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Dermatology OAU > VIRAL SKIN INFECTIONS > Flashcards

VIRAL SKIN INFECTIONS Flashcards

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1
Q

Viruses are facultative intracellular micro org (T/F)?

A

False

They are obligate intracellular!

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2
Q

What are the structural components of a virion particle?

A

central core of nucleic acid; DNA or RNA,ss or ds
A protein coat (capsid)
Envelope (in some viruses)

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3
Q

What are the two main groups of viruses?

A

DNA viruses

RNA viruses

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4
Q

Viral infections causing skin pathology which can either be ?

A

exanthematic

non-exanthematic (enanthematic)

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5
Q

What does an exanthema mean?

A

Involving only skin eruptions accompanied by systemic illnesses such as malaise and fever

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6
Q

Outline 3 examples of exanthematic viral infections?

A

Chicken pox
Roseola infantum
Ptyriasis rosea

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7
Q

What does an enanthema mean?

A

involves mucosal eruptions especially in association with skin.

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8
Q

Outline 3 examples of enanthematous viral infections?

A

herpes
warts
Kaposi sarcoma

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9
Q

Outline the major groups of virus families?

A 
Herpesviridae
Human papilloma virus
Paramyxoviridae 
Enteroviruses 
Retroviruses
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10
Q

Latent, lytic and recurrent infections are typical of the herpes viruses (T/F)?

A

True

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11
Q

Herpes viruses refers to a large group of RNA viruses capable of infecting animals and humans with about 25 known to infect humans (T/F)?

A

False
They are DNA viruses
Only about 8 are known to infect humans out of 100

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12
Q

Itemize the 3 subfamilies of the herpes viruses family?

A

Alphahepesvirinae
Betaherpesvirinae
Gammaherpesvirinae

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13
Q

Outline the 9 herpes viruses known to infect man?

A 
HSV-1------HHV1
HSV-2------ HHV2
VZV----------HHV-3
EBV ---------HHV-4
CMV--------HHV-5
HHV-6A and HHV-6B
HHV-7
Kaposi's sarcoma ------ HHV-8
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14
Q

What viruses make up the alphaherpesvirinae?

A

herpes simplex virus 1 and 2

varicella-zoster virus

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15
Q

Itemize 4 essential features of the alphaherpesvirinae

A

extremely short reproductive cycle (hours) prompt destruction of the host cell
they have a wide host range
establish latent infection in sensory nerve ganglia.

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16
Q

Itemize 4 essential features of the betaherpesvirinae

A

They have a restricted host range
Their reproductive life cycle is long (days) with infection progressing slowly in cell culture systems.
their ability to form enlarged cells
These viruses can establish latent infection in secretory glands, cells of the reticuloendothelial system, and the kidneys.

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17
Q

What viruses make up the betaherpesvirinae ?

A

human cytomegalovirus

HHV-6 and HHV-7

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18
Q

Itemize 4 essential features of the gammaherpesvirinae

A

They infect and become latent in lymphoid cells. their associations with cancer and cellular proliferation

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19
Q

What viruses make up the gammaherpesvirinae?

A

EBV (HHV-4)

HHV -8

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20
Q

What are the 2 main types of herpes simplex virus?

A

HSV-1 (oro-facial)

HSV-2 (genital)

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21
Q

How is HSV transmitted?

A

DIRECT CONTACT of a susceptible person with droplets from infected secretions

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22
Q

What facilitates transmission of HSV?

A

Trauma?

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23
Q

What is the usual route of spread of HSV-1?

A

spread by respiratory droplets or by direct contact with infected saliva

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24
Q

What is the usual route of transmission of HSV-2?

A

usually transmitted by genital routes; sexual route, virus shed on toilet seats

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25
Q

What category of people are at risk of HSV-1 infection?

A

nail biters. CHILDREN!
thumb suckers
nipples of breastfeeding mother
dentists

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26
Q

Infection with HSV-1 may confer immunity against HSV-2 (T/F)?

A

False

Infection with either confers no immunity against the other.

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27
Q

Oropharyngeal HSV-1 infections result in latent infections in the sacral ganglia (T/F)?

A

False

Trigeminal ganglia!

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28
Q

Genital HSV-2 infections lead to latently infected trigeminal ganglia (T/F)?

A

False

Sacral ganglia

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29
Q

Lesions seen in primary HSV infections are usually less numerous than recurrent infections (T/F)?

A

False

The are more

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30
Q

Systemic diseases commonly accompany primary HSV infections (T/F)?

A

False

Only rarely does systemic disease develop.

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31
Q

Primary HSV infections are usually subclinical with most being asymptomatic (T/F)?

A

True!

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32
Q

In what group of patients would widespread organ involvement occur in primary HSV infection?

A

Immunocompromised patients

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33
Q

reactivations will still occur spontaneously in spite of HSV-specific humoral and cellular immunity in the host. (T/F)

A

True!

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34
Q

Most recurrences are very symptomatic, reflected by viral shedding in secretions (T/F)?

A

False

Many recurrences are asymptomatic, reflected only by viral shedding in secretions, thanks at least to our immune system.

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35
Q

Recurrences occur without triggers in HSV-1 infections (T/F)?

A

False

In HSV-2

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36
Q

HSV recurrent infections are less extensive and less severe in Immunocompromised patients (T/F)?

A

False.

In immunocompetent ptx

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37
Q

Itemize 5 trigger factors of HSV-1 infection?

A 
febrile illnesses
fatigue
emotional stress
premenstrually
exposure to sunlight
dental surgery
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38
Q

HSV Recurrence is often preceeded by what?

A

A prodrome of itching and burning!

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39
Q

Outline the natural history of recurrence of HSV infections?

A

Recurrence is often preceeded by a prodrome of itching and burning
Within 24h, red papules appear at the site progress to blisters over 24h
form erosions over the next 24h – 36h
and heal in another 2 to 3 days

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40
Q

What is the total duration of a typical outbreak of genital herpes?

A

7 days

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41
Q

How would you differentiate recurrent from primary genital herpes infection?

A

lesions usually occur in grouped blisters.
Vesicles are smaller
unlike initial infection they tend to occur in the same anatomic region, but not always on identical sites.

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42
Q

In what situation would recurrent herpetic infections be increased in incidence and severity, running a prolonged and atypical course ?

A

Situation of reduced immunity!

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43
Q

What term is used to describe the acquisition of HSV at a new site in an individual previously infected ?

A

“non-primary, first episode” infection

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44
Q

Orolabial herpes typically lasts for about 6days (T/F)?

A

False

Lasts for abt 2 weeks

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45
Q

What is the most striking and common lesion seen in orolabial herpes?

A

Gingivitis (swollen, tender gums)

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46
Q

Primary infections of orolabial herpes in adults commonly cause what?

A

pharyngitis
tonsillitis
Localized lymphadenopathy

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47
Q

Recurrent disease in orolabial herpes may be precipitated by what?

A

respiratory tract infections (cold sores) ultraviolet radiation
menstruation
stress

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48
Q

The cluster of vesicles seen In orolabial herpes is most commonly localized where?

A

at the border of the lip

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49
Q

Intense pain associated with orolabial herpes is usually constant throughout the illness (T/F)?

A

False

occurs at the outset but fades over 4–5 days

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50
Q

Lesions seen in orolabial herpes usually heal with minimal scarring (T/F)?

A

False

Lesions heal without scarring!

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51
Q

Outline the natural history of orolabial herpes illness?

A

Lesions progress through the pustular and crusting stages, and healing without scarring is usually complete in 8–10 days

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52
Q

Mention 4 complications of orolabial herpes?

A 
Maurice syndrome
Recurrent lymphocytic meningitis
Encephalitis
Keratoconjunctivitis
Recurrent postherpetic erythema multiforme (HLA DQw3)
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53
Q

Primary genital herpes is usually mild lasting for any 1week (T/F)?

A

False
It can be severe
Lasting about 3 weeks

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54
Q

How would you describe the characteristic lesions seen in primary genital herpes infection?

A

VESICULOULCERATIVE lesions of the penis of the male or of the cervix, vulva, vagina, and perineum of the female.

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55
Q

Lesions in primary genital herpes may be painless (T/F)?

A

False

It’s painful!

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56
Q

Itemize 4 associated symptoms seen in primary genital herpes infection?

A

fever
malaise
dysuria
inguinal lymphadenopathy

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57
Q

Viral excretion in primary genital herpes persists for how long?

A

about 3 weeks

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58
Q

Recurrences of genital herpetic infections are less common but tend to be severe when they occur (T/F)?

A

False

Recurrences of genital herpetic infections are common and tend to be mild.

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59
Q

How would you differentiate recurrent from primary genital herpes infection clinically?

A

A limited number of vesicles appear and heal in about 10 days.

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60
Q

symptomatic recurrence of genital herpes infection usually indicate a person shedding virus can transmit the infection to sexual partners. (T/F)?

A

False
Whether a recurrence is symptomatic or asymptomatic, a person shedding virus can transmit the infection to sexual partners.

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61
Q

Recurrent genital herpes lesions are always painful (T/F)?

A

False

Some recurrences are asymptomatic!

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62
Q

How would you differentiate genital herpeticum lesion from the chance seen in syphyllis clinically?

A

Erosions or ulcerations from genital herpes are usually VERY TENDER and NOT INDURATED as opposed to the chancre of primary syphilis

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63
Q

Recurrent genital herpes usually heals without scarring unless the lesion is secondarily infected (T/F)?

A

True

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64
Q

The favored site for recurrent genital herpes particularly in women is? and why is this so?

A

The buttocks

may be due to post-coital inoculation!

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65
Q

What is the most common non-specific test used in the diagnosis of HSV infection? and what is seen?

A

TZANCK SMEAR

Multinucleated giant cells

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66
Q

Itemize the specific diagnostic methods used in suspected HSV infection?

A

Viral culture of blister fluid
Direct fluorescent antibody
Polymerase chain reaction
Skin biopsy; viropathic changes

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67
Q

What are the treatment options for HSV infection?

A

Recurrent herpetic lesion is self-limiting and dries up in about a week if uncomplicated by bacterial infection

LIPS
–zinc oxide ointment and castor oil (soothes and protects from sunlight)
– 5% IDOXURIDINE in dimethyl sulphoxide should be applied to affected area 2hourly for 2 days.
– 0.1% IDOXURIDINE in water solution is useful in treatment of the eye.
TOPICAL ANTISEPTIC or ANTIBIOTIC
GENTAMYCIN or OXYTETRACYCLINE ointment 3 times daily for bacterial superinfection.

GENITAL HERPES
BETADINE or POTASSIUM PERMANGANATE solution sit baths 3 times daily.
ZINC OXIDE and CASTOR OIL to soothe, or SULPHUR 5% in zinc oxide.
Alternatively BETADINE ointment or OXYTETRACYCLINE ointment 3 times daily.

SEVERE INFECTIONS or INFECTIONS in IMMUNODEFICIENT patients
if available give ACYCLOVIR 200-400 mg
5 times daily for 5-10 days.

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68
Q

Zoster is a mild, highly contagious disease, chiefly of children (T/F)?

A

False

Varicella (chickenpox)

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69
Q

Varicella is a sporadic, incapacitating disease of children resulting from the reactivation of the residual latent virus in a partially immune person. (T/F)?

A

False
Zoster (shingles)
It’s seen in adults not children

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70
Q

Varicella is usually mild in adults and the Immunocompromised (T/F)?

A

False

It’s more severe!

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71
Q

Both Varicella and zoster are caused by the same organism (T/F)?

A

True

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72
Q

How would you differentiate Varicella from zoster?

A

VARICELLA is the acute disease that follows primary contact with the virus
whereas ZOSTER is the response of the partially immune host to reactivation of varicella virus present in latent form in neurons in sensory ganglia

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73
Q

Varicella has a worldwide distribution as opposed to shingles (T/F)?

A

False

They both occur worldwide!

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74
Q

A killed vaccine is available for the VZV (T/F)?

A

False

live attenuated vaccine

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75
Q

Varicella is also known as what?

A

Chicken pox

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76
Q

How do you get chicken pox?

A

spread by the respiratory route

direct contact with lesions.

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77
Q

What is the incubation period for Varicella?

A

about 14 days [10-21 days]

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78
Q

Viral replication of HSV occurs first where?

A

at the site of infection.

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79
Q

Viral replication of VZV occurs first where?

A

Regional lymph nodes

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80
Q

replication of VZV in liver,spleen, lungs associated with secondary viremia (T/F)?

A

False

It’s primary viremia

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81
Q

Infection of mononuclear cells by VZV and development of typical rash is associated with primary viremia (T/F)?

A

False

It’s secondary viremia

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82
Q

Skin Lesions in chicken pox are described as what?

A

“teardrop” vesicles on an erythematous base

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83
Q

Outline the natural history of Varicella infection?

A

Slight malaise is followed by the development of papules, which turn rapidly into clear vesicles, (lesions appear in crops and are often itchy) the contents of which soon become pustular.

Over the next few days the lesions crust and then clear, sometimes leaving white depressed scars.

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84
Q

Which area of the body are more and less affected in chicken pox?

A

Lesions are most profuse on the TRUNK and least profuse on the periphery of the LIMBS .

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85
Q

Lifelong immunity usually follows chicken pocks infection (T/F)?

A

True!

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86
Q

Second episodes of chicken pox would indicate what?

A

immunosuppression

another viral infection

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87
Q

Itemize 5 possible complications of Varicella infection?

A

secondary bacterial infection with S.aureus or streptococcal organisms
Pneumonia
Cerebellar ataxia and encephalitis
Reye syndrome (acute hepatitis + encephalopathy due to use of aspirin)
Maternal infection during the first 20weeks may result in congenital malformations or spontaneous abortions.
Neonatal varicella.

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88
Q

What are the contraindications of administering VZV vaccine?

A

patients with immunodeficiencies or blood dyscrasias

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89
Q

What are the treatment options for chicken pox?

A

A live attenuated vaccine is now available, and being more widely used

IN MILD ATTACKS
CALAMINE LOTION topically can be used.

SEVERE ATTACKS and for IMMUNOCOMPROMISED patients
Acyclovir, famciclovir and valaciclovir should be reserved

for the latter, prophylactic aciclovir if given within a day or two of exposure

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90
Q

The skin lesions of zoster are histopathologically distinct from those of varicella (T/F)?

A

False

They are identical

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91
Q

an acute inflammation of the sensory nerves and ganglia is a common finding in chicken pocks (T/F)?

A

False

It’s zoster!

92
Q

What is the single most important risk factor in the development of herpes zoster?

A

waning immunity!

Virus travels down the nerve to the skin and induces vesicle formation.

93
Q

The clinical manifestations of herpes zoster are caused by a newly acquired virus (T/F)?

A

False

It’s due to virus acquired in the past!

94
Q

Describe the natural history of herpes zoster?

A

Attacks usually start with a burning pain, soon followed by erythema and grouped, sometimes bloodfilled, vesicles scattered over a dermatome.
The clear vesicles quickly become purulent, and over the space of a few days burst and crust.

95
Q

Occasions when pain is not followed by the eruption in herpes zoster is known as?

A

zoster sine eruption

96
Q

Keloids is a known complication of zoster scars (T/F)?

A

True

97
Q

Zoster is characteristically bilateral (T/F)?

A

False

It’s unilateral

98
Q

Zoster may affect more than one adjacent dermatome (T/F)?

A

True!

99
Q

patients with zoster cannot transmit the virus to others (T/F)?

A

False

They can transmit the virus to others in whom it will cause chickenpox.

100
Q

The thoracic segments and the ophthalmic division of the trigeminal nerve are often involved disproportionately in zoster (T/F)?

A

True!

101
Q

Persistent herpetic neuralgia is most common in what group of patients?

A

Elderly

102
Q

What are the components of Ramsay hunt syndrome?

A

facial palsy
ear pain
associated vesicles

103
Q

Itemize 5 complications of herpes zoster?

A

SECONDARY BACTERIAL INFECTION
Zoster of the ophthalmic division of the trigeminal nerve can lead to corneal ulcers and scarring. (HUTCHINSON SIGN which indicates involvement of the nasociliary nerve)
PERSISTENT HERPETIC NEURALGIA
MOTOR PALSY (uncommon) but has led to paralysis of ocular muscles, the facial muscles, the diaphragm and the bladder.
DISSEMINATED HERPES ZOSTER
HERPES ZOSTER OTICUS
CNVIII involvement may result in vertigo, dizziness and hearing loss

104
Q

How is herpes zoster diagnosed?

A

TZANCK SMEAR show multinucleated giant cells and a ballooning degeneration of keratinocytes, indicative of a herpes infection.

CULTURE

105
Q

What are the treatment options for herpes zoster?

A

EARLY STAGE of diagnosis of the disease
–It is essential that systemic treatment should start within the first 5 days of an attack!
ACICLOVIR; 800mg every 4hrs for 7-10 days FAMCICLOVIR ; 500mg evry 8hrs for 7 days VALACICLOVIR; 1000mg every 8hrs for7 days

Administration of GABAPENTIN in conjuction with antivirals during the acute phase may protect against POST HERPETIC NEURALGIA

LATE DIAGNOSIS
treatment should be SUPPORTIVE with REST, ANALGESICS and bland applications such as CALAMINE.
Secondary bacterial infection should be treated appropriately.

106
Q

What is the treatment of post HERPETIC neuralgia?

A 
gabapentin
pregabalin
lidocaine patch 5%
opioid analgesics
TCA
107
Q

Roseola infantum is also known as what?

A

Exanthem subitum or 6th Disease

108
Q

What age group are commonly affected by Roseola infantum?

A

infants aged under two years

109
Q

What’s the incubation period for Roseola infantum?

A

10-15 days

110
Q

Outline the natural history of the 6th disease?

A

Begins with Prodromal symptoms: There is fever for a 2 or 3 days which suddenly drops on the fourth accompanied by the rose coloured rash

The Initial rash is A rose pink maculopapular eruption which appears on the neck and trunk,buttocks,sometimes face and extremities

The rash may affect the face and limbs before clearing over one to two days

111
Q

The mucous membrane are rarely spared in Roseola infantum (T/F)?

A

False

They are spared!

112
Q

How is Roseola infantum diagnosed?

A

diagnosed from its clinical features!

113
Q

What is a very important complication of the 6th disease?

A

febrile convulsions.

114
Q

What are the treatment options for exanthema subitum?

A

CONTROL FEVER
Fever can be controlled with wet dressings or tepid water sponge baths, supplemental fluids and antipyretics

HHV-6 is insensitive to current antiviral agents, but in immunocompromised children with severe disease some authorities recommend treatment with GANCICLOVIR

115
Q

an acute, self healing exanthem xterised by oval erythemato-squamous lesions of the trunk and limbs is the correct description for what?

A

Ptyriasis rosea!

116
Q

What viral agents have been implicated in causing Ptyriasis rosea?

A

HHV-6

HHV-7

117
Q

What age groups are commonly affected by Ptyriasis rosea?

A

affects children and young adults[10-35yrs]

118
Q

Second attacks of Ptyriasis rosea are very common after initial resolution (T/F)?

A

False

Second attacks are rare!

119
Q

What body regions are usually spared in Ptyriasis rosea?

A

face
scalp
palms
soles

120
Q

Ptyriasis rosea is a highly contagious infection (T/F)?

A

False

It seems not to be contagious!

121
Q

an oval pink or red plaque 2-5cm in diameter, with a finely scaling borders which marks the beginning of Ptyriasis rosea infection is called what?

A

HERALD or MOTHER PATCH

122
Q

Describe the natural history of Ptyriasis rosea infection?

A

Typical Ptyriasis rosea begins with a solitary patch called herald patch or mother patch.

It enlarges progressively to abt >= 3cm

Soon after, many smaller oval lesions with scale at their borders appear on the trunk and (upper) arms.
Typically the lesions take on the direction of the langer’s cleavage lines forming a “Christmas tree pattern” on the back and disappear spontaneously within 2 months.

123
Q

Ptyriasis rosea lesions are typically itchy and painful (T/F)?

A

False

They usually cause no pain or itch

124
Q

A majority of patients have associated systemic symptoms such as aching and tiredness in Ptyriasis rosea infection (T/F)?

A

False

It’s a minority!

125
Q

How long do Ptyriasis rosea eruptions last before they resolve?

A

eruption lasts between 2 and 10 weeks

126
Q

Spontaneous resolution of Ptyriasis rosea lesions sometimes occur leaving hyperpigmented patches that fade away more slowly (T/F)?

A

False

It’s hypopigmented patches

127
Q

How would you differentiate between pityriasis rosea and secondary syphilis?

A

It is difficult
However unlike Ptyriasis rosea, Secondary syphilis involves palms and soles with generalized lymphadenopathy!

serological tests for syphilis should be performed!

128
Q

What important investigation must always be carried out in a case of Ptyriasis rosea?

A

Serological test for syphyllis!

129
Q

Mention 5 differentials of Ptyriasis rosea?

A

Secondary syphilis; except it involves palms and soles with generalized lymphadenopathy

Seborrhoiec dermatitis; but here it’s profuse in presternal and infrasternal areas with scalp involvement

Nummular eczema; except it’s pruritic or vesicular.

Lichen planus; diff in histopathology

Pityriasis lichenoides chronica; no herald patch, histopathology

130
Q

What are the treatment options for pityriasis rosea?

A

No treatment is curative, and active treatment is seldom needed!

A moderately potent topical steroid or calamine lotion will help the itching if present

One per cent salicylic acid in soft white paraffin or emulsifying ointment reduces scaling.

Sunlight or artificial UVB often relieves pruritus and may hasten resolution

131
Q

a vascular neoplasm that affects skin and mucosa, and less commonly involves other organs like lymph nodes, lungs and GI tract describes what?

A

Kaposi sarcoma!

132
Q

What viruses has been linked to Kaposi sarcoma?

A

HHV-8

133
Q

What are the variants of Kaposi sarcoma?

A

classical
endemic
epidemic/ HIV-related

134
Q

purple-black papules and rounded nodules usually on one leg which progress very slowly or remain stationary, patient can survive for over a decade. This describes what variant of KS?

A

Classical KS

135
Q

Patients with classical KS rarely survive up to 2 years (T/F)?

A

False

Patient can survive for over a decade!

136
Q

The most aggressive variant of KS is known as?

A

Epidemic/ HIV-related KS

137
Q

The epidemic variant of KS has 4 variants (T/F)?

A

False

It’s the endemic variant!

138
Q

Itemize the 4 types of endemic KS?

A

benign nodular
aggressive
florid
lymphadenopathic

139
Q

The florid endemic KS variant progresses much faster than any other variant of KS (T/F)?

A

False

It’s the epidemic/ HIV-related variant

140
Q

What body regions are commonly affected by KS?

A

the face
the trunk
the genitalia
the proximal limbs especially the thighs

141
Q

What complications may arise from KS lesions?

A

Lesions may be warty, tumorous, may ULCERATE and they may cause GROSS OEDEMA, especially in the face, penis and scrotum

142
Q

KS often presents with generalised lymph node enlargement or pleural lesion (T/F)?

A

True!

143
Q

KS lesions usually affect the lower extremities bilaterally (T/F)?

A

False

It’s unilateral

144
Q

What important examination must always be carried out in a suspected KS patient?

A

Always examine the mouth!

Plaques, nodules and tumours in the mouth, especially on the hard palate and tonsils are very common

145
Q

What investigations are carried out in the diagnosis of KS?

A 
PCR ASSAYS
Viral DNA can be detected in patient specimens 
(Direct virus culture is difficult)
SEROLOGICAL ASSAYS are available to measure persistent antibody to KSHV, using 
*indirect immunofluorescence
*Western blot
*ELISA formats.
SKIN BIOPSY 
CHEST X-RAY 
UPPER & LOWER GI ENDOSCOPY.
146
Q

Treatment for KS is mostly palliative (T/F)?

A

True!

147
Q

What are the treatment options for KS?

A

Treatment options depend on

  • extent of tumor and growth rate
  • HIV viral load
  • general condition of the patient.

LIMITED SKIN DISEASE
may be treated with
*CRYOTHERAPY
*INTRALESIONAL VINBLASTINE / VINCRISTINE *RADIATION THERAPY

148
Q

Most people will have a wart at some time in their lives (T/F)?

A

True

149
Q

Their prevalence is highest in adolescents (T/F)?

A

False

Childhood!

150
Q

What viral agents is implicated in causing warts?

A

Human papilloma virus(HPV)

151
Q

Itemize the well recognized types of viral warts and what they cause?

A

HPV 1,2,4 —COMMON WARTS
HPV 6,11 —- ANOGENITAL WARTS
HPV 16,18—GENITAL DYSPLASIA/CERVICAL CA

152
Q

How do you get viral warts?

A

close contact; direct or indirect!

Viral particles are released from the surface of papillomatous lesion

153
Q

Why do we have different kinds of warts?

A

Papillomaviruses cause infections at cutaneous and mucosal sites, sometimes leading to the development of different kinds of wart

154
Q

What is the pathogenesis of viral warts?

A

It is likely that microlesions allow infection of proliferating basal layer cells at other sites or within different hosts.

155
Q

HPV Genital warts are usually acquired through?

A

sexually transmitted

156
Q

Mention the HPV types implicated in common warts?

A

HPV 1, 2, 4, 27, 57 and 63

157
Q

Common warts are most commonly seen in what group of individuals?

A

Teenagers!

158
Q

How is common wart spread?

A

By contact

Auto-innoculation

159
Q

What is usually the first sign of common wart infection?

A

smooth skin-coloured papule.

160
Q

Common warts can occur at any age (T/F)?

A

True

161
Q

Describe the typical history of common wart infection?

A

The first sign is a smooth skin-coloured papule which enlarges into an irregular hyperkeratotic surface giving it the classic ‘warty’ appearance

162
Q

What HPV types are implicated in plantar warts?

A

HPV 1, 2, 4, 27, and 57

163
Q

Common warts can be painful urging the patient to seek treatment (T/F)?

A

False

It’s plantar warts!

164
Q

How can plantar warts be differentiated from corns?

A

Presence of bleeding capillary loops allows plantar warts to be distinguished from corns

165
Q

Common warts are associated with presence of bleeding capillary loops (T/F)

A

False

It’s plantar warts!

166
Q

This kind of warts has a rough surface, which protrudes only slightly from the skin and is surrounded by a horny collar. This describes what?

A

Plantar warts!

167
Q

What are the treatment options for palmoplantar warts?

A

KERATOLYTIC THERAPY
SALICYLIC ACID 25% ointment twice daily. followed by CUTTING or SCRAPING the warts with a pumice stone, callus file or a knife twice a week.
Preparations of SALICYLIC ACID 5-20% and LACTIC ACID 5-20% in COLLODION are easier to use.
Light ELECTRO DISSECTION and CURETTAGE.
FREEZE with LIQUID NITROGEN when available

168
Q

Warts resolve spontaneously in the healthy as the immune response overcomes the infection (T/F)?

A

True

169
Q

Warts resolve spontaneously within 2 weeks without treatment (T/F)?

A

False

6 mnths to 2yrs

170
Q

Plane warts most commonly affects which area of the body?

A

the face and brow

the backs of the hands.

171
Q

smooth flat-topped papules usually skin-coloured or light brown that become inflamed as a result of an immunological reaction, just before they resolve spontaneously correctly describes what?

A

Plane warts!

172
Q

What kinda warts exhibit positive koebners phenomena?

A

Common warts

Plane warts

173
Q

Plain warts are usually multiple and painful (T/F)?

A

False

They are multiple and painless!

174
Q

What are the treatment options for plane warts?

A

SALICYLIC ACID 2-5% ointment twice daily for 4-8 weeks.
LIMITED NUMBER OF LESIONS
CURETTAGE with a SHARP CURETTE.
ELECTROSURGERY may be carefully tried but may leave hypopigmented scars.
CAUSTIC PENCIL (=silver nitrate pencil) daily.

If lesions are WIDESPREAD and salicylic acid 2-5% ointment is not successful, it is BEST to LEAVE!!

175
Q

What is the risk of electrosurgery therapy in TX of plane warts?

A

May leave hypopigmented scars!

176
Q

Low-risk genital HPV types are implicated in anogenital warts (T/F)?

A

True

HPV 6 & 11

177
Q

most HPV induced genital dysplasias are caused by HPV 6 and 18 (T/F)?

A

False!

It’s HPV 16 & 18

178
Q

What are the various routes of transmission of condyloma acuminata?

A

by DIRECT CONTACT
usually through SEXUAL INTERCOURSE,
sometimes by INFECTED HANDS
from MOTHER TO CHILD during CHILDBIRTH.

179
Q

The lesion seen in anogenital warts can be described as?

A

Papillomatous cauliflower-like lesions, with a moist macerated vascular surface which may coalesce to form huge lesions causing discomfort and irritation.

180
Q

The vaginal and anorectal mucosae may be affected in condyloma acuminata (T/F)?

A

True!

181
Q

What agent is used in the treatment of anogenital warts in pregnant women?

A

Trichlorocacetic acid 50-88% solution

182
Q

What are the treatment options for anogenital warts?

A

Women with anogenital warts, or who are the partners of men with anogenital warts, should have their cervical cytology checked regularly

PODOPHYLLOTOXIN (0.5% solution or 0.15% cream)
IMIQUIMOD (5% cream).
**Both are irritants and should be used carefully

Apply podophyllin carefully to the warts with the back of a matchstick. Leave it on for 4 to 6 hours then wash off with water and soap. Repeat weekly until cleared.

TRICHLOROACETIC ACID (50-88%) solution, applied in the clinic, may be used in pregnancy.
CRYOSURGERY with LIQUID NITROGEN .
CAUTERISATION of large and/or refractive genital warts. This can be a very useful procedure but is controversial

Topical 5% 5-FU cream (EFUDIX) may be used once daily to once weekly for up to 6 months after any of these treatments to prevent recurrences!

183
Q

What viruses is implicated in Molluscum contagiosum?

A

Pox virus!

184
Q

How is Molluscum contagiosum spread?

A

spread by DIRECT CONTACT;
SEXUALLY
SHARING A TOWEL at the swimming bath

185
Q

What group of individuals are commonly affected by Molluscum contagiosum?

A

Children!

186
Q

Molluscum contagiosum lesions are commonly present on what body regions?

A

Face
eyelids
occasionally on the limbs and trunk

187
Q

Whatbis the incubation period for Molluscum contagiosum?

A

ranges from 2 to 6 weeks?

188
Q

Several members of the family are often affected by Molluscum contagiosum (T/F)?

A

True!

189
Q

A typical description of Molluscum contagiosum lesions will include?

A

Individual lesions are shiny, white or pink, and hemispherical with central punctum, which may contain a cheesy core, giving the lesions their characteristic umbilicated look.

190
Q

Distribution of Molluscum contagiosum lesions depends on what?

A

The mode of infection

191
Q

Multiple lesions are rarely seen in Molluscum contagiosum infection (T/F)?

A

False

Multiple lesions are commonly seen

192
Q

What group of individuals are prone to extensive lesions in Molluscum contagiosum infection?

A

Atopic individuals
immunocompromised
spread by scratching
use of topical steroids

193
Q

Untreated lesions In Molluscum contagiosum usually clear in 2 months (T/F)?

A

False

6-9 months

194
Q

Individual lesions rarely persist for more than 6-9 months in Molluscum contagiosum infection (T/F)?

A

False

2 months

195
Q

Lesions in Molluscum contagiosum infection are usually accompanied by a brief local inflammation before complete resolution (T/F)?

A

True!

196
Q

Mention 2 complications seen in Molluscum contagiosum infection ?

A

Large solitary lesions may take longer.
Some leave depressed scars
Traumatized or overtreated lesions may become secondarily infected

197
Q

Diagnosis in Molluscum contagiosum is by?

A

PCR can detect viral DNA sequences

ELECTRON MICROSCOPY can detect poxvirus particles.

198
Q

What is an effective therapy for Molluscum contagiosum in children?

A

Cantharidin!

199
Q

Why may treatment of Molluscum contagiosum be difficult?

A

because of the closeness of lesions to the eyes!

200
Q

Outline treatment options for Molluscum contagiosum infection?

A
  • Can be FROZEN with ETHYL- CHLORIDE SPRAY and CURETTED.
  • Spiking the umbilicated centres with a sharp-pointed tooth pick stick which has been dipped in strong IODINE SOLUTION.
  • CAUSTIC PENCIL (silver nitrate pencil) for small molluscum.
  • Caustic treatment with 80% PHENOL or 50-88% TRICHLOROACETIC ACID.
  • CANTHARIDIN is an effective therapy in children.
201
Q

Measles infection confers lifelong immunity (T/F)?

A

True

202
Q

Measles is a chronic infection (T/F)?

A

False

It’s an acute infection

203
Q

acute, highly infectious disease characterized by fever, respiratory symptoms, and maculopapular rash correctly describes what infection?

A

Measles infection!

204
Q

Measles virus is highly contagious with multiple serotype and has no animal reservoir (T/F)?

A

False

It has a single serotype

205
Q

Inapparent infections are rare in measles (T/F)?

A

True

206
Q

How is measles transmitted?

A

predominantly via the respiratory route (by inhalation of large droplets of infected secretions).

207
Q

What is the incubation period for measles virus?

A

9-12 days

208
Q

Measles is an epidemic throughout the world (T/F)?

A

False

It’s an endemic

209
Q

In general, epidemics of measles recur regularly every 5–6years (T/F)

A

False

Every 2-3 years

210
Q

What determines the severity of measles infection in any community?

A

A population’s state of immunity is the determining factor.

The disease will flare up when there’s accumulation of susceptible children

211
Q

Not all ages will develop clinical measles (T/F)

A

False

All ages!

212
Q

Where does the measles virus undergo replication?

A

Reticuloendothelial cells!

213
Q

Secondary viremia is typically associated with replication of measles virus in the reticuloendothelial system (T/F)?

A

False

It’s Primary viremia

214
Q

Primary viremia is typically associated with seeding of epithelial surfaces of the body, including the skin, respiratory tract, and conjunctiva (T/F)

A

False

It’s secondary viremia

215
Q

Focal replication of measles virus typically occurs where?

A

Epithelial surfaces

216
Q

What is typically seen in lymphoid tissues throughout the body (lymph nodes, tonsils, appendix) in measles infection?

A

Multinucleated giant cells with intranuclear inclusions

217
Q

Describe the typical natural history of measles illness?

A

1) An incubation period of 9-12 days
2) Its typically a 7- to 11-day illness (with a prodromal phase of 2–4 days followed by an eruptive phase of 5–8 days).
3) The fever and cough persist until the rash appears and then subside within 1–2 days
4) The rash, which starts on the head and then spreads progressively to the chest, the trunk, and down the limbs, appears as light pink, discrete maculopapules that coalesce to form blotches, becoming brownish in 5–10 days.

5)The fading rash resolves with desquamation.
Symptoms are most marked when the rash is at its peak but subside rapidly thereafter.

218
Q

When does the maculopapular rash of measles appear?

A

The characteristic maculopapular rash appears about day 14 after exposure.

219
Q

The maculopapular rash of measles appears just as circulating antibodies become detectable thus the viremia disappears and the fever falls T/F)?

A

True!

220
Q

The prodromal phase of measles is characterized by what?

A 
fever
malaise
sneezing
coughing
running nose
conjunctivitis
Koplik's spots
221
Q

The cough and coryza of measles reflect what?

A

reflect an intense inflammatory reaction involving the mucosa of the respiratory tract

222
Q

What are koplik spots and what do they contain?

A

They are small, bluish-white ulcerations on the buccal mucosa opposite the lower molars pathognomonic for measles

These spots contain giant cells and viral antigens

223
Q

When do the koplik spots of measles appear?

A

appear about 2 days before the rash.

224
Q

Mention 5 complications of measles infection?

A

Giant cell pneumonia, more common in adults
Otitis media
Post-measles encephalitis
Subacute sclerosing panencephalitis (SSPE)
Thrombocytopenic purpura
Fetal death in pregnancy

225
Q

Measles pneumonia is more common In children (T/F)?

A

False

In adults

226
Q

How is the diagnosis of measles made?

A 
CLINICALLY
Characteristic fever
koplik spots
conjunctivitis
respiratory symptoms
typical exanthema.

Antigen detection from epithelial cells in respiratory secretions and urine

SEROLOGY— ELISA

227
Q

What are the treatment options for measles?

A

Ribavirin
Vitamin A
Prevention is with live attenuated measles vaccine

Dermatology OAU (10 decks)

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