171: Endemic (Nonvenereal) Treponamatosis Flashcards

1
Q

What are the key differences between endemic treponematoses and syphilis?

A
  1. Nonvenereal form of transmission
  2. Endemic occurrence in specific geographic areas
  3. Tendency to affect children rather than sexually active adults
  4. Less likely risk for congenital transmission
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2
Q

What is Pinta and how does it differ from other endemic treponematoses?

A

Pinta is a chronic infectious and contagious disease recognized by the World Health Organization as a neglected tropical disease. It is the most benign of the endemic treponematoses, affecting only the skin, and is characterized by:
- Clinical manifestations limited to the skin, including vitiligo-like achromic lesions and hyperpigmented lesions.
- Affects people of all ages.
- Not sexually transmitted nor congenitally acquired.

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3
Q

What is the epidemiology of Pinta?

A
  • Most patients acquire the infection during childhood.
  • There is no difference between the two sexes in terms of infection rates.
  • The indigenous population is the most affected group.
  • Pinta is thought to be present focally in the Brazilian and Venezuelan rainforests.
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4
Q

What are the key differences between endemic treponematoses and syphilis in terms of transmission and affected populations?

A
  1. Transmission: Endemic treponematoses are nonvenereal, while syphilis is sexually transmitted.
  2. Affected Populations: Endemic treponematoses tend to affect children rather than sexually active adults, whereas syphilis primarily affects sexually active adults.
  3. Congenital Transmission: There is a lower risk of congenital transmission in endemic treponematoses compared to syphilis.
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5
Q

What are the clinical implications of the disease progression in endemic treponematoses, particularly in relation to morbidity?

A

Significant morbidity is associated with the progression of endemic treponematoses, which primarily affects the skin, bone, and cartilage. This can lead to:
- Disfigurement: Visible skin lesions and deformities.
- Pain: Chronic pain due to bone and cartilage involvement.
- Disability: Impairment in physical function.
- Social Isolation: Stigmatization and social withdrawal due to visible symptoms.

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6
Q

What are the two clinical stages of Pinta and their characteristics?

A

Pinta is classified into two clinical stages:

  1. Primary Stage:
    • Early Phase: Appears 7 to 20 days after treponema inoculation, characterized by erythematous scaly papules on the face and extremities.
    • Secondary Phase: Occurs within 6 months to 2-3 years, presenting hypochromic, erythematous patches that enlarge and coalesce, referred to as pintides.
  2. Late Stage:
    • Appears 2 to 5 years after the first lesion, characterized by achromic patches on body prominences, large hypochromic areas, and various hyperchromic lesions.
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7
Q

What are the characteristics of the primary lesions in Pinta?

A

The primary lesions in Pinta consist of:
- One to several erythematous scaly papules, commonly affecting the face and extremities.
- Lesions tend to grow in extension, producing erythematosquamous or hyperpigmented plaques.
- They vary in size and shape (arciform, circinate, polycyclic, serpiginous).
- Generally asymptomatic, but pruritus may occur.
- Regional lymphadenopathy is common.

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8
Q

What changes occur in the lesions during the secondary phase of Pinta?

A

During the secondary phase of Pinta, the lesions present:
- Variable degrees of hyperkeratosis.
- Small and occasionally nummular morphology.
- Gradual enlargement and coalescence, affecting large areas of the body, with centers resembling normal skin, referred to as pintides.
- Pintides initially appear red to violaceous and later change to slate-blue, brown, gray, or black.

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9
Q

What are the key features of the late or tertiary stage of Pinta?

A

The late or tertiary stage of Pinta is characterized by:
- Achromic patches on body prominences (hands, wrists, elbows, tibia, ankles, feet).
- Large hypochromic areas on upper extremities, trunk, and thighs.
- Cutaneous atrophy and multiple hyperchromic lesions in a mottled pattern.
- Hypochromic patches with irregular borders and macules, especially on buttocks.
- Sparing of the groin, genital area, and inner thighs.
- Appearance of hyperchromic and hyperkeratotic patches on exposed areas of extremities, with frequent plantar hyperkeratosis.

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10
Q

A child from a rural community presents with erythematous scaly papules on the face and extremities. What is the likely diagnosis and the causative organism?

A

The likely diagnosis is Pinta, caused by Treponema carateum.

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11
Q

A patient presents with hypochromic patches on the dorsum of the hands and anterior tibia, sparing the groin and genital area. What stage of Pinta is this, and what are the characteristic findings?

A

This is the late or tertiary stage of Pinta. Characteristic findings include achromic patches, cutaneous atrophy, and hyperchromic patches on exposed areas.

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12
Q

A child presents with erythematous, hyperpigmented plaques of varying shapes on exposed areas. What is the likely stage of Pinta, and what are the lesions called?

A

This is the primary stage of Pinta, and the lesions are erythematosquamous or hyperpigmented plaques.

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13
Q

A patient with Pinta has lesions that are initially red to violaceous and later become slate-blue or black. What are these lesions called, and in which phase do they appear?

A

These lesions are called pintides, and they appear during the secondary phase of the primary stage.

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14
Q

A child in a humid environment develops erythematous scaly papules that coalesce into plaques. What is the likely diagnosis, and what is the causative organism?

A

The likely diagnosis is Pinta, caused by Treponema carateum.

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15
Q

A patient with Pinta has lesions with a polymorphic clinical picture. What does this indicate about the disease stage?

A

This indicates the secondary phase of the primary stage, where lesions from different periods coexist.

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16
Q

A patient with Pinta has hyperkeratotic patches on the palms and soles. What stage is this, and what are the associated findings?

A

This is the late or tertiary stage of Pinta. Associated findings include hyperpigmented and achromic patches with hyperkeratosis.

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17
Q

A patient with Pinta has lesions that appear slate-blue and later turn black. What is the progression of these lesions, and what are they called?

A

These lesions are called pintides. They progress from red to violaceous, then to slate-blue, brown, gray, or black.

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18
Q

A patient with Pinta has erythematous scaly papules that grow into plaques. What is the morphology of these plaques?

A

The plaques vary in size and shape, including arciform, circinate, polycyclic, and serpiginous morphologies.

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19
Q

A patient with Pinta has hypochromic patches with irregular borders on the buttocks. What stage is this, and what are the associated findings?

A

This is the late or tertiary stage of Pinta. Associated findings include cutaneous atrophy, achromic dot-like lesions, and hyperchromic lesions in a mottled pattern.

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20
Q

A patient with Pinta has lesions that coalesce into large areas with normal skin centers. What are these lesions called?

A

These lesions are called pintides.

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21
Q

What are the characteristics of the primary stage of Pinta, including its phases and lesion types?

A

The primary stage of Pinta is characterized by two phases:
1. Early phase (initial period): Appears 7 to 20 days after treponema inoculation, with primary lesions consisting of erythematous scaly papules affecting the face, upper and lower extremities.
2. Secondary phase (cutaneous dissemination): Occurs within 6 months to 2-3 years after the first lesions, presenting hypochromic, erythematous, or erythematohypochromic patches that gradually enlarge and coalesce into lesions called pintides. These lesions are initially red to violaceous and later become slate-blue, brown, gray, or black.

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22
Q

Describe the late or tertiary stage of Pinta and its clinical features.

A

The late or tertiary stage of Pinta appears 2 to 5 years after the first lesion and is characterized by:
- Achromic patches over body prominences (e.g., dorsum of hands, wrists, elbows, tibia, ankles, and foot).
- Large hypochromic areas on upper extremities, trunk, and thighs.
- Cutaneous atrophy and multiple hyperchromic lesions in a mottled pattern.
- Hypochromic patches with irregular borders and macules, especially on buttocks.
- The groin, genital area, and inner/upper thighs are often spared.
- Hyperchromic and hyperkeratotic patches on exposed areas of the upper and lower extremities, with frequent plantar hyperkeratosis.

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23
Q

What is the significance of pintides in the secondary phase of Pinta, and how do they change over time?

A

Pintides are significant in the secondary phase of Pinta as they represent the progression of the disease. They are characterized by:
- Initially appearing as red to violaceous lesions.
- Over time, they change color to slate-blue, brown, gray, or black.
- They gradually enlarge and coalesce, affecting large areas of the body, with centers resembling normal skin.
- Pintides may present variable degrees of hyperkeratosis and are small and occasionally nummular in morphology.

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24
Q

What are the complications associated with pinta lesions after treatment?

A

Although early pinta lesions heal within several months after specific treatment, the therapy cannot reverse the skin changes of late pinta. Unlike other treponematoses, destructive skin and bone lesions, nor cardiovascular and neurologic manifestations are seen in patients with pinta.

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25
Q

What is the primary cause of pinta and how is it transmitted?

A

Pinta is caused by T. carateum, which is morphologically and antigenically identical to the etiologic agents of syphilis and yaws. It is usually acquired during early childhood and thought to spread mostly via direct contact with an infected person, although transmission may also occur via fomites. The treponeme enters the skin through small cuts, scratches, or other skin damage.

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26
Q

What laboratory tests are used for diagnosing pinta?

A

Serology remains the cornerstone of diagnosis for pinta. The T. pallidum particle agglutination (TPPA) and hemagglutination (TPHA) assays are used to detect Treponema-specific antibodies. The venereal disease research laboratory (VDRL) and rapid plasma reagin (RPR) tests are nonspecific but more accurate in reflecting disease activity than TPPA or TPHA, with titers falling rapidly after successful treatment.

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27
Q

What are the histopathologic features of primary and secondary lesions in pinta?

A

The primary lesions in pinta are characterized by mild acanthosis and spongiosis, with lymphocyte migration and vacuolar degeneration of the basal cell layer. In the dermis, changes consist of a slight lymphohistiocytic and plasmocytic infiltrate and mild vascular reaction. The hypochromic lesions from the secondary phase present with moderate hyperkeratosis, acanthosis, and spongiosis, along with a superficial infiltrate around the thickened vessels.

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28
Q

A patient with Pinta has lesions with hyperkeratosis and acanthosis. What stage is this, and what are the histopathologic findings?

A

This is the secondary phase of the primary stage. Histopathologic findings include hyperkeratosis, acanthosis, and spongiosis.

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29
Q

What are the key characteristics of the complications associated with pinta, particularly in relation to skin changes after treatment?

A
  • Early pinta lesions heal within several months after specific treatment.
  • The therapy cannot reverse the skin changes of late pinta.
  • Unlike other treponematoses, destructive skin and bone lesions, nor cardiovascular and neurologic manifestations are seen in patients with pinta.
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30
Q

How does the etiology and pathogenesis of pinta differ from other treponematoses in terms of transmission and environmental factors?

A
  • Pinta is caused by T. carateum, morphologically and antigenically identical to syphilis and yaws.
  • It is found in warm and humid environments and is usually acquired during early childhood.
  • Transmission occurs mainly through direct contact with an infected person, but may also occur via fomites.
  • The treponeme enters the skin through small cuts, scratches, or other skin damage. The only known reservoir is human beings.
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31
Q

What role does serology play in the diagnosis of pinta, and how do the different serological tests compare in specificity and accuracy?

A
  • Serology is the cornerstone of diagnosis for pinta.
  • The T. pallidum particle agglutination (TPPA) and hemagglutination (TPHA) assays detect Treponema-specific antibodies, which usually remain positive for life.
  • The venereal disease research laboratory (VDRL) and rapid plasma reagin (RPR) tests are nonspecific but more accurate in reflecting disease activity than TPPA or TPHA, with titers falling rapidly after successful treatment.
  • However, serologic techniques cannot distinguish pinta from syphilis or other nonvenereal treponematoses.
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32
Q

What are the histopathological features observed in the primary and secondary lesions of pinta?

A
  • Primary lesions: Characterized by mild acanthosis and spongiosis, with lymphocyte migration and vacuolar degeneration of the basal cell layer.
  • Secondary lesions: Present with moderate hyperkeratosis, acanthosis, spongiosis, and a superficial infiltrate around the thickened vessels. The dermis shows slight lymphohistiocytic and plasmocytic infiltrate and mild vascular reaction.
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33
Q

What are the histological features observed in erythematous and squamous lesions of yaws?

A

In erythematous and squamous lesions, the following features are observed:
- Acanthosis, hyperkeratosis, and spongiosis in the epidermis.
- Lymphohistiocytic infiltrate in the dermis with edema and vascular proliferation in the papillary dermis.

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34
Q

What is the recommended treatment for pinta, and how quickly does it render lesions noninfectious?

A

The recommended treatment for pinta is a single or divided dose of long-acting Benzathine penicillin (1.2 MU for adults).

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35
Q

What are the key histopathological features observed in erythematous and squamous lesions of yaws?

A

The key histopathological features include:
- Acanthosis, hyperkeratosis, and spongiosis in the epidermis.
- Lymphohistiocytic infiltrate in the dermis with edema and vascular proliferation in the papillary dermis.

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36
Q

What is the recommended treatment for pinta?

A

The recommended treatment for pinta is:
- A single or divided dose of long-acting Benzathine penicillin (1.2 MU for adults; 0.6 MU for children).

This treatment renders the lesions noninfectious in less than 24 hours.

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37
Q

What is yaws and what organism causes it?

A

Yaws is an infectious disease caused by T. pallidum ssp. pertenue. The clinical appearance of a typical lesion resembles a raspberry, which is reflected in one of its names, framboesia tropica.

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38
Q

What are the primary and secondary lesions of pinta, and how do they resolve?

A

The primary and secondary lesions of pinta may resolve spontaneously. However, despite treatment, patients may present with lifelong late lesions.

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39
Q

What is the significance of the term ‘framboesia’ in relation to yaws?

A

The term ‘framboesia’ refers to the clinical appearance of a typical lesion of yaws, which resembles a raspberry.

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40
Q

What is the primary mode of transmission for Yaws?

A

Yaws is transmitted by direct skin contact with an infectious lesion, facilitated by abrasion or erosion of the skin.

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41
Q

What age group is most commonly affected by Yaws?

A

Children up to 15 years of age are most commonly affected, with a peak incidence between 6 and 10 years.

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42
Q

What are the characteristics of the primary lesion of Yaws?

A

The primary lesion of Yaws is usually a papule that develops 21 days after initial contact, evolving into a proliferative, exudative, papillomatous lesion 2 to 5 cm in diameter.

43
Q

What are secondary lesions in Yaws and when do they appear?

A

Secondary lesions appear after 1 to 2 months (up to 24 months) and represent hematogenous and lymphatic spreading to the skin and bone.

44
Q

What is the clinical significance of the lesions on the palms and soles in Yaws?

A

On the palms and soles, lesions can be exudative papules or papulosquamous plaques, keratodermic, with a tendency to form fissures.

45
Q

What is Pianic onychia in relation to Yaws?

A

Pianic onychia is a paronychia that originates from hyperkeratotic lesions in the nail folds, associated with Yaws.

46
Q

What is the diagnosis for a child with a raspberry-like lesion on the leg that resolves spontaneously after 3 months?

A

The diagnosis is Yaws, and the lesion is called ‘mother yaws’ or ‘maman pian.’

47
Q

What is the term for the peculiar gait caused by painful acral lesions in Yaws?

A

The term for the gait is ‘crab yaws,’ caused by tender or painful acral lesions.

48
Q

What is the morphology of dry, papulosquamous lesions on the face in Yaws?

A

The lesions have annular or discoid morphology with a squamous collaret, and the condition is called tinea yaws.

49
Q

What stage is characterized by angular cheilitis and exudative lesions around natural orifices in Yaws?

A

This is the secondary stage of Yaws, and the lesions are mucosal lesions presenting as bilateral exudative angular cheilitis.

50
Q

What condition is characterized by hyperkeratotic lesions in the nail folds leading to paronychia in Yaws?

A

This condition is called pianic onychia.

51
Q

What is the clinical significance of keratodermic lesions on the palms and soles in Yaws?

A

These lesions are tender or painful, leading to a peculiar gait known as crab yaws.

52
Q

What happens to Yaws lesions in a dry climate?

A

In a dry climate, the lesions become scarce and restricted to intertriginous areas.

53
Q

What are the associated findings of mucosal lesions resembling angular cheilitis in Yaws?

A

This is the secondary stage of Yaws. Associated findings include exudative papules and papulosquamous lesions.

54
Q

What are the primary and secondary lesions associated with Yaws?

A

Primary lesions:
- Usually a papule that develops 21 days after initial contact.
- Evolves into a proliferative, exudative, papillomatous lesion (2 to 5 cm in diameter).

Secondary lesions:
- Appear after 1 to 2 months (up to 24 months).
- Represent hematogenous and lymphatic spreading to the skin and bone.

55
Q

What populations are most affected by Yaws?

A

Yaws predominantly affects:
- Children: Most commonly those up to 15 years of age.
- Rural communities: Individuals living in poor sanitary conditions in tropical areas.

56
Q

What clinical features can be observed in the cutaneous manifestations of Yaws?

A

The clinical features of Yaws lesions include:
- Exudative papules: Generalized, bilateral, and symmetrical.
- Dry, papulosquamous papules: Resembling psoriasis or seborrheic dermatitis.

57
Q

What happens to secondary yaws lesions if left untreated?

A

If left untreated, secondary yaws lesions resolve either spontaneously or after treatment, healing with or without scarring.

58
Q

What are the common manifestations associated with late-stage yaws?

A

The most common manifestations associated with late-stage yaws include:
1. Subcutaneous gummatous nodules with massive tissue destruction.
2. Complete destruction of the nasal cartilage leading to a deformity known as gangosa.

59
Q

What is the prognosis for patients in the latent stage of yaws?

A

Up to 10% of patients in a latent stage may evolve into the most disfiguring, disabling late stage after 5 years of untreated infection.

60
Q

What is meant by ‘attenuated yaws’?

A

‘Attenuated yaws’ refers to a milder form of the disease that can be seen in areas of reduced transmission.

61
Q

What stage is characterized by subcutaneous gummatous nodules and serpiginous ulcerations in Yaws?

A

This is the late or tertiary stage of Yaws. Common manifestations include tissue destruction.

62
Q

What is the deformity caused by the destruction of nasal cartilage in late-stage Yaws?

A

The deformity is called gangosa, caused by the destruction of nasal cartilage.

63
Q

How long can relapses occur in Yaws after the initial infection?

A

Relapses can occur for up to 5 years after the initial infection, representing the latent stage.

64
Q

What are the potential outcomes for secondary yaws if left untreated?

A

Secondary yaws can resolve either spontaneously or after treatment, healing with or without scarring.

65
Q

What are the characteristics of late-stage yaws lesions?

A

Late-stage yaws lesions may include:
1. Subcutaneous gummatous nodules with massive tissue destruction.
2. Complete destruction of nasal cartilage leading to gangosa.

66
Q

What is the recommended treatment regimen for yaws in patients older than 10 years?

A

The recommended treatment regimen for yaws in patients older than 10 years is a single dose of 1.2 million units of long-acting penicillin.

67
Q

What alternative medications can be used for adults allergic to penicillin in the treatment of yaws?

A

Alternative medications for adults allergic to penicillin include oral tetracyclines, doxycycline, and erythromycin.

68
Q

What is the causative agent of Bejel?

A

The causative agent of Bejel is the spirochete T. pallidum ssp. endemicum.

69
Q

In which age group is Bejel primarily found?

A

Bejel primarily involves children from 2 to 15 years of age, but can also be seen in adults belonging to nomadic people.

70
Q

What are the clinical outcomes expected after therapy for yaws?

A

After therapy for yaws, the expected clinical outcomes are:
1. Yaws lesions become noninfectious within 24 hours after therapy.

71
Q

What are the advantages of azithromycin treatment over penicillin for Yaws?

A

Advantages include ease of administration by less skilled workers, reduced risk of anaphylaxis, and suitability for mass control programs.

72
Q

What is the recommended treatment regimen for yaws in patients younger than 10 years?

A

For those younger than 10 years, the recommended dose is 0.6 million units.

73
Q

What are the common clinical features of Bejel?

A

Common clinical features of Bejel include:
- Primary lesions that are not easily identified.
- Secondary lesions may mimic condyloma lata.

74
Q

What are the common clinical features of Bejel?

A

Common clinical features of Bejel include primary lesions that are not easily identified, secondary lesions that may mimic condyloma lata or angular stomatitis, and tertiary lesions including gumma and gangosa.

75
Q

What is the primary population affected by Bejel?

A

The main population affected by Bejel are children younger than 15 years of age. Factors that facilitate the infection include overcrowding, poor sanitary conditions, and poor personal hygiene.

76
Q

How does the epidemiology of Bejel differ in dry versus humid climates?

A

Bejel predominates in countries with dry climates, while in nearby countries with more humid climates, yaws is the predominant disease.

77
Q

What are the characteristics of the primary lesion in Bejel?

A

The primary lesion in Bejel is infrequently observed and is described as a painless and superficial mucosal ulceration in the mouth or the nasopharynx.

78
Q

What are the secondary lesions associated with Bejel?

A

The secondary lesions in Bejel are similar to those seen in syphilis and are characterized by oval, almost painless patches with a whitish, slightly elevated cap, lesions of angular stomatitis, generalized nonitchy skin eruptions, generalized lymphadenopathy, and laryngitis.

79
Q

What are the potential noncutaneous findings in patients with Bejel?

A

Patients with Bejel may develop noncutaneous findings such as osteitis and periostitis of long bones and hands, complaints of nocturnal pain, and bone changes may evolve into saber tibias.

80
Q

What is the causative agent of Bejel?

A

Bejel is caused by T. pallidum ssp. endemicum. The disease is acquired during childhood and is transmitted through the skin.

81
Q

What is the likely diagnosis for a patient with painless mucosal ulceration and generalized lymphadenopathy?

A

The likely diagnosis is Bejel, caused by Treponema pallidum ssp. endemicum.

82
Q

What stage is characterized by destructive ulcerations and nasal cartilage collapse?

A

This is the tertiary stage of Bejel, and the deformity is called gangosa.

83
Q

What is the underlying pathology for saber tibias and nocturnal bone pain in Bejel?

A

The underlying pathology is osteitis and periostitis, which are less severe in Bejel compared to Yaws.

84
Q

What stage is indicated by condylomata lata-like lesions in Bejel?

A

This is the secondary stage of Bejel. Other findings include generalized lymphadenopathy, laryngitis, and painless mucosal patches.

85
Q

What is the mode of transmission for Bejel?

A

The mode of transmission includes nonvenereal direct mucosal or skin contact and sharing utensils or drinking vessels.

86
Q

What are the primary epidemiological characteristics of Bejel?

A

Bejel is prevalent in the Near East and the African Sahel, particularly in rural areas of Saudi Arabia. It predominates in countries with dry climates.

87
Q

What are the key cutaneous findings associated with Bejel?

A

Key cutaneous findings in Bejel include primary lesions as painless mucosal ulceration, secondary lesions like oval patches, angular stomatitis, generalized skin eruptions, and condylomata lata-like lesions.

88
Q

How do the noncutaneous findings in Bejel compare to those in Yaws?

A

Noncutaneous findings in Bejel include osteitis and periostitis of long bones, nocturnal pain, and saber tibias, which are less severe than in Yaws.

89
Q

What is the etiology of Bejel?

A

Bejel is caused by T. pallidum ssp. endemicum. The disease is typically acquired during childhood through direct transmission via the skin.

90
Q

What is the primary method for diagnosing Bejel?

A

Most cases of Bejel are diagnosed on the basis of clinical findings.

91
Q

What laboratory tests are used to diagnose Bejel?

A

Results of nontreponemal agglutination tests such as RPR and VDRL, as well as specific treponemal tests like TPHA, TPPA, and FTA-ABS, are positive.

92
Q

What are the expected epidermal changes in early lesions of Bejel?

A

In early lesions, epidermal changes such as hyperplasia and spongiosis are expected.

93
Q

What imaging findings are associated with Bejel?

A

Periostitis and bone involvement can be seen on radiographs, similar to findings in yaws.

94
Q

What is the recommended treatment for Bejel according to the WHO?

A

The WHO recommends 1.2 million units of benzathine penicillin for treatment of all stages in adults; half the dose is used in children younger than 10 years.

95
Q

What laboratory tests can confirm the diagnosis of Bejel?

A

Laboratory tests include RPR, VDRL, TPHA, TPPA, and FTA-ABS. The challenge is differentiating Bejel from venereal syphilis.

96
Q

What other findings are common in the tertiary stage of Bejel?

A

Other findings include gummas, destructive ulcerations, and nasal cartilage involvement leading to gangosa.

97
Q

What imaging findings are expected for a patient with saber tibias and nocturnal bone pain?

A

Imaging findings include periostitis and bone involvement, similar to Yaws.

98
Q

What is the treatment for gummas in the tertiary stage of Bejel?

A

Treatment is benzathine penicillin. The recommended dose for children under 10 years is 0.6 million units.

99
Q

What are the key diagnostic criteria for Bejel?

A

Bejel is primarily diagnosed based on clinical findings. The differential diagnosis with venereal syphilis can be challenging.

100
Q

What challenges are associated with distinguishing Bejel from venereal syphilis?

A

The challenge lies in similar positive test results, necessitating a thorough patient history.

101
Q

What are the typical pathological findings in cutaneous lesions of Bejel?

A

The cutaneous lesions typically show a superficial dermal lymphoplasmacytic infiltrate. Early lesions may exhibit epidermal changes such as hyperplasia and spongiosis.

102
Q

What imaging findings in Bejel are similar to those in Yaws?

A

Imaging findings in Bejel include periostitis and bone involvement, which are similar to findings seen in yaws.

103
Q

What is the recommended treatment for Bejel, and how does it differ for children?

A

The treatment of choice for Bejel is penicillin. The WHO recommends 1.2 million units for adults; for children under 10 years, the recommended dose is half.