Difference between revisions of "Talk:Yaws"

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==Description of Yaws==
 
==Description of Yaws==
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The symptoms of yaws usually appear in 3 stages: primary, secondary, and tertiary. The primary stage involves the entry and initial development of <span style="font-style: italic;">T. pallidum pertenue</span>. The secondary stage is characterized by varying skin lesions and is highly infectious. Secondary lesions may go on to develop into tertiary stage, during which secondary lesions may come and go. <br />
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<span style="font-weight: bold;">Primary stage:</span><br />
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After an incubation period of <span style="font-style: italic;">T. pallidum pertenue</span> of approximately 3 weeks, the primary lesion (mother yaw) develops after a scratch, bite, or abrasion on exposed skin. The mother yaw develops a honey-brown crust and enlarges horizontally 1-5 cm in diameter. The crust hardens and then sloughs off and reveals a raspberry-like base. This raspberry-like base is filled with treponemes, making these lesions highly infectious. During this stage, infected persons may experience lymphadenopathy (swollen lymph nodes), fever, and joint pain. The mother yaw resolves spontaneously in 2-9 months, leaving an atrophic scar with central hypopigmentation and peripheral hyperpigmentation (10).<br />
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<span style="font-weight: bold;">Secondary stage:</span><br />
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About 6-16 weeks after the primary stage, an eruption of skin lesions, bone lesions, and constitutional symptoms appears. The cutaneous lesions (daughter yaws) resemble the mother yaw but are smaller (up to 2 cm in diameter) and are usually located next to the mouth and nose. The daughter yaws expand, ulcerate, and excrete a fluid swarming with treponemes, which dries into a crust. These bumps on the skin surface can form thick, hyperkeratotic plaques that may become fissured or eroded. Macular and hyperkeratotic lesions on the palms of the hands and the soles of the feet (similar to lesions found in syphilis patients) may also be present. Infected persons may also experience painful osteopetrosis (bone hardening). Some of these early bone changes can be observed on radiographs. Manifestations during this stage are generally non-scarring and reversible. Patients may develop relapses for up to 5 years after the initial infection. The disease then enters a noninfectious latent period where patients do not exhibit any signs or symptoms (10).<br />
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<span style="font-weight: bold;">Tertiary stage:</span><br />
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After 5-15 years of latency, a late stage develops and is characterized by destructive skin lesions, bone lesions, and possible neurological and ophthalmologic damage. Enlarging and painless subcutaneous nodules develop and undergo abscess formation, necrosis, and ulceration. Lesions have well-defined edges and an indurate base with granulation tissue and yellowish slough. The ulcers that develop in this stage may become infected and lead to devastating destruction of underlying structures. Furthermore, these ulcers may coalesce and form tracts that heal with keloid formation, which leads to crippling deformities and contractures (10). <br />
  
 
===Description of the microbe===
 
===Description of the microbe===

Revision as of 01:43, 28 August 2009

Introduction

Yaws is a bacterial infection that enters through an open lesion and affects the skin, bones, and joints of its host if left untreated. This infection is caused by a microaerophilic spirochete bacterium, Treponema pallidum pertenue, which flourishes in tropical regions with poor living conditions, such as India, Africa, and South America. Yaws was nearly eradicated in the mid 1900s, but has recently become a major problem in many countries, specifically, India. The ecological, governmental, and social aspects of India and the nature of the microbe itself contribute to the spread of the disease. 


Description of Yaws

The symptoms of yaws usually appear in 3 stages: primary, secondary, and tertiary. The primary stage involves the entry and initial development of T. pallidum pertenue. The secondary stage is characterized by varying skin lesions and is highly infectious. Secondary lesions may go on to develop into tertiary stage, during which secondary lesions may come and go.

Primary stage:
After an incubation period of T. pallidum pertenue of approximately 3 weeks, the primary lesion (mother yaw) develops after a scratch, bite, or abrasion on exposed skin. The mother yaw develops a honey-brown crust and enlarges horizontally 1-5 cm in diameter. The crust hardens and then sloughs off and reveals a raspberry-like base. This raspberry-like base is filled with treponemes, making these lesions highly infectious. During this stage, infected persons may experience lymphadenopathy (swollen lymph nodes), fever, and joint pain. The mother yaw resolves spontaneously in 2-9 months, leaving an atrophic scar with central hypopigmentation and peripheral hyperpigmentation (10).

Secondary stage:
About 6-16 weeks after the primary stage, an eruption of skin lesions, bone lesions, and constitutional symptoms appears. The cutaneous lesions (daughter yaws) resemble the mother yaw but are smaller (up to 2 cm in diameter) and are usually located next to the mouth and nose. The daughter yaws expand, ulcerate, and excrete a fluid swarming with treponemes, which dries into a crust. These bumps on the skin surface can form thick, hyperkeratotic plaques that may become fissured or eroded. Macular and hyperkeratotic lesions on the palms of the hands and the soles of the feet (similar to lesions found in syphilis patients) may also be present. Infected persons may also experience painful osteopetrosis (bone hardening). Some of these early bone changes can be observed on radiographs. Manifestations during this stage are generally non-scarring and reversible. Patients may develop relapses for up to 5 years after the initial infection. The disease then enters a noninfectious latent period where patients do not exhibit any signs or symptoms (10).

Tertiary stage:
After 5-15 years of latency, a late stage develops and is characterized by destructive skin lesions, bone lesions, and possible neurological and ophthalmologic damage. Enlarging and painless subcutaneous nodules develop and undergo abscess formation, necrosis, and ulceration. Lesions have well-defined edges and an indurate base with granulation tissue and yellowish slough. The ulcers that develop in this stage may become infected and lead to devastating destruction of underlying structures. Furthermore, these ulcers may coalesce and form tracts that heal with keloid formation, which leads to crippling deformities and contractures (10).

Description of the microbe

Treponema pallidum subspecies pertenue, the causative agent of yaws, cannot be distinguished by means of histopathologic, serologic, immunologic or therapeutic methods from other treponemal bacteria such as Treponema pallidum subspecies pallidum, which causes syphilis and Treponema pallidum subspecies carateum, which causes pinta (16). These treponematoses are only differentiated by mode of transmission, and the clinical criteria and infection of laboratory animals and humans (16). However, a recent study discovered an antigenic difference established by a single amino acid residue at position 40 in the proteins, namely glutamine in TpF1 of subspecies pallidum and arginine in TyF1 of subspecies pertenue (8).

Treponema pallidum is a spirochete bacterium — spiral-shaped with outer and cytoplasmic membranes and a thin peptidoglycan layer. It has periplasmic flagella (or endoflagella), which lie in the periplasmic space and expand from both ends toward the middle of the organism. The flagellar filament has a sheath and core structure, and is composed of at least four major polypeptides (15). T. pallidum contains at least eight major membrane-associated lipoporoteins. The small number of intramembranous protein particles (~70 per mm2) in the outer membrane contributes to its unusual structure compared to other spirochetes and gram-negative bacteria that possess sevenfold the amount of protein. The sparsely distributed and uniformly sized outer membrane particles indicate that there are few different types of protein in the outer membrane. It is hypothesized that the low concentration of surface-exposed protein antigens decrease the reactivity of antibodies and immune cells enabling T. pallidum to avoid immune response, thus causing its pathogenesis (15).

T. pallidum was recently discovered to be a microaerophilic organism with a doubling time greater than 30 hours. Its slow growth and fastidious character in vivo and in vitro suggest that it may have metabolic limitations and growth requirements yet to be identified (15). However, previous studies indicate that it is capable of glucose metabolism and the synthesis of DNA, RNA, and protein. T. pallidum is a parasite and depends on host cells for protection against oxygen radicals because the bacterium need oxygen for metabolism but are highly susceptible to its toxicity (15).

Transmission of disease

How is it transmitted? Is there a vector (animal/insect)?

Prevention

Why is this disease a problem in [name of country]

What is being done to address this problem

Include anything being done by the local government or groups as well as efforts by non-local groups.

What else could be done to address this problem

Are there solutions that could be successful but haven't been implemented due to political or economic reasons? Are there successful efforts in other countries? Are there reasons why these efforts may or may not be successful in the country you've focused on? etc. etc.

References

[Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.

Edited by [insert your names here!], students of Rachel Larsen



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