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1. Integument Forms the boundary between the human and

the environment
Formed by the skin, hair, nails, and sweat and
oil glands

2. Epidermis 25 cells thick, dead cells that have igrated from

the deepest layer

3. Keratin gives cell the ability to withstand damage and

water penetration

4. Stratum basale several layers below the stratum corneum, at-

tached to the dermis, source of cells that make
up the dermis

5. Dermis -composed of connective tissues instead of

epithelium

-rich matrix of fibroblast cells, collagen,

maxrophages and mast cells

6. sebaceious glands oil glands

7. Defense of the skin antimicrobial peptides, sebum, sweat, ly-

zoenyzme

8. Antimicrobial peptides positively charged chemicals that act by dis-

rupting the negatively charged membranes of
bacteria

9. Sebum low ph makes the skin inhospitable to microor-

ganism
- oily due to its high concentration of lipids
-Lipids serve as nutrient for normal microbiota

10. Sweat Inhibitory to microorganisms due to low pH and

high salt
concentration

11. Lyzozyme
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-enzyme found in sweat, tears, and saliva
- Specifically breaks down peptidoglycan
found in the cell
walls of bacteria

12. Skin normal biota Streptococcus, Staphylococcus, Corynebac-

terium, Propionibacterium, Pseudomonas,
Lactobacillus; yeasts such as Candida

13. MRSA skin and soft tissue methicillin-resistant staphylococcus aureus

infection

14. MRSA skin and soft tissue • Coagulase is a diagnostic species

infection pathogenesis and characteristic
virulence factor
• Also produce hyaluronidase,
staphylokinase, DNase, and lipase

15. Culture and/or Diagnosis PCR

(MRSA) Isolation on blood agar or mannitol salt agar
Catalase distinguishes S. aureus from other
staphylococcal species.
Coagulase test

16. Prevention and treatment • Prevention is only possible with good hygiene
(mrsa)
• Treatment through incision of lesion and pus
drainage

• Antimicrobial treatment should include more

than one
antibiotic (vancomycin is recommended in
U.S.)

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17. Maculopapular Rash Dis- Skin eruptions caused by a variety of microbes
eases • Flat to slightly raised colored bumps

18. Measles Also known as rubeola

19. Measles signs and symp- • Sore throat

toms • Dry cough
• Headache
• Conjunctivitis
• Lymphadenitis
• Fever
• Oral lesions called Koplik's spots
• Red, maculopapular exanthem
that erupts on the head and
progresses to the trunk and
extremities

20. Measles Sequelae and •Laryngitis

Complications •Bronchopneumonia
•Secondary bacterial infections such as ear
and sinus infections
•Pneumonia
•Encephalitis resulting in CNS changes rang-
ing from disorientation to coma
•Can result in permanent brain damage or
epilepsy

21. Measles: Subacute Scle- SSPE

rosing Panencephalitis •Appearance years after initial measles infec-
tion
•Direct viral invasion of neural tissue

22.
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Measles pathogenesis and Course of infection:
virulence factors -Virus implants on respiratory mucosa and in-
fects the tracheal and bronchial cells.
-It travels to the lymphatic system where it
multiplies and enters the bloodstream.
-Viremia carries the virus to the skin and vari-
ous organs.
Syncytia:
-Giant cells with many nuclei
-Result of fusion of adjacent cell membranes
caused by the virus

23. Measles Transmission and One of the most contagious infectious dis-
Epidemiology eases
transmitted by respiratory droplets & humans
are the only reservoir

24. Measles culture and diag- • Clinical presentation

nosis • ELISA to test for IgM to measles antigen

25. Measles Prevention • MMR vaccine contains live, attenuated

measles virus that confers
protection for up to 20 years
• Recommended for healthy children aged 12
to 15 months, with a
booster before the child enters school

26. Measles treatment • Reducing fever

• Suppressing cough
• Replacing lost fluid
• Remedies to relieve neurological and respira-
tory symptoms and to
sustain nutrient, electrolyte, and fluid levels
• Vitamin A supplements are recommended

27. Rubella • Also known as German measles, its name is

derived from Latin for "little red"

• Relatively minor rash disease with few com-

plications
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• Serious damage can occur to the fetus in

utero

• Women of childbearing years must be sure to

have been vaccinated before
they plan to conceive

28. Postnatal rubella -Rash of pink macules and papules

-Appears first on the face and progresses
down the trunk and toward the extremities
-Advances and resolves within 3 days
-Milder than measles rash
-Adult rubella characterized by joint inflamma-
tion and pain rather than rash

29. Congenital Rubella • Most common defect is deafness, but cardiac

abnormalities, ocular lesions, deafness, and
mental and physical retardation can occur in
varying combinations

• Other sequelae include anemia, hepatitis,

pneumonia, carditis, and bone infection

30. Teratogenic Causes harm to the detus

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31. Rubella causative agent Rubivirus from the family Togaviridae

32. Rubella Transmission and -Worldwide distribution

Epidemiology -Initiated through contact with respiratory se-
cretions and occasionally urine
-Virus is shed through prodromal phase and
up to a week after the rash appears
-Congenitally infected infants are contagious
for a much longer time
-Virus is only moderately communicable; close
living conditions are required for its spread
-Declared eliminated from the U.S. in 2004,
and from the Americas in 2015

33. rubella culture and diagno- -Because it mimics other diseases, rubella
sis should not be diagnosed on clinical grounds
alone.

-IgM antibody detected through ELISA or latex

agglutination

34. rubella prevention and Attenuated rubella vaccine is given in MMR at

treatment 12 - 15 months and a booster at 4 - 6 years.

Postnatal rubella is usually benign and re-

quires only
symptomatic treatment.

No specific treatment is available for congeni-

tal rubella.

35. Fifth disease also known as erythema infectiosum

- cause rashes in children: scarlet fever,

measles, rubella, and another rash thought to
be distinct

36. Fifth disease signs and -Mild disease that results in a "slapped cheek"
symptoms appearance that begins on the face
-Within 2 days, rash spreads on the body but
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is most prominent on arms, legs, and trunk.
-Rash may occur for several weeks and may be
brought on by any activity that increases body
heat.

37. Fifth disease causative Parvovirus B19

agent

38. Fifth Disease Diagnosis -Clinical presentation

-Rule out rubella by testing for IgM antibodies

39. fifth disease transmission respiratory secretions, blood, blood products

very contagious

40. fifth disease prevention • No vaccine and no treatment

and treatment
• Usually mild disease

41. Roseola Common disease in young children and

babies; sometimes known as "sixth disease"

42. Roseola signs and symp- -Can result in a maculopapular rash, but up to
toms 70% of cases proceed without the rash stage

-Usually accompanied by a high fever (41°C or

105°F) that comes on quickly and lasts up to 3
days

-Seizures may occur during this period.

-On the fourth day, the fever disappears and

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the rash appears, first on chest and trunk, then
less prominently on the face and limbs.

43. Roseola causative agent Human herpesvirus 6 (HHV-6)

44. Roseola Transmission and It is thought that 100% of the U.S. population
Epidemiology is infected with the virus by adulthood

45. Roseola prevention and No treatment, no vaccine

treatment

46. Impetigo Superficial bacterial infection that causes the

skin to flake or peel

47. Impetigo causative agent Staphylococcus aureus and Streptococcus

pyogenes or can be both

(S. pyogenes begins but S. aureus takes over

and prroduces a bacteriocin)

48. Impetigo signs and symp- -Lesion: peeling skin, crusty and flaky scabs,
toms or honey-colored crusts
-Lesions found most around the mouth, face,
and extremities

49. Impetigo caused by Exfoliative toxins A and B cause characteristic

Staphylococcus aureus blistering and facilitate the spread of the bac-
terium.

50. Impetigo caused by Strep- Gram-positive coccus, beta-hemolytic on

tococcus pyogenes blood agar

Causes streptococcus pharyngitis, scarlet

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fever, pneumonia, puerperal fever, necrotizing
fasciitis, serious bloodstream infections, and
poststreptococcal conditions

51. Impetigo caused by Strep- • Possesses a huge arsenal of enzymes and

tococcus pyogenes patho- toxins
genesis and virulence fac-
tor • Rarely, impetigo caused by S. pyogenes can
be followed
by acute
poststreptococcal glomerulonephritis

• Strains that cause impetigo never cause

rheumatic fever.

• S. pyogenes is more often the cause of im-

petigo in
newborns; S. aureus is more often the cause
of impetigo
in older children; both can cause infection in
either age
group

52. Cellulitis Caused by a fast-spreading infection in the

dermis and in the
subcutaneous tissues

53. Cellulitis signs and symp- Pain, tenderness, swelling, and warmth
toms
Fever and swelling of the lymph nodes in the
area may also occur

54. Lymphangitis
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red lines leading away from the area are vis-
ible, the result of microbes and inflammatory
products being carried by the lymphatic sys-
tem

55. Bacteremia bacteria in the blood

56. Cellulitis causative agents Streptococcus pyogenes and

Healthy Individuals occasionally Staphylococcus aureus

57. Cellulitis causative agents almost any bacterium

immunocompromised indi- and some fungi
viduals

58. Cellulitis causative agents group B streptococci

Infants

59. Cellulitis Transmission and •Generally follows introduction of bacteria or

Epidemiology fungi into the dermis:
•Trauma
•Subtle means; no obvious break in the skin

60. Cellulitis culture/diagnosis Diagnosis through clinical signs and symp-

toms

61. cellulitis prevention and -Mild cellulitis responds well to oral antibiotics
treatment effective against S. aureus and S. pyogenes
-More involved infections and infections in im-
munocompromised patients require IV antibi-
otics.
-Surgical debridement is required with exten-
sive tissue damage.

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62. Staphylococcal Scalded Dermolytic condition caused by Staphylococ-
Skin Syndrome cus aureus

63. SSSS signs and symptoms Bullous lesions:

-Split occurs in the epidermal tissue layers just
above the stratum basale.
-Appear first around the umbilical area in
neonates or in the axilla
Widespread desquamation of the skin follows.

64. SSSS transmission and -Transmission may occur when caregivers car-
epidemiology ry the bacterium from one baby to another.
-Adults in the nursery can directly transfer S.
aureus.
-30% of adults are asymptomatic carriers, har-
boring the organism in the nasopharynx, axilla,
perineum, and vagina

65. SSSS prevention and treat- • Eliminate carriers in contact with neonates
ment • Immediate treatment with systemic antibi-
otics

66. Chickenpox very

common and mostly
benign

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67. Pox individual lesions that contain fluid

68. Chickenpox signs and Fever and abundant rash appear after an incu-
symptoms bation period of 10 to 20 days
rash begins on the scalp, face, and
trunk, and radiates in sparse crops to
the extremities
Skin lesions progress quickly from macules
and
papules to itchy vesicles filled with a clear fluid
encrust and drop off after several days
heal completely or may leave a small scar
lesions can number from a few to hundreds;
more abundant in adolescents and adults

69. lesion distribution Centripetal

70. shingles (herpes zoster) Characteristic asymmetrical distribution on the

sign and symptoms skin of the
trunk or head

71. Chickenpox and shingles Human herpesvirus 3 (HHV-3) AKA varicella,

causative agent an enveloped
DNA virus

72. Chickenpox and shingles HHV-3 enters the respiratory tract, attaches to
pathogenesis and viru- respiratory
lence factors mucosa, and invades and enters the blood-
stream

• Viremia disseminates the virus to the skin,

where it causes
adjacent cells to fuse and lyse, causing char-
acteristic lesions

• The virus then enters sensory nerves and

dorsal root ganglia

• Ability to remain latent in nerve ganglia is an

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important virulence
factor

73. postherpetic neuralgia inflammation of the ganglia and nerve path-

ways that causes pain and tenderness and can
last for several months

74. Chickenpox and shingles • Humans are the only natural host for HHV-3
transmission and epidemi-
ology • Harbored in the respiratory tract:
• Communicable from both respiratory droplets
and fluid from active
lesions
• People can acquire chickenpox from expo-
sure to fluid of shingles
lesions
• Infected persons are infectious a day or two
prior to the
development of the rash
• Chickenpox is so contagious that if you are
exposed to it,
you will almost certainly get it

75. chickenpox and shingles -Live attenuated vaccine licensed in 2006

prevention -Zostavax approved by the FDA in 2006 to
prevent shingles

76. chickenpox and shingles Uncomplicated varicella is self-limiting and re-

treatment quires no therapy aside from alleviation of
discomfort. Secondary bacterial infections are
treated with topical or systemic antibiotics. Oral
acyclovir should be administered to those con-
sidered at risk for complications.
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do not administer aspirin as this may lead to

reye's syndrome

77. Smallpox A highly contagious viral disease character-

ized by fever, weakness, and skin eruption with
pustules that form scabs; responsible for killing
Native Americans.

78. Variola Major highly virulent, caused toxemia, shock, and

intravascular coagulation

79. Signs and symptoms of • Prodrome period of high fever and malaise
smallpox • Rash emerges, first in the mouth
• Severe abdominal and back pain
• Rash spreads throughout the body within 24
hours

80. Smallpox causative agent variola virus:

- orthopoxvirus
- enveloped DNA virus

81. Smallpox prevention and postexposure prophylaxis

treatment
-Tecovirimat and cidofovir

82. Leishmaniasis localized infection of the capillaries of the skin

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83. Leishmaniasis causative • Cutaneous leishmaniasis: L. tropica

agent
• Mucocutaneous leishmaniasis: L.
brasiliensis

84. Leishmaniasis transmis- sand flies

sion

85. Leishmaniasis culture and microscopic visualization

diagnosis

86. Cutaneous anthrax Papule that becomes necrotic and later rup-
tures to form a painless, black eschar.

87. Cutaneous anthrax Bacillus anthracis

causative agent

88. Cutaneous anthrax culture -Culture on blood agar

and diagnosis -Serology
-PCR performed by CDC

89. Cutaneous and Superficial ringworm

Mycoses

90. Dermatophytes
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A type of fungi that causes skin, hair, and nail
infections.

91. Ringworm of the scalp This mycosis results from the fungal invasion
(Tinea Capitis) of the scalp and the hair of the head, eyebrows,
and eyelashes.

92. Ringworm of beard (tinea This tinea, also called barber's itch, affects the
barbae) chin and beard of adult males. Although once
a common after effect of unhygienic barbering,
it is now contracted mainly from animals.

93. Ringworm of body (tinea This extremely prevalent infection of humans

corporis) can appear nearly anywhere on the body's
glabrous (smooth and bare) skin.

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94. ringworm of the groin Sometimes known as jock itch, crural ring-
(Tinea crusis) worm occurs mainly in
males on the groin, perianal skin, scrotum,
and, occasionally, the
penis. The fungus thrives under conditions of
moisture and humidity
created by sweating.

95. Ringworm of the Foot Tinea pedis has more colorful names as well,
(Tinea Pedis) including athlete's foot and jungle rot. Infec-
tions begin with blisters between the toes that
burst, crust over, and can spread to the rest of
the foot and nails.

96. ringworm of the nail (Tinea Fingernails and toenails, being masses of ker-
Ungulum) atin, are often sites for
persistent fungus colonization. The first symp-
toms are usually
superficial white patches in the nail bed. A
more invasive form
causes thickening, distortion, and darkening of
the nail.

97. Ringworm causative agent Trichophyton, Microsporum, Epidermophyton

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98. ringworm pathogenesis Dermatophytes have the ability to digest ker-
and virulence factors atin
Fungi do not invade deeper epidermal layers.

99. Supeficial Mycoses Involve the outer epidermal surface:

• Innocuous infections with cosmetic rather

than disease-causing effects

100. Superficial Mycoses Malassezia

causative agent

101. Conjunctivitis sign and • Most bacterial infections produce a milky dis-
symptoms charge
• Viral infections produce a clear, watery exu-
date

• Patients often wake up in the morning with

the eye "glued"
shut by secretions that have accumulated and
solidified
overnight

• Some conjunctivitis cases are caused by an

allergic
response and a clear, watery fluid is formed

• Common name is pinkeye

102. neonatal eye infections - neisseria gonorrhoeae

caused by - chlamydia trachomatis
- herpes simplex

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103. Conjunctivitis causative Staphylococcus epidermidis, Streptococcus
agent pyogenes, Streptococcus
pneumoniae, Haemophilus influenzae, or
Moraxella

• N. gonorrhoeae and C. trachomatis conjunc-

tivitis result from
autoinoculation from a genital infection or sex-
ual activity

104. Conjunctivitis prevention Ciprofloxacin is a common choice because it

and treatment covers all possible
bacterial infections

105. Keratitis Invasion of deeper eye tissues

• Can lead to complete corneal destruction

106. Keratitis causative agent Miscellaneous bacteria

Herpes simplex virus

107. Keratitis culture and diag- -Clinical diagnosis

nosis -Viral culture or PCR, if needed

108. keratitis treatment Trifluridine or acyclovir or both

109. Acanthamoeba keratitis Amoeba causes keratitis in people who

wear contact lenses:
• Free-living amoeba live in tap water,
freshwater lakes, etc.
• Associated with less-than-rigorous contact
lens hygiene or previous trauma to the eye

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