Gram- Spirals Flashcards
List the Gram- Spirals.
Treponema pallidum
Borrelianburgdorferi
Outline features of T. Palladium
- Very delicate, easily killed by drying or heating at 42C for an hr.
- Antigenicity – 3 types of Antibodies are produced
- Non specific - Reagin Ab
- Group specific – found in T. pallidum & Reiter strains.
- Species specific – polysaccharide Antigen of T. pallidum
What are some symptoms of T. Palladium infection/disease it causes?
Causes Syphilis
Symptoms include:
Discoloured warts around genitals
Rashs around the body
Fever, chills, flu like symptoms, etc…
Explain the Pathogenesis of T. Palladium and VF
VF:
-Outer membrane proteins
-Virulent spirochetes produce hyaluronidase
-Coated with host cell fibronectin
- Sexually transmitted disease.
- Entry through abrasions on mucosa/ skin
- Incubation period (10 to 90 days).
- Infectivity maximal during first 2 yrs of disease
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4 Stages:
- Primary
- Secondary
- Latent
- Later Tertiary Stage
Primary Syphilis
- Enters host through break in skin/ penetration of mucous membranes in genitals
- Tissue destruction
- Microbial hyaluronidase destroys hyalurionic acid and glycosaminoglycan in ECM
Chancres
- form due to immune response
- Painless, avascular, ulcerated lesion covered in thick exudate rich in Treponema
- Heals in 10 -40 days
Secondary Syphilis
- Most infectious stage
- Sets in 2-6 months after primary lesion heals.
- Pt is asymptomatic but widespread dissemination occurs via blood
- Maculopapular skin rashes
- Mucous patches in the oropharyngeal area
Latent Syphilis
- Quiescent stage which follows secondary stage
- Serological proof of infection without signs or symptoms
Early (2 yrs or less) or Late (>2 years)
- Early latent syphilis is treated with IM injection of penicillin
- Late latent syphilis – 3 injections per week
- Late tertiary or quaternary syphilis –neurosyphilis: tabes dorsalis or general paralysis of insane
Discuss the methods of diagnosis/diagnostic tools to identify T. Palladium
Laboratory diagnosis of Syphilis
- Cannot be cultured - Does not grow on artificial media
Microscopy
- Dieterle Stain (uranium & Ag Nitrate) & Dark field
- Serology: Treponema pallidum particle agglutination assay
- Non specific test/ standard tests for syphilis (FTA-ABS)
- direct fluorescent antibody test- DFA-Tp
- fluorescein isothiocyanate (FITC)-conjugated monoclonal or polyclonal antibodies
Laboratory Host
- Virulent strains can be maintained in rabbit testis by serial passages
- Nichol’s strain – used for diagnosis & research
- Reiter’s strain – a non-pathogenic strain cultivated for diagnosis
Discuss the treatment options/prevention of T. Palladium
Screening
- All pregnant woman at first prenatal visit
- Individuals with other STDs
- High risk behaviours (drug use, prostitution, etc.);
- again at 28 weeks gestation if pregnant
Exposure
- Reporting of contacts and tracing of sexual partners
- Education
Treatment
- Patient and sexual partner(s) should be treated
- Antibiotic therapy
- Penicillin – preferred in pregnancy
- Doxycycline
- Tetracycline
Outline features of B. Burgdoferi
Morphology:
- Irregular/loose spirals
- 10-30 µm long x 0.3 µm
- Highly flexible
- Stain readily
- Larger than treponemes
Culture & growth characteristics
- Can be cultured in liquid media containing blood, serum, or tissue
- Multiplication is rapid in chick embryos
- Survives at 4C for months in infected blood or culture media
- Pass from generation to generation in some ticks, but not in lice
What are some symptoms of B. Burgdoferi infection/disease it causes?
Causative agent of Lyme disease
- Blood- transmitted by the bite of Ixodid ticks
- predominant in North America, but also present in Europe
- Characteristic rash BULL’S EYE
Symptoms include: insomnia, swollen joints, hearing loss, heart complications, etc…
Explain the Pathogenesis + VF of B. Burgdoferi
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Spirochete Morphology:
- Helical Shape: Borrelia species, including B. burgdorferi, are spiral-shaped bacteria called spirochetes. This unique helical morphology contributes to their motility, allowing them to move through various tissues and evade host defenses.
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Adhesion and Tissue Invasion:
- Outer Surface Proteins (Osps): Borrelia expresses a family of outer surface proteins, such as OspA and OspC, which play a role in adhesion to host cells and tissues.
- Tissue Tropism: Different Osps are expressed during various stages of the Borrelia life cycle, facilitating tissue invasion and adaptation to different host environments.
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Antigenic Variation:
- VlsE (Variable Major Protein-Like Sequence Expressed): Borrelia undergoes antigenic variation by changing the expression of VlsE. This helps the bacterium evade the host immune system by altering its surface antigens.
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Motility:
- Flagella (Periplasmic Flagella): Borrelia spirochetes have internal, periplasmic flagella that contribute to their motility. This motility is crucial for their ability to disseminate through tissues and reach different organs.
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Host Immune Evasion:
- Complement Evasion: Borrelia has developed mechanisms to evade the host complement system, which is a crucial part of the immune response. This includes binding to host complement regulators and avoiding complement-mediated lysis.
- Antigenic Variation: As mentioned earlier, antigenic variation, particularly in VlsE, helps Borrelia evade adaptive immune responses by changing its surface antigens.
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Biofilm Formation:
- Exopolysaccharides: Borrelia can form biofilms, particularly in the midgut of ticks. This biofilm formation may contribute to bacterial survival and persistence in the tick vector.
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Tick Saliva Interaction:
- Tick Saliva Proteins: During transmission from ticks to humans, Borrelia interacts with tick saliva, modulating the host immune response and potentially facilitating successful colonization.
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Inflammatory Response:
- Induction of Inflammation: The presence of Borrelia in tissues triggers an inflammatory response, leading to the characteristic symptoms of Lyme disease. This includes the erythema migrans rash, joint pain, and other systemic manifestations.
Discuss the methods of diagnosis/diagnostic tools to identify B. Burgdoferi
First test is and EIA or IFA, if positive result wait for symptoms, if symptoms appear in less than 30 days conduct IgM and IgG western blot if more than 30 days only IgG.
If first test is negative consider and alternative diagnosis.
CDC
Discuss the treatment options/prevention of B. Burgdoferi
- Early: Amoxycillin, tetracyclin, doxycyclin, cephalosporins
- Late disease: Ceftriaxone
