place of least resistance” (locus minoris
resistentiae) that was subsequently infected during
what would otherwise have been a transient, self-
limited bloodstream infection. Whereas most
patients with tropical pyomyositis have no
underlying disease, about 60% of patients with
pyomyositis in temperate climates have a defect in
host defenses.
Pyomyositis usually affects the large muscles of the
lower extremities or trunk. The illness typically
unfolds over several weeks. Most patients present
with pain and tenderness localized to the body of a
muscle, but an occasional patient will present with
an acute illness with marked systemic toxicity.
Unusual presentations include toxic shock syndrome
and infection of the abdominal wall resembling the
presentation of acute abdomen. Untreated,
pyomyositis often progresses to severe sepsis with
shock and death.

23. Figure 9
The foot of this patient is swollen due to gonococcal
arthritis. Gonorrhea is the most frequently reported
communicable disease in the U.S. Disseminated
gonococcal infection is most often the cause of acute
septic arthritis in sexually active adults, and the
reason for most hospitalizations due to infective
arthritis. CDC
Figure 10
This patient presented with cutaneous foot lesions
that were diagnosed as a disseminated gonococcal
infection. CDC ACUTE SEPTIC ARTHRITIS
(ACUTE INFECTIOUS ARTHRITIS)
Here, the term septic arthritis will be used for acute
infectious arthritis of bacterial etiology. This
condition is uncommon in the general population
(annual incidence 2 to 5 per 100,000 persons), but is
more common in patients with rheumatoid arthritis
(28 to 38 per 100,000) and in persons with a joint

24. prosthesis (40 to 68 per 100,000). The disease
usually affects a single joint, most commonly the
knee. S. aureus is the most common pathogen, but
special note should be taken of N. gonorrhoeae in
sexually active young adults and of a wide range of
bacteria under special circumstances.
Septic arthritis usually results from hematogenous
seeding of the synovium, a highly vascular tissue
that lacks a basement membrane. Especially
vulnerable patients include young infants because of
the rich vascularity surrounding their epiphyseal
growth plates and patients with chronic arthritis,
joint implants, recent trauma, or chronic debilitating
diseases including the frail elderly. Septic arthritis
can also be secondary to penetrating trauma. Septic
arthritis of the hands and wrists is commonly caused
by trauma including animal and human bites.
In newborn infants the usual etiologies are group B
streptococci, aerobic gram- negative rods, and S.
aureus. H. influenzae type b was formerly the usual
cause of septic arthritis in toddlers, but wide use of
the conjugate vaccine has virtually eliminated this
disease. Kingella kingae, a fastidious gram-negative

25. rod, is emerging as an important joint pathogen in
children. After age 2, S. aureus becomes the most
common cause of septic arthritis in persons other
than sexually active young adults, in whom
gonococcal arthritis (figure 9) is common.
Streptococci (not only group A but also groups B, C,
and G) are relatively common causes. Pasteurella
multocida causes particularly aggressive disease
after a cat bite. Aerobic gram-negative rods cause up
to one-fifth of cases, usually in the setting of chronic
underlying disease or injection drug use.
Streptococcus pneumoniae occasionally causes
septic arthritis, especially in children with sickle cell
disease. A wide variety of bacteria cause occasional
cases. Septic arthritis due to Pseudomonas
aeruginosa and occurring in unusual places (e.g.,
sternoclavicular joints, sacroiliac joints, or pubic
symphysis) is well documented among injecting
drug users.
Acute septic arthritis usually presents with pain,
swelling, and limitation of motion of the affected
joint. Most patients are febrile. A single large joint is
involved in about 90% of children and about 80% to
90% of adults. The knee is the most commonly
involved joint, followed by the hip and the shoulder.

26. Patients with rheumatoid arthritis are more likely to
have multiple joint involvement. Patients with
gonococcal arthritis also have involvement of
multiple large and small joints, but on closer
inspection there is often little or no joint effusion
despite prominent inflammation of the adjacent
tendons (tenosynovitis). Associated vesiculopustules
strongly suggest the gonococcal arthritis-dermatitis
syndrome.
SEPTIC BURSITIS
Septic bursitis most commonly involves the
olecranon or prepatellar bursae. S. aureus causes
most cases of acute septic bursitis; chronic cases can
be due to a wide range of microorganisms. Minor
trauma is likely to be a precipitating factor,
especially when bursae of the lower extremities are
involved. Chronic infectious bursitis, which
typically follows minor trauma, is associated with a
wide variety of bacteria and fungi of low virulence.
Examples include fungi that are soil contaminants
and non-tuberculous mycobacteria. Septic bursitis
presents with some combination of pain, tenderness,
erythema, warmth, and swelling over the affected
bursa in a person vulnerable to recurrent trauma such

27. as a painter or brick mason. The presentation may be
acute when due to S. aureus or subacute or chronic
when due to an organism of lesser virulence.
Absence of pain on movement of the joint helps
distinguish septic bursitis from arthritis. Although
septic bursitis is an uncommon lesion, the diagnosis
is easily made on clinical grounds when suspected
and confirmed by aspiration or open exploration of
the bursa.
VIRAL ARTHRITIS
Arthritis, usually symmetric and self-limited, is a
prominent feature of several viral infections. Most
cases result from viral invasion of the synovium
and/or deposition of circulating immune complexes.
Presentations vary according to the etiology:
Rubella usually causes a polyarthritis in adult
women most often affecting the small joints of
the hands. The knees, wrists, and ankles can also
be involved. The arthritis usually begins
simultaneously with the rash or within the next
72 hours. Effusions can be sufficiently large to
permit aspiration for synovial fluid analysis,
which usually discloses a predominance of
mononuclear cells.

28. Mumps typically causes a polyarthritis that
involves multiple small and large joints. The
arthritis usually begins shortly before the onset
of parotitis or within the next 2 weeks. Effusions
are uncommon.
Parvovirus B19 causes arthritis that is usually
symmetric and involves the joints of the upper
or lower extremities. Carpal tunnel syndrome
sometimes occurs. A rash that can be
maculopapular, reticular, or hemorrhagic usually
accompanies the arthritis. A history of exposure
to a child with fifth disease (erythema
infectiosum, manifested by a “slapped cheeks”
facial rash) is often obtained. (The major
complications of parvovirus B19 infection
derive from its effect on developing red blood
cells and include erythoblastosis fetalis with
fetal loss and aplastic crisis in persons who need
rapid production of erythrocytes).
Acute hepatitis B causes, in about 20% of
patients, a symmetric arthritis affecting (in order
of frequency) the hands, knees, and ankles. The
arthritis usually begins within 2 days before the
onset of symptoms and signs of liver disease
such as jaundice.

29. Most cases of viral arthritis are self-limited, but
some patients may have prolonged joint pain and the
issue whether viral arthritis precipitates chronic
rheumatic diseases remains an open.
Figure 11
This patient’s arm shows the effects of the fungal
disease sporotrichosis, caused by the fungus
Sporothrix schenckii. The first symptom is usually a
small painless bump that’s red, pink, or purple. This
is followed by one or more additional
bumps/nodules which open and may resemble boils.
Eventually lesions look like open sores, or
ulcerations, and heal slowly. CDC/Dr. Lucille K.
Georg
CHRONIC MONOARTICULAR ARTHRITIS
DUE TO INFECTION
Chronic arthritis involving a single joint, when due
to infection, is usually caused by mycobacteria
(including M. tuberculosis), fungi, nocardia,
brucellosis, or Whipple’s disease. Most cases of

30. chronic monoarticular arthritis arise by
hematogenous infection. Sporothrix schenckii
(sporotrichosis) (figure 11) is perhaps the most
common fungal etiology in non-
immunocompromised patients and most often
involves the knee. Brucella species are notorious
causes of chronic arthritis in parts of the world
where brucellosis remains prevalent. Whipple’s
disease, recently attributed to a bacterium named
Tropherma whippelii, can also cause chronic
monoarticular arthritis.
ACUTE HEMATOGENOUS
OSTEOMYELITIS
Hematogenous osteomyelitis results when
microorganisms enter the bloodstream from a distant
source (such as a minor skin lesion), enter bone
through a nutrient artery, and establish infection.
The disease occurs most often in infants and
children, but can occur at any age group.
Hematogenous osteomyelitis in adults most often
involves the spine (vertebral osteomyelitis) and is
discussed separately.
Acute hematogenous osteomyelitis is nearly always

31. caused by a single organism. S. aureus is common in
all age groups and is the most common cause in
adults. Group B streptococci and E. coli commonly
cause the disease in infants, and group A
streptococci often cause the disease in older
children. H. influenzae was a common cause of
osteomyelitis in young children before the wide use
of the vaccine. Salmonella species not infrequently
cause hematogenous osteomyelitis in patients with
sickle cell disease or other hemoglobinopathies.
The occurrence of hematogenous osteomyelitis is
best explained by the fragile nature of the arterial
supply to the metaphyseal regions of bones, and
especially those of growing children. Minor trauma
such as the “lumps and bumps” of childhood
disrupts the delicate capillary loops of these regions,
causing small areas of necrosis that provide safe
harbors for any bacteria that chance to come their
way through the bloodstream. In infants less than 1
year of age, the growth plates of bone have a rich
blood supply and therefore hematogenous
osteomyelitis often affects the epiphyses of long
bones. Thereafter the growth plates lose their blood
supply, causing osteomyelitis to be confined to the

32. metaphysis and diaphysis.
Symptoms vary according to age but can be subtle in
all age groups. In neonates, findings often consist of
localized swelling and decreased motion in an
extremity, often (about 60% of cases) accompanied
by an effusion in the adjacent joint. About one-half
of children with osteomyelitis present with an acute
or subacute illness over several weeks with fever and
other constitutional symptoms accompanied by signs
of inflammation over the affected bone. In many
children and in most adults, the illness evolves over
a month or longer with vague constitutional
symptoms and non-specific bone pain.
VERTEBRAL OSTEOMYELITIS AND
DISKITIS
Vertebral osteomyelitis typically involves two
adjacent vertebrae and the intervertebral disk; when
the disk alone is involved the process is called
diskitis. Vertebral osteomyelitis often presents as a
subacute or chronic illness with constitutional
symptoms and localized back pain. Occasionally, it
presents as acute fever with back pain. Fever is
absent in about one-half of patients. Complications
include paraspinous abscess, epidural abscess, and

33. spinal cord compression. Neurologic symptoms such
as weakness in the lower extremities or impaired
bladder or bowel function indicate spinal cord
compression. The disease occurs mainly in adults. In
children, the initial complaint is usually refusal to
walk, a limp, or back pain.
Most cases are of hematogenous origin, but
occasional cases result from inoculation of bacteria
during spinal surgery, lumbar puncture,
myelography, or other medical procedures. S. aureus
is the most common pathogen. Aerobic gram-
negative rods are relatively common causes
especially in patients with chronic urinary tract
infections. Tuberculosis of the spine (Pott’s disease)
should always be considered. Occasional cases are
caused by fungi or unusual pathogens.
OSTEOMYELITIS FOLLOWING NAIL
PUNCTURE WOUNDS
Nail puncture wounds can result in various
combinations of cellulitis, abscess, osteochondritis,
septic arthritis, and osteomyelitis. Osteomyelitis

34. complicates about 1% to 2% of nail puncture
wounds in children. Most of these infections occur
during the warm summer months. Osteomyelitis due
to Pseudomonas aeruginosa is strongly associated
with wearing tennis shoes at the time of the injury
(up to 93% of cases). Staphylococcus aureus is the
other major pathogen, and in one series both Ps.
aeruginosa and S. aureus were isolated in about one
half of the cases.
INFECTIONS OF THE HAND
Acute paronychia, usually caused by S. aureus, is an
infection involving the lateral fold of soft tissue
surrounding the fingernail. Trauma to the nail
including nail biting, foreign bodies, manicures, or
hangnail is the usual predisposing cause. Injury to
the seal between the nail plate and the nail fold
allows bacteria to enter, causing cellulitis and/or the
abscess.
Herpes whitlow, caused by the herpes simplex virus
(HSV-1 or HSV-2), usually involves the fingertip
including structures related to the nail bed. This

35. lesion is an occupational hazard for health care
workers, being encountered not infrequently among
nurses, surgeons, and dentists. Patients with herpetic
gingivostomatitis and genital herpes are also at risk.
Chronic paronychia is usually associated with
Candida albicans (about 95% of cases) but a wide
range of bacterial, fungal, and mycobacterial
pathogens have been recovered. There is typically a
history of frequent immersion of the hands in water.
Persons at risk include housewives, dishwashers,
swimmers, bartenders, and persons with diabetes
mellitus or who are immunosuppressed. The
condition most commonly affects women between
the ages of 30 and 60 years. Recurrent episodes of
pain, inflammation, and swelling eventually lead to
chronic induration around the nail, often involving
the eponychium (the thin membrane on the proximal
aspect of the nail that serves as a seal between the
nail wall and the nail plate).