Bacterial/Parastitic Lecture Flashcards
Prokaryotes
No membrane bound nucleus
Gram staining
Gram positive: thick cell wall of peptidoglycan
Gram negative: peptidoglycan sandwiched between two membranes
Classification
Shape
Anerobic/anaerobic
Mechanisms of bacterial injury
Adhere to host cells, invade or deliver toxins
Virulence genes confer these properties
- Pathogenicity island (genes are bound together)
Biofilms
Within extracellular polysaccharides that adhere to host tissues or devices as catheters
Makes them inaccessible to immune systems
Adhesins
Surface molecules on bacteria that bind to host cells
Entry into host?
Opsonization (coated with antibody and taken in) and phagocytosisinto macrophages
Inside the host?
Replicate, inhibit host protein synthesis, lyse hotst cells
Bacterial toxins?
Endotoxins (components of bacterial cells):
Lipopolysaccharids (gram - bacteria) which activate protective immunity but can cause septic shock
- Exotoxins (secreted by bacteria): enzymes, intracellular toxins and neurotoxins (superantigens)
Injurious effects of host immunity?
Granulomatous reaction in TB (tries to engulf the bacteria but it is hypersensitive so you have huge influx of macrophages that form granulomas)
Antibodies react against strept proteins begin to act against heart
Poststrep glomerulonephritis
— Type 3 hypersensitivity (lots of antibody/antigen complexes forming) deposit in the joints
Gram Positive Bacterial Infections
Diptheria Listeriosis Anthrax Streptococcal infection Staphylococcal Infections
Diptheria
corynebacterium diptheriae
- Produce toxin that blocks host cell protein synthesis
- Immunization: protects against leathal effects of toxin
- EF2 (elongation factor): conversion from RNA to protein is blocked
Listeriosis
Listeria monocytogenes
Food borne
Causes menigitis
ACTA: allows it to escape the lysosomes and move to adjacent cells
IFN-gamma activates macrophages to phagocytose and kill bacteria
- Internalins + E-cadherins: internalization
Anthrax
Bacillus anthracis
Has a polyglutamyl capsule: prevent anthrax toxins
Two parts: can’t act without B
Heptamer: interacts with edema factor or lethal factor –» forms an acidic pH
Edema fact: interacts with calmodulin convert AMP to cAMP causing water efflux leading to edema
Lethal factor: protease that works on MAPK and causes cell death
Steptococcal infections
Rheumatic fever, glomerulonephritis
Pneumonia and meningitis
Dental caries
Rheumatic fever, glomerulonephritis
S. pyogenes
Pneumonia and meningitis
S. pneymoniae
Dental caries
S. mutans
Staphylococcal infections
Multiple toxins and enzymes
Superantigens
Antibiotic resistance
Multiple toxins and enzymes
S. aureus
Superantigens
Huge release of antigens causing shock
S. aureus and S. pyogenes
Antibiotic resistance
MRSA
Methicillin resistance
Gram negative bacterial infections
Neisserial Infections Whooping Cough Pseudomonas Infections Plague Chancroid Granuloma Inguinale (donovanosis)
Neisserial Infections
N. menigitidis and V gonorrheae
Whooping cough
Bordetella pertussis
Inspiratory whoop
PCR
Infects bronchial epithelium and macrophages
Pertussis toxin- paralyzes the respiratory cilia –> inactivates G proteins
Whooping Cough mechanism
Virulence factors: BVGS is activated and phosphorylates BVGA
BVGA regulates transcription of mRNA for adhesions and toxins
Necrotizing pneumonia
Pseudomonas aeruginosa
Plague from human by fleabites
Yersinia pestis
Chancroid: acute sexually transmitted ulcerative infection
Hemophilus ducreyi
Granuloma Inguinale (Donovanosis): inflammatory disease
Klebsiella granulomaris/calymmato-bacterium donovant
Myobacterial Infections
Slender aerobic rods
Mycolic acid in cell wall- acid fast (retains even with acid or alcohol)
TB
Leprosy
Tuberculosis
TB Mycobacterium TB Myobacterium bovis HIV = immunocompromised Infection: leads to delayed hypersensitivity to M tuberculosis antigens TB skin test
TB skin test
Won’t work 0-3 weeks
3+ weeks: IFN-gamma works on activated macrophages and breaks down bacterial genomes; creates TNF which works against TB
Leprosy
Mycobacterium leprae
- Obligate intracellular bacteria
- Two forms: tuberculoid and lepromatous/anergic (severe)
- People with robuts Th1 response (tuberculoid)
- Lepromatous leprosy – weak Th1 response
Spirochete infections
Syphilis and lyme’s disease
Syphilis
Treponema pallidum subsp. Pallidum Sexual contact Congenital syphilis (transplacental) Immune response to the spirochete - controls it but accounts for pathology - Jerisch-Herxheimer reaction
Herisch-Herxheimer reaction
You give antibiotics to a patient with high bacterial contents, you have high flow of exotoxins with will release a lot of cytokines leading to shock
Lyme disease
Borrelia burgdorferi
Transmitted by ixodes deer ticks
Stages of Lyme disease
Stage 1: acute illness- tick bite
Stage 2: dissemination - demyelination, heart block
Stage 3: late chronic form - arthritis
Anaerobic bacterial infections
Can cause abscessess
- Head and neck with facultative aerobic bacteria
Closterdial infections
C perfringens and C speticum
cellulitis and myonecrosis of woulds
C. botulinum
Blocks neuromuscular transmission by blocking release of ACh- sever paralysis
C. tetani
tetanus
Violent spastic paralysis – block GABA release
C. difficile
colitisis
Obligate intraceullular bacterial infections
Proliferate only within host cells
Chlamydial Infections
Chlamydia trachomatis
Elementary body (inactive) Reticulate body (active)
Genital infection
STD with gonorrohoea
Riskettsia prowazekii
epidemic typhus
Orienta tsutsugamushi
scrub typhys
Rickettsia tickettsii
Spotted fever
Ehrlichia ewingii
Infect neutrophils
Ehlichia chaffeenis
Infect macrophages
Richettsial infections
Enter and lyse the endothelial cells- hypovolemic shock, edema
- Mediated by NK cells and CTLs
Protozoal infections
Unicellular eukaryotic organisms Microscopic exams Malaria Leishmaniasis African Trypanosomiasis Chagas Disease
Malaria
Plasmodium falciparum Mosquito Anemia Cerebral malaria RBCs clump causing ischemia --> cerebral malaria
Leishmaniasis
Chronic inflammation
Promastigote (extracellular) and amastigote (macrophages)
Promastigotes injected by bite, phagocytosed by macrophages and the acidity of the phagosomes convert them to amastigotes
Amastigotes multiple and are released from macrophages –> infect more
Promastigotes
for virulence: lipophosphoglycan and gp63
- Lipophosphoglycan: activates and inhibits complement
GP63: promotes promastigote adhesion to macrophages
— Parasite specific CD4 response (AIDS)
African trypanosomiasis
Trypanosoma brucei rhodesiense
Trypanosoma brucei gambiense
Chagas disease
Trypanosoma cruzi
Brief exposure to acidic phagolysosome to develop into the amastigotes
- Amastigotes develop flagella, lyse host cells, enter bloodstream and penetrate smooth, skeletal and heart muscles
– Cardiac damage, inflammation
Chagas autoimmune mechanism?
Cross react with host cells and extracellular proteins such as laminin
Metazoal infections
Multicellular eukaryotic organisms
Microscopic examination of tissue and serology
Schistosomiasis
Lymphatic filariasis
Schistosomiasis
Schistosoma mansoni, S. Japonicum, S. mekongi
Snails
Eggs in circulation cause inflammation –> granuloma formation and hepatic fibrosis
TH1 and TH2 mediated immune response
— excessive immune response
Lymphatic filariasis
Mosquitos
Wucheria bancorfti and brugia malayi
Category A
Highest risk, person to person, high mortality
Small pox, anthrax
Category B
Moderate morbidity, low mortality
Typhys fever
Category C
Engineered pathogens for mass dissemination
High damage potenial
Nipah virus and hantavirus
