Selected human infectious diseases part 2

1. Staphylococcal scalded skin
syndrome. Neonate with large
denuded areas of the skin
where bullae have burst.

2. Staphylococcal scalded skin
syndrome. Large areas of
epidermal loss, with some bullae
still intact.

3. Staphylococcal scalded skin
syndrome. Red raw denuded
areas where skin has sloughed
off.

4.  The peeling is caused by the toxin which
produces a cleavage plane high in the
epidermis at the stratum granulosum level.
 As the areas of exfoliation dry, a flaky
desquamation and then replacement with
new epidermis occurs within two weeks.

5.  SSSS is treated with a penicillinase-resistant
penicillin, given intravenously, together with
measures to counter hypovolaemia.

6.  A clinically identical syndrome to SSSS,
termed toxic epidermal necrolysis or Lyell's
syndrome, is seen in older children or adults
as a manifestation of drug allergy
(particularly to sulphonamides) or viral
infections.

7.  Many advocate the use of high-dose
corticosteroids for the treatment of toxic
epidermal necrolysis
 differentiation from SSSS by means of a skin
biopsy is important.

8. Toxic epidermal necrolysis (Lyell’s syndrome). Loss of
epidermis in a black child associated with sulphonamide
therapy.

9.  This is a necrotizing infection of
subcutaneous tissues usually occurring as a
result of trauma or operations in the
perineum, abdomen or lower extremities.

10.  It may be caused bynclostridial species
sometimes by aerobic bacteria such as
streptococci, staphylococci and coliforms.

11.  There is a gradual onset of swelling and
erythema and frank crepitus in the involved
area.

12. Postoperative gangrenous cellulitis. A huge area of
ulceration filled with gangrenous skin and slough lies
adjacent to the wound. There is surrounding cellulitis and a
further area of necrotic skin in the flank.

13. The cellulitis has resolved and the ulcerated area is filled
with black necrotic tissue.

14.  There is little pain
 There may be a foul smelling discharge from the
wound.
 In clostridial anaerobic cellulitis the discharge is thin
and dishwater-like
 In non-clostridial infection it is thicker and darker in
colour.
 Radiology may show gas in the tissues. Exploration
of the wound should be performed to ensure that
there is no myonecrosis.

15. Considerable amount of gas (G)
in the tissues of the thigh of a
patient with anaerobic infection
following intravenous drug abuse.

16.  Treatment consists of surgical debridement
and parenteral antibiotic therapy.

17. Clostridial cellulitis, following a compound fracture of the
tibia. Crepitus was noted on examination and the presence
of gas was confirmed radiologically.

18.  Gas gangrene (clostridial myonecrosis) is a
fulminant life-threatening infection of skeletal
muscle caused by Clostridium perfringens.
 C. perfringens produces a number of powerful
toxins
 it is the a-toxin which is associated with the
severe toxicity, haemolysis and myositis of gas
gangrene.

19. Histology showing typical “box-car” appearance of C.
perfringens in necrotic tissue. Spores are rarely seen in
clinical specimens. Gram’s stain.

20.  The incubation period is 1-4 days
 the earliest symptom is severe pain at the site
of the wound.
 skin is pale and then assumes a bronze
discolouration, followed by the appearance
of haemorrhagic bullae.
 There is often a distinctive, sweetish odour to
the serosanguinous discharge.

21. Amputation stump with discoloration of skin and
hemorrhagic bullae typical of gas gangrene.

22.  Tachycardia and apprehension are prominent
 there may be haemolysis and renal failure. In
suspected cases it is imperative to examine
the muscles for myonecrosis

23.  A Gram stain of the exudate or the muscle
will show numerous gram-positive bacteria,
but this finding does not determine the need
for treatment.
 Affected muscles initially are pale and fail to
bleed or contract on electrical stimulation
later they become beefy red and then
gangrenous and friable.

24. There is a serosanguinous discharge from the lower end of
the surgical wound and the affected muscles show pallor
and failure to bleed.

25.  If myonecrosis is present then immediate,
extensive surgical debridement of involved
muscles and fasciotomy to decompress the
oedema is the only hope.
 Penicillin, chloramphenicol or metronidazole,
gas gangrene antitoxin and hyperbaric
oxygen are of help but must be regarded as
of secondary importance to emergency
surgery.

26.  Animal bites
 Bites from domestic dogs and cats are frequent and
range from the trivial to the life-threatening.
 Infections are caused by the animals' oral bacterial
flora.
 The most important organism in both dog and cat
bites is Pasteurella multocida, a small gram-
negative coccobacillus.

27.  Staphylococci, streptococci and anaerobic
bacteria are the other common pathogens.
 An infected animal bite usually presents with
a localized cellulitis, a malodorous wound
exudate and a low-grade fever .
 Many bites occur close to bones or joints and
septic arthritis, tendonitis and osteomyelitis
sometimes occur.

28. Infected wound of finger following bite of domestic cat.
Pasteurella multocida was isolated from the wound.

29.  Penicillin or ampicillin is very suitable but
erythromycin and the penicillinase-resistant
penicillins are less effective.
 Amoxicillin/clavulanic acid will cover all the
likely pathogens and tetracycline can be used
in the penicillin-allergic individual.
 Tetanus and/or rabies prophylaxis should also
be considered.

30.  Human bites
 The normal human oral flora is capable of
causing severe infections, either as a result of
bites or in clenched fist injuries

31.  The organisms responsible are a-haemolytic
streptococci and various anaerobes including
Fusobacterium spp. Bacteroides spp. and Eikenella
corrodens.
 The latter is particularly important as it often
produces an indolent infection and is resistant to
clindamycin, metronidazole, penicillinase-resistant
penicillins and some cephalosporins.

32.  managed with primary closure
 require irrigation, debridement,
immobilization, elevation and close
observation.
 Penicillin plus a penicillinase-resistant
penicillin or amoxicillin/clavulanic acid are the
drugs of choice.

33. Etiologic agent: Neisseria meningitidis
- Human are the only natural hosts
- Nasopharynx is the portal of entry
- Fulminant meningococcemia is more severe,
with high fever, and hemorrhagic rash; there
may be disseminated intravascular
coagulation and circulatory collapse
(Waterhouse-Friderichsen syndrome)

34. Meningococcaemia
 The rash of meningococcal septicaemia varies a
good deal in distribution and extent, as well as in
the character of the individual lesions.
 The lesions of acute meningococcaemia are mixed
petechial and maculopapular rash most prevalent
on the extremities and extensor surfaces.

35. *meningitis – is the most common
complication of meningococcemia
- Usually begins suddenly, with intense
headache, vomiting, and stiff neck, and
progress to coma within few hours

36. Acute meningococcemia. Note the variable size of the lesions and
their peripheral distributions. Some of the lesions are obviously
purpuric, others macular or papular.

37. Purpuric lesions of variable size on buttocks and thighs.

38.  The rash starts as erythematous macules that
are at first not purpuric, then becomes
brown-stained appearance.
 Purpuric lesions vary in size between
petechiae and ecchymoses of up to several
centrimetres in diameter with an irregular
edge.
 Petechiae may also be seen in the
conjunctivae.

39. Petechiae on the ankle of a young
child with meningococcemia

40. Large ecchymoses of variable size and with an irregular edge.

41. Petechia on bulbar conjunctiva.

42.  Clinical meningitis is common and the
organism is often seen in the cerebrospinal
fluid deposit.
 Gram-negative diplococci can occasionally be
seen on smears obtained from the skin
lesions of acute meningococcaemia.

43. Ecchymoses have undergone central ulceration in the aftermath of
the acute illness with subsequent skin necrosis. Skin grafting was
required.

44.  In the most severe form of meningococcal
septicaemia, accompanied by
 hypotension
 disseminated intravascular coagulation
 peripheral gangrene
 purpura fulminans

45. Gangrene of the extremities following a near-fatal illness with
hypotension.

46. Gangrene of both legs in a black man with acute meningococcal
infection. Bilateral below-knee amputations were later required.

47.  Chronic meningococcaemia is an infrequent
syndrome of recurrent episodes of fever,
arthralgia and rash occurring over a few
weeks.
 The lesions may be maculopapular, petechial,
vesicular or pustular
 paralysis and cardiac toxicity are rare.

48. Chronic meningococcemia. Maculopapular lesions over the
dorsum of the foot of a young woman with recurrent arthralgia and
fever. Neisseria miningitidis was isolated from blood culture.

49. Vesiculopustular lesions on the leg of a hemosexual man with N.
meningitidis bactaeremia. The lesion is similar to that seen in
gonococcal septicemia, which was the initial clinical diagnosis in
this man.

50. Erythema nodosum
 This condition consists of red, raised, painful,
tender, discrete yet ill-defined nodules (Fig 10.105),
usually occurring on the shins (Fig 10.106), but less
commonly on the upper limbs and face. The lesions
are usually symmetrical. They progress over days or
weeks to a more indolent purple-brown appearance
before gradually subsiding.

51. Close-up of purple-red
nodular lesions on shins.

52. Lesions are typically
symmetrical over lower legs.

53.  Fever, malaise and painful swelling of the
ankles are common accompaniments.
Erythema nodosum is a form of cutaneous
vasculitis that represents a hypersensitivity
reaction with numerous clinical associations.

54.  The most frequent are sarcoidosis, primary
tuberculosis, b-haemolytic streptococcal infections,
leprosy, yersiniosis, coccidioidomycosis and
histoplasmosis. It may also be precipitated by drugs,
inflammatory bowel disease and certain collagen
diseases. Rarely, the following infections have also
been associated with erythema nodosum:cat-
scratch disease, psittacosis, other chlamydial
infections and measles.

55.  Therapy should be directed at eliminating the
underlying cause. Symptoms are treated with
aspirin or anti-inflammatory therapy.

56. Erythema multiforme
 Erythema multiforme is a hypersensitivity
reaction that develops in response to an
infection or to drugs or other chemicals. The
skin lesions appear suddenly over any body
area, including the palms and soles.

57.  As its name implies, the lesions of erythema
multiforme vary greatly; maculopapular,
petechial and vesicular elements may all be
seen, but the characteristic element is the
target lesion, in which the initial lesion
spreads in an annular fashion, followed by the
development of a new spot in the middle of
the ring.

58. Typical target lesions on the
palm.

59. Annular target-like vesicular
lesions.

60. Purpuric lesions over the foot.
Although these lesions are not
as typical as those shown
above, the target-like
configuration of some of these
lesions can still be discerned.

61.  Usually only the skin is affected but
inflammation and sometimes ulceration of
the oral, ocular and genital mucosal surfaces
may also occur: it is then termed the Stevens-
Johnson syndrome.

62. Stevens-Johnson syndrome.
Lesions of erythema
multiforme can be seen on the
face, together with
involvement of the mouth.

63. Stevens-Johnson syndrome.
Severe illness with marked
cutaneous and mucous
membrane lesions of
erythema multiforme.

64.  The best established infective associations of
erythema multiforme are herpes simplex and
Mycoplasma pneumoniae; others include
histoplasmosis, coccidioidomycosis and infections
caused by coxsackie virus B5, adenoviruses,
Salmonella, Yersinia and Mycobacterium species.
The other well established association is drug
exposure, notably to sulphonamides and
phenylbutazone.

65. protozoal and helminth infection

66. Trichinosis
 Trichinosis is a ubiquitous disease of man
and animals acquired by eating raw or
undercooked meat containing encysted
larvae of the roundworm, Trichinella
spiralis.
 In most cases the meat is pork or wild boar,
but recently a number of cases have been
traced to bear or walrus meat and even
(occasionally) horsemeat.

67.  Following ingestion, the cyst walls are digested
in the stomach and the viable larvae pass into
the small intestine.
 They attach to the mucosal lining and develop
into adult worms.
 Each fertilized female releases several hundred
larvae over a period of about two weeks before
she dies.
 The newborn larvae burrow into the intestinal
lymphatics, then move via the thoracic duct to
the general circulation, by which means they are
distributed throughout the body.

68.  In most tissues they are killed by the
inflammatory response which they elicit, but
in skeletal muscle (particularly in the
diaphragm, chest wall, biceps and
gastrocnemius) they become encysted and
remain viable and infectious.
 After many years they die and the lesions
eventually calcify.

69. Early stage of infection
showing larva of Trichinella
spiralis in skeletal muscle
before encystment.

70. Coiled encysted larva of T.
spiralis (L) in muscle of
tongue.

71. High powered view of coiled
larva of T. spiralis in fully
formed cyst within striated
muscle of tongue, showing
hyaline capsule of the cyst. H
& E stain.

72. Coiled encysted larva of T. spiralis (L) in striated muscle
showing intense inflammatory reaction around cyst.
Trichrome stain.

73.  Most infections are asymptomatic but heavy
exposure may cause diarrhoea or an illness
characterized by fever, muscle pain, and
periorbital oedema.
 Diarrhoea and abdominal pain is caused by
the adult worms in the intestine and is
usually seen only in the first few days after
ingestion. The other symptoms are
associated with the burden of larvae in the
muscles.

74.  Occasionally conjunctivitis and
haemorrhages in the conjunctivae and nail
beds are present.
 In extremely heavy infections a fatal
myocarditis or encephalitis may occur.
 The systemic symptoms are usually maximal
after 2-3 weeks and then subside slowly.

75. Splinter haemorrhages in the nail beds.

76. Cysticercosis
 Infection with the larvae of Taenia solium
(cysticercosis) most often produces
symptoms referable to the central nervous
system but the larvae may also develop in
skeletal muscle.
 After a few years the organism dies and the
wall of the cyst eventually calcifies.

77.  The condition is usually clinically silent and
is generally only recognised when soft
tissue x-rays are taken in asymptomatic
patients with other conditions and the
characteristic calcified cysts are seen.

78. Radiograph of leg showing characteristic elongated
calcified cysts of T. solium. At this site they produce no
symptoms.

80. Tinea versicolor
 Tinea (or pityriasis) versicolor is a superficial
dermatomycosis
 caused by the lipophilic yeast, Malassezia
furfur.
 is a normal commensal of skin and what
triggers transformation into hyphal forms
and infection is not clear.
 most common in teenagers and young
adults and is more likely in hot weather.
 The asymptomatic lesions are irregular,
hypo- or hyper-pigmented, and may be
circumscribed or diffuse.

81. Brownish-red diffuse lesions over the trunk and arms of a
young man.

82. Superficial, brownish-red lesions
over the back of a young man.

83.  They have a dust-like scale but are not itchy.
 They usually occur on the trunk or proximal
aspects of the limbs, but occasionally affect
other areas of the skin.
 stained with methylene blue (the so called
`spaghetti and meatballs' appearance).

84. Sticky tape strip showing typical cluster of round budding
cells and mycelial elements of Malassezia furfur.
Methylene blue stain.

85.  Treatment for several weeks with local
application of selenium sulphide
suspension or a topical azole
antifungal cream is effective.

86.  Candida organisms are small budding yeasts
that cause various conditions in humans.
 are normal commensals of humans but are
capable of causing infections whenever the
normal defense mechanisms are interrupted.
 For the prevention of cutaneous candida
infection, the most important defense
mechanism is an intact integument.
 Any factor that causes maceration of the
skin predisposes to candida invasion, as does
diabetes mellitus.

87.  The most common form of cutaneous
candidiasis is spread of vaginal infection to
the perineum.
 The vulva and labia are red and intensely
pruritic and there are usually irregular
patches of affected skin, often with much
scaling and spread to adjacent areas.

88. Candidiasis of the perinium. Large areas of denuded skin with
rather well-defined edges and some scaling. Satelite lesions are
visible beyond the edges. This is often associated with candidiasis.

89.  In infants, the wearing of wet nappies
(diapers) causes maceration of the skin:
candida infection produceas a similar
appearance termed napkin (diaper) rash (Fig
11.99). The perianal skin is another site (Fig
11.100) and candidal intertrigo is often seen
in moist sites where skin surfaces are
adjacent, as under the breasts or in the groin.

90. Candida napkin rash. Inflammation affecting the napkin
areas, including the scrotum with prominent satellite
pustules.

91. Perineal candidiasis. A common
distribution spreading from the
perianal area along the perineum.

92.  Candida is a common cause of paronychia.
The acute phase of inflammation is followed
by discolouration, ridging and thickening of
the nail.
 Paronychia are more common in those whose
hands are frequently immersed in water and,
as for many of the other manifestations of
cutaneous candidiasis, in diabetic patients.

93. Candida paroncyhia. Ridged nails with indolent
inflammatory tissue lateral to the nails.

94. Generalized acute cutaneous candidiasis. Rounded, slightly raised
erythematous patches of various size developing as a generalized
eruption following a napkin (diaper) rash.

95.  All the above mild or moderate forms of
cutaneous candidiasis are treatable
topically with nystatin or imidazoles such
as clotrimazole or miconazole.

96.  Chronic mucocutaneous candidiasis is a
persistent infection of the mucous
membranes, skin, hair and nails associated
with a number of immune defects, mainly of
T-cell function.
 Some patients also have associated
endocrine disorders, especially
hyperparathyroidism or Addison's disease.

97.  The clinical illness usually begins in
childhood with oral candidiasis but
subsequent syndromes vary greatly from
mild but chronic infections,
 for example, candidal paronychia and
angular stomatitis, to severe disfiguring
granulomatous lesions.

98. Chronic mucocutaneous candidiasis. Chronic angular
stomatitis and onychomycosis due to candida in a 12-year
old child with impaired T-cell response to candida antigens.

99. Chronic disfiguring candida
infection of the scalp in a
child.

100.  Treatment with a variety of
immunostimulants has been of limited
success and the treatment of choice now
appears to be long term ketoconazole or
fluconazole.

101.  Disseminated candidiasis, which tends to
occur in the immunocompromised or those
with candida endocarditis, can be
associated with cutaneous lesions.
 These are typically pink to red
macronodules, up to 1cm in diameter, and
can be single or multiple.

102. Disseminated
candidiasis. The typical
skin lesions are pinkish-
red nodules, here seen
on the ankle of a patient
with acute leukemia.
Candida can be
visualized in punch
biopsies.

103.  This chronic infection is caused by
Sporothrix schenckii
 a widely distributed saprophytic fungus.
 Most cases of infection in man are the
result of minor trauma and inoculation of
the organism through the skin.

104. Histological section showing small yeast-like organism
of Sporothrix schenki. Gomori-methenamine silver stain.

105.  At the site of entry (often on the hands) a
small, painless, pink or purple, verrucous,
nodular or ulcerative cutaneous lesion develops
anything from 1 week to several months later.
 In 75% of cases the chronic primary inoculation
lesion is associated with multiple painless
nodules distributed along the lymphatic vessels
draining the primary lesion.

106. Lympocutaneous sporotrichosis. A large verrucous and
ulcerative lesion on the dorsal surface of the fourth finger. A
single satellite lesion is present on the dorsum of the hand,
probably along a lymphatic vessel draining the primary lesion.

107. A chronic crusting primary lesion involving the nail bed
of the third finger, with multiple painless nodules along
the lymphatic channels draining the lesions.

108.  Sometimes these lesions ulcerate. No
constitutional symptoms develop unless
secondary bacterial infection develops. The
organism is readily cultured from purulent
exudate or biopsy material placed on
Sabouraud's medium, but is rarely seen on
direct examination of the tissue. The
histopathological response to sporotrichosis
involves granulomas and microabscesses.

109.  Pseudoepitheliomatous hyperplasia may be
present. Lymphocutaneous and cutaneous
sporotrichosis usually responds to oral therapy with
potassium iodide (3-4ml every 8 hours until the skin
lesions disappear), but occasional cases require
systemic treatment with amphotericin B, especially
when deeper tissues are involved. Preliminary
reports suggest that itraconazole may also be
effective. Relapse is very rare.

110.  are a group of fungal infections of the skin
caused by organisms (the dermatophytes)
which invade only the superficial stratum
corneum of the skin and other keratinized
tissues such as hair and nails.

111. Tinea corporis (ringworm of the body)
- is most often seen in children and is caused by
various species of the genera Trichophyton,
Epidermophyton and Microsporum.
- Some of these species, such as T. rubrum, are
exclusively human pathogens, transmitted
through infected skin squames, and some, such as
M. canis, are transmitted to humans from animals
(in this case cats or dogs).

112. Spiral hyphae of Trichophyton mentagrophytes.

113.  The lesions are often found on the trunk or
legs and usually have a prominent edge
with a central scaly area - tinea circinata -
although granulomata involving deeper
layers may also be seen.

114. Typical lesions of tinea
circinata, with margins more
inflamed than the centres.

115. Tinea corporis. Annular erythematous lesion due to
Microsporum species showing an advancing active
periphery and scaling in the central area.

116. Inflammatory infection due
to the zoophilic fungus T.
mentagrophytes in a
farmer.

117. Tinea barbae (barber's itch)
 is a chronic infection of the beard area of the face and
neck, with both superficial lesions and deeper lesions
involving the hair follicles.
Tinea pedis (athlete's foot)
is a chronic fungus infection of the feet, involving
particularly the toes, toe webs, and soles usually
caused by T. rubrum or E. floccosum.
 The intertriginous areas of the toe web usually show
the most severe involvement with cracking and
severe maceration of the skin. The major symptom is
itching.

118. Tinea barbae (barber’s itch). Dermatophytic infection of
beard area.

119. Tinea pedis (athelete’s foot). Scaling erythematous
pruritic patches in the characteristics location involving
the toes, toe webs and sole of the foot.

120.  Treatment involves careful drying of the feet
after bathing, followed by application of
various topical antifungal agents.
 The same two dermatophytes are the usual
cause of infection in the groin (tinea cruris)
and similar symptoms occur.
 Unlike candidal groin infection,
dermatophytes tend to spare the scrotum.
Dermatophytes can be diagnosed by the
examination of KOH preparations of skin
scrapings.

121. Tinea cruris. Scaling rash over the thighs. Unlike
candida infection the scrotum is usually spared.

122. The laboratory diagnosis can be made by softening
skin scrapings in 10-20% KOH and examining under
the microscope for fungal hyphae.

123.  Most cases of dermatophyte infections
respond readily to topical agents, either
keratolytic agents such as salicylic and
benzoic acid compound (Whitfield's ointment)
or antifungal agents such as the imidazoles,
given for 2-4 weeks.
 Very occasionally, chronic dermatophyte
infections can cause scarring with keloid
formation.

124. Keloid scarring on the thigh as a
result of chronic tinea corporis
in a South American man.

125. Tinea capitis (ringworm of the scalp)
 is chiefly a disease of children and is also caused
by Trichophyton or Microsporum species.
 It causes scaly erythematous scalp lesions with
loss of hair.
 Different species may produce arthrospores within
the hair shaft (endothrix infections) or on the
outside of the hair shaft (ectothrix infections).
There are variable degrees of inflammation
present: cases acquired from cattle and due to T.
verrucosum often are very inflammatory and form
large pustular lesions called kerions.

126. Tinea capitis. Scaling of
the scalp and hair loss due
to infection with
Microsporum canis.

127. Infected hair shaft showing many arthrospores of
Trichophyton tonsurans.

128. Keroin. In some forms of tinea capitis there is severe
inflammation causing a pustular lesion with an
exudative crust.

129. Infection due to T. schoenleinii causes a
condition called favus.
 Here the hairs are infected but not
structurally damaged or shed until late into
the disease.
 This produces a marked inflammatory crust
with matted hairs over the scalp.

130. Favus. An inflammatory response develops around
individual hairs and the scalp appears to be covered
with a thick crust. This is caused by T. schoenleinii.

131.  Diagnosis of Microsporum infection may be suspected
by demonstration of green fluorescent hairs under
Wood's light, but hairs infected by T. tonsurans do not
exhibit fluorescence.
 Fungus can be detected by microscopic examination
of the hair (preferably a broken stub) in KOH
preparations.
 Scalp infections do not respond to topical therapy and
are usually treated with 6-12 weeks of oral
griseofulvin.

132. Onychomycosis (tinea unguium)
 is a chronic fungal infection of the nails,
usually associated with infection of the
adjacent skin due to T. rubrum (Fig 11.95).
 There is thickening of the nail which
becomes white, brown or yellow.

133.  The presence of heaped-up debris
containing the organism under the nail
differentiates onychomycosis due to
dermatophytes from that due to chronic
candida infection of the nails (Fig 11.96).

134. Deformity and ridging of nails due to candida infection.

135. Onychomycosis. Chronic infection with Trichophyton
rubrum in a diabetic patient, showing brittle,
discoloured, nail with separation of nail bed by fungus-
containing debris.

136.  Treatment involves the removal of as much
of the infected nail as possible and long
term (6-12 months) systemic therapy with
griseofulvin, but the infection is extremely
difficult to eradicate and more than 50%
relapse.