Gram- Cocci Flashcards
Name/list Gram- Coccid pathogens.
Chlamydia trachomatis
Rickettsia rickettsia
Neisseria gonorrhoea
Neisseria meningitis
Outline features of C. Trachomatis.
- Obligate, aerobic intracellular parasites, coccoid/rod.
- Cell walls of Gram –ve bacteria, but lack muramic acid & PG.
- Energy parasites that use ATP produced by the host cell.
- A Giemsa stain can be used to visualize chlamydial inclusions in tissues.
- Chlamydia trachomatis is a non-motile STI.
- Have Elementary Bodies & reticulate bodies.
- First cultured in yolk egg sacs in 1957(because it could not be grown on agar this more suitable to infect cell culture)
Three Biovars (???)
- Ab, B, Ba, or C – cause trachoma, inclusion conjuctivitis
- D-K –urethritis, PID, ectopic pregnancy, infant pneumonia
- L1, L2, and L3 – lymphogranuloma venereum (the most serious)
- Reiter’s Syndrome (reactive Arthritis)
- Plastic genome!- extrachromosomal plasmid
What are some symptoms of C. Trachomatis infection/disease it causes?
Painful urination, fever, pus, fatigue, etc…
C. Trach causes chlamydia (STD)
Explain the Pathogenesis of C. Trachomatis & VF
Chlamydiae are obligate intracellular bacteria. They lack several metabolic and biosynthetic pathways and depend on the host cell for intermediates, including ATP. Chlamydiae exist as two stages: (1) infectious particles called elementary bodies and (2) intracytoplasmic, reproductive forms called reticulate bodies. (DRAW FROM NOTION)
- LPS Membrane with no peptidoglycan (beta lactam resistance)
- Cysteine-rich proteins inhibit phagolysosome fusion.
- LPS can cause shock.
- Antigenic variation
- Adhere to sialic acid receptors on mucous membranes
- It sticks on sites where phagocytes, B cells and T cells cannot access
- Pathogenicity Islands encode projection (injects proteins into cell cytoplasm- avoids lysosomes)
- Intracellular replication
- Survival of infectious EBs as a result of cross-linkage of membrane proteins.
Discuss the methods of diagnosis/diagnostic tools to identify C. Trachomatis
Agar: NO
Haemolysis: ?
-Obligate, aerobic intracellular parasites
-Gram- coccoid/rod (Cell walls of Gram –ve bacteria, but lack muramic acid & PG)
OTHER DIAGNOSTIC METHODS (+PROS/CON)
-Giemsa stain can be used to visualise chlamydial inclusions in tissues.
-Direct fluorescent antibody (DFA)
-NAATs- Gold Standard
Biochemical tests: ?
Discuss the treatment options/prevention of C. Trachomatis
Treatment
-Azithromycin
-Erythromycin
-Doxycycline
Outline features of R. Rickettsia
- Obligate intracellular parasites (almost virus-like) which infects capillary cells & Insect Vectors.
- Defective bacteria - leaky plasma membranes.
- Gram –ve very small 0.3-1.0 µm.
What are some symptoms of R. Rickettsia infection/disease it causes?
Typhus fever group
- Epidemic typhus/Brill-Zinsser typhus - Rickettsia prowazekii
- Endemic typhus
Spotted fever group
- Rocky Mountain spotted fever (Rickettsia rickettsia)
- Siberian tick typhus Rickettsia sibirica
Symptoms/complications:
-Bronchopneumonia
-Congestive heart failure
-Multi-organ failure
-Deafness
-Disseminated intravascular coagulopathy (DIC)
Explain the Pathogenesis of R. Rickettsia.
Rickettsiae are transmitted to humans by the bite of infected ticks and mites and by the feces of infected lice and fleas. They enter via the skin and spread through the bloodstream to infect vascular endothelium in the skin, brain, lungs, heart, kidneys, liver, gastrointestinal tract, and other organs. Rickettsial attachment to the endothelial cell membrane induces phagocytosis, soon followed by escape from the phagosome into the cytosol. Rickettsiae divide inside the cell.Rickettsia prowazekiiremains inside the apparently healthy host cell until massive quantities of intracellular rickettsiae accumulate and the host cell bursts, releasing the organisms. In contrast,R rickettsiileaves the host cell via long, thin cell projections (filopodia) after a few cycles of binary fission. Hence, relatively fewR rickettsiiorganisms accumulate inside any particular cell, and rickettsial infection spreads rapidly to involve many other cells. Perhaps because of the numerous times the host cell membrane is traversed, there is an influx of water that is initially sequestered in cisternae of cytopathically dilated rough endoplasmic reticulum in the cells more heavily infected withR rickettsii.
Discuss the methods of diagnosis/diagnostic tools to identify R. Rickettsia
Agar: ?
Haemolysis: ?
-Obligate intracellular parasites (almost virus-like)
-Infects capillary cells & Insect Vectors
-Defective bacteria - leaky plasma membranes,
-Gram –ve very small 0.3-1.0 µm
OTHER DIAGNOSTIC METHODS (+PROS/CON)
-Microscopy Geimsa stain - pleomorphic coccobacillus
-Isolated from experimental animals
-Serology(used very often)
Discuss the treatment options/prevention of R. Rickettsia
Treatment & Prophylaxis of Rickettsia
-Treatment should be started early in the first week of illness.
-Doxycycline (first choice)
-Tetracycline (alternate)
Vaccines
-Live vaccine & killed vaccine are available but not very effective.
Discuss general information on Nisseria.
-Gram –ve cocci, non-motile, aerobic bacteria often arranged as diplococci.
-Oxidase positive
Neisseria generally are very exacting in their nutritional requirements. They require enriched media (chocolate blood agar) + extra CO2.
(N. gonorrhoeae being more exacting than N. meningitidis)
Selective medium is:
-Thayer Martin medium
-Chocolate blood agar
-V.C.N.T
- Vancomycin
- Colistin
- Nystatin
- Trimethoprim
Outline features of N. Gonorrhoea
Neisseria gonorrhoea is an obligate pathogen with invasive infection of anogenital, oropharyngeal, and conjunctival mucous membranes.
- Neisseria gonorrhoeae, also known as gonococcus, or gonococci, is a species of Gram-negative diplococci bacteria.
- This bacteria has long Fimbriae (Type IV Pili-STRONG) which also assists in biofilm formation.
- Transmitted via sexual contact, ocular during birth.
- A highly plastic genome acquires and spreads new genes.
- AMR resistant strains:
- “Super gonorrhoea”
What are some symptoms of N. Gonorrhoea infection/disease it causes?
BOTH
- Maybe asymptomatic.
- Urethritis(i.e. discharge of pus)
IN MEN:
- Inflammation & infection that extends along the urethra.
- Abscess and multiple discharging sinuses.
IN WOMEN:
- Vulvovaginitis.
- Salpingitis.
- Pelvic inflammatory disease.
Explain the Pathogenesis of N. Gonorrhoea + VF
- Acquired through sexual contact
- Establishes infection in the urogenital tracts
- Interacts with non-ciliated epithelial cells
- Infection leads to inflammation and PMN leuk. influx
- lower female genital tract is typically asymptomatic.
- N. gonorrhoeae engulfed by PMN are secreted in PMN-rich exudate.
- TNF from phagocytes and peptidoglycan and LPS
- Causes toxic damage to ciliated epithelial cells
(DRAW FROM NOTION)
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Pilin Antigenic Variation:
- Type IV Pili: Neisseria gonorrhoeae uses Type IV pili for adhesion to and colonization of host mucosal surfaces. These pili are hair-like appendages on the bacterial surface.
- PilE Gene Variation: The gene encoding the major subunit of Type IV pili is called pilE. Neisseria gonorrhoeae has a repertoire of pilE alleles (variant forms of the pilE gene), and only one allele is expressed at a time.
- Switching Expression: The bacterium can switch the expression of different pilE alleles through a process known as pilin antigenic variation. This involves the recombination of pilE alleles into the expression locus, leading to the production of pili with different antigenic properties.
- Escape from Immune Recognition: As the bacterium changes the expression of pilin variants, it can escape recognition by the host immune system. This continual alteration in the surface antigens helps Neisseria gonorrhoeae evade the host’s adaptive immune response, including antibody-mediated immune recognition.
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Immunoglobulin A1 (IgA1) Protease:
- Function in Antigenic Variation: IgA1 protease is another virulence factor in Neisseria gonorrhoeae that contributes to immune evasion.
- Cleavage of Antibodies: IgA1 protease cleaves immunoglobulin A1 (IgA1), an antibody that is present in mucosal secretions and plays a role in immune defense.
- Reduction of Antibody-Mediated Immunity: By cleaving IgA1, the bacterium can reduce the effectiveness of antibody-mediated immunity, aiding in the evasion of the host’s mucosal immune defenses.
