Bacteriology II PDF

Gram - LPS- endotoxin (structure is triggering the response) ○ Sepsis (damaging, over-reactive immune response) Especially with bacteremia (bacteria in blood) Thin peptidoglycan doesn’t bind to stain Gram Negatives: Many uses capsules Endotoxins (sepsis)...

Gram - LPS- endotoxin (structure is triggering the response) ○ Sepsis (damaging, over-reactive immune response) Especially with bacteremia (bacteria in blood) Thin peptidoglycan doesn’t bind to stain Gram Negatives: Many uses capsules Endotoxins (sepsis) Secretion systems Many have flagellas (movement) 3 major antigens ○ O=somatic, K= capsular, H (H=flagella) O and H used for typing Phase variation Gram (-) diplococci Coccus (pink coloration in gram stain) Genus: Neisseria ○ Gonorrheae ○ Meningitdis Epidemiology Only in humans Virulence factor: N. gonorrheae and N. meningitis ○ Pili (exists outside of cell; hollow tubes that allow material in and out of cell) Attachment (suction cup on the end of tubes) Transfer of DNA (hollow tubes allow the transfer of DNA, giving DNA to other bacteria, toxin and drug resistance) Motility (can physically move short distances around body) ○ Porin proteins Block neutrophil function (block it from killing bacteria) Cell invasion ○ IgA protease (found on mucosal surfaces) ○ avoid lysosomes (no degradation in phagocytosis) N. Meningitdis ○ Capsule (make it slippery and unlikely for macrophages to phagocysize) Gonorrheae: Disease: Some individual are asymptomatic ○ Ping pong effect (get it again if partner doens’t get treated; does get worse for repeatedly infected individuals) When we have asymptomatic individuals, theres a change of reinfection  Asymptomatic people serve as a harbor for disease Transfer higher male→ female, male→male Oral infections Rare cases→systemic (joint infection)- bacteria moving away from oral and vaginal area Chronic infection→sterility Tranmission Sexual transmission -gonorrheae in the eye Birth Treatment Antibiotic ○ Resistance Prevention: Safe sex Education Birth preparedness Meningitidiis Disease: Some individuals are asymptomatic ○ Symptomatic is immunosuppressed (controlling of bacteria) Normally respiratory infection ○ Cough, chest pain Rare systemic infection: ○ Meningitis Toxic shock Treatment Antiobiotics ○ Resistance Prevention: Vaccine ○ Some strains (capsule) building antibody toward structure to result in opsonization for degradation of bacteria Gram (-) Coccobacilus Genus: Haemophilus Bordetella Haemophilus genus Influenzae Epidemiology:  Faculative anaerobic Fermentative Normal flora (certain genes turned in and certain turned off in certain conditions) ○ Lack capsule Virulence factor: Capsule Adhesion ○ Impaire ciliary function (damages respiratory tract) IgA proteases - IgA produced is broken down and unable to carry out function Transmission: Respiratory Treatment: Antibiotics ○ Not resistant Prevention: Vaccination ○ Capsule (not going to affect normal flora) Bordetella Pertussis ○ Whooping cough (making a comeback) Epidemiology Strict aerobe Mostly restricted to humans Virulence factor: Adhesions (hard for us to remove bacteria from respiratory tract) Exotoxin ○ Local toxin Block ciliary action (preventing movement) Tissue damage (specifically lung; prevent uptake of O2) => worrying about secondary infection (bacteria getting in to tissue damaged) ○ Systemic toxin Pertussis toxin Interfere with signaling pathways resulting in higher amount of respiratory secretion and mucus production (mucus high in bacteria) Sep 27, 2024 Why is whooping cough dangerous from a public standpoint? Asymtomatic: you’re spreading it when you don’t know you’re sick You don’t know when people are infected when they have already spreaded it Also happened with COVID Transmission Respiratory Coughing (masks preventing transmission) Treatment: Antibiotic ○ Not a lot of resistance (good) Prevention Vaccination: ○ Pertussis toxoid + other B. pertussis antigens ○ DPT/DTap => use whole inactivated/ uses few antigens, doesn’t work well or last as long Gram (-) rods: LPS still there Genus: Echerichia Salmonella Shingellla Legionella Yersinia Pseudomonas Echerichia Genus E. coli (ground beef) Gram Negatives: Many uses capsules Endotoxins (sepsis) Secretion systems Many have flagellas (movement) 3 major antigens ○ O, K, H (H=flagella) O and H used for typing Phase variation (most bacteria are able to do to stay ahead of immune system; changes epitope antigens produced are targeting; contain many outer proteins they can use; immune system is constantly catching up to these epitope changes)  Epidemiology: Normal flora ○ Humans and animals ○ Opportunistic infections (only bad when it gets in the wrong place; need e.coli, it does stuff for us but ONLY IN THE GI TRACT; if out, it gets dangerous) ○ Acquired additional genes (toxins and antibiotic resistance) Plasmids Transduction E.coli induced gastroenteritis Organism abbreviatio Site of infection Mechanisms Disease n Enterotoxigenic ETEC Small intestine Heat stable and heat liable Travelers diarrhea (local people are naturally immunized) Enteropathogenic EPEC Small intestine Plasmids encoded virulence Malabsorption and diarrhea factor that result in microvilli damage (causes disease) Pick up plasmids Enteroaddregative EAEC Small intestine Plasmid encoded virulence Malabsorption, diarrhea and factor that result in E. coli hemorrhaging aggregates, induce microvilli enteroinvasive EIEC Large intestine Plasmid encoded virulence Malabsorption, diarrhea and factors that result in hemerrhaging epithelial cell Shiga STEC Large intestine EPEC+ shiga toxin Malabsorption, diarrhea and toxin-producing hemerrhaging e.coli (O157 H7) -defining which O and H antigen it has What is causing the diarrhea/hemorrhaging? In healthy, epithelial cells have villi that increase surface area that allows you to acquire more nutrients The first damage that can happen is taking away these fingers (villi) that can decrease it’s ability to absorb these nutrients The next level is breaking the tight function that is breaking the cells together. The tight junction disables cells to go between tissue. When you have toxins that causes the tight junction to go away, things can go in and out freely. Fluid is going out making diarrhea watery. E. coli with flagella can go inside body. If there is internal damage, blood can go out hence hemorrhaging. Other sites of infection: UTI (fecal contamination) Neonatal meningitis (with certain types) => vaginal area, if it gets to the brain bad things happen (rare) Transmission: Fecal-oral ○ Fecal contamination Seen more in food, especially cows (O157 H7) does nothing to the cow In slaughtering the cow, if the knife knicks the GI tract, there’s contamination on the knife getting into the meat Treatment: Mild cases: ○ Self limiting or commensal (symbiotic relationship, becomes normal flora) Severe cases ○ Antibiotics (able to explode e.coli that can release toxins making it more damaging) ○ Risks: antibiotic-induced sepsis (aka antibiotic-induced toxic shock) Prevention: Minimize exposure ○ Hygiene ○ Cooking food properly E.coli is mostly on surface Safe with steak because there’s less outer surface Not safe with ground beef because there is MORE outer surface Salmonella Genus: Enterica** Typhi Epidemiology/ transmission Enterica ○ Contaminated food Poultry, eggs, and dairy No disease in other animal host (natural host-where pathogen can exist but not cause disease)=> normal flora in these animals ○ Fecal-oral Typhi ○ Restricted to humans ○ Fecal-oral ○ Asymptomatic colonization (carriers) Typhoid mary:  ○ A cook and when she was cooking food she would have her dirty hands in it and infect everyone Virulence factor: Enterica and thyphi ○ Replicate and endocytic vesicle No fusion to lysosome (able to replicate inside macrophages) Regulated genes in pathogenicity island (collection of genes located together carrying out a certain function) Series of regulated genes usually found in genome, sometimes in plasmids that contain virulence genes Typhi ○ Replication and macrophages (get outside of GI tract) Uses macrophages as a way to move around the body Disease: Enterica ○ Nausea, vomiting, nonbloody diarrhea Typhi ○ Asymptomatic ○ Nausea, vomiting, nonbloody diarrhea ○ Septicemia: systemic (usually childern and immunocompromised) Taraphoid fever Milder version Typhoid fever More severe Only when you don’t have healthy immune system Treatment GI=> gets to other locations when outside GI tract ○ Self limiting Septicemia (blood poisoning) or carrier ○ Antibiotics Prevention: Minimize exposure ○ Cooking food properly=> raw chicken on a cutting board and cross contamination ○ Hygiene => washing hands ○ Endemic areas=> location where this bacteria is constantly spreading Vaccination (typhi) Only utilize when people are going to an endemic area  Oct 2, 2024 Shigella Dysenteriae Epidemiology Restricted to humans Transmission Fecal-oral contamination ○ Most common in children ○ Not usually via water supply Virulence factors: Induce phagocytosis=> wants to be acquired into macrophages and reproduce, hides from immune system (antibodies are unable to bind) ○ Replicate cytoplasm ○ Induce apoptosis => cell dies, releasing bacteria doing damage (finding more macrophages), using our own cells against us “Shoot” themselves into neighboring cells=> one cell infected, this bacteria will shoot itself into another cell Exotoxin (Shiga toxin) ○ A-B type (5 B units form complex to allow A entrance) Blocks translation=> death of cell Disease: Diarrhea, bloody stools, abdominal cramps Treatment: Self-liming (good immune system) Prevention: Hygiene (prevent fecal contamination) Legionella Pneumophila (pneumonia) Epidemiology: Obligate aerobe (has to have O2 to survive) Often associated with contaminated water supply lines (dangerous with those with weakened immune system) ○ Air conditioners, ice machines, hot tub etc. Disease: Respiratory infection ○ Mild: Pontiac fever ○ Severe pneumonia- legionnaires disease Virulence factor: Grow in ameba (water, by living in ameba, its a way for it to grow/reproduce in water) and alveolar macrophages=> good at living in cells especially macrophages in lung LPS mediated damage=> our reaction to LPS (endotoxin) Resistant to typical intracellular defenses=> living in cells and cell have no way to destroy it  Resistant to typical cleaning agents ○ Bleach => doesn’t kill legionella Transmission Contaiminated water ○ Usually mist or ice Treatment: Antibiotics=> catching it early Prevention: Resistant to typical cleaning agents ○ Bleach Filters Yersinia Petis (aka bubonic plague) Epidemiology Natural host: rats (asymptomatic) Zoonotic infection (humans dead and end host) Disease: Rapid onset (less than a week) ○ Bubonic plague Bacteremia ○ Pneumonic plague Pneumonia Virulence factor: Resistance to phagocytic killing Cytotoxin ○ Disrupt actin filament=> important in movement of material within cell ○ Suppress cytokine production=> recruitment of adaptive and innate cells Plasmid encoded ○ Capsule=> hard for macrophages to pick up ○ Complement degrading genes=> MAC aren’t forming Transmission Fleas Pneumonic ○ Person- to person Treatment: antibiotics Prevention rodent/flea control Pseudomonas Aeruginosa Epidemiology: Moist environment ○ Soil, vegetation, water ○ Hospitals Equipment, fixtures Minimal growth requirements ○ Requires little Carbon and Nitrogen ○ Grows 4℃ to 42 ℃ Virulence factor: (no not need to remember but it basically have every bad thing) Biofilms Capsules Adhesions Exotoxins ○ Block proteins synthesis Pigments ○ Toxic forms of oxygen ○ Stimulate cytokines Enzymes ○ Lipases ○ Elastes ○ Break down complement ○ Inhibit neutrophils Disease: High prevalence in individuals ○ Cystic fibrosis ○ Immunocompromised ○ With burns ○ On broad-spectrum antibiotics Disease: Bronchial infection ○ Range of diseases Asymtomatic=> inflammation=> necrotizing bronchopneumonia Skin infections UTI Ear infections (swimmer's ear) Corneal ulcers Bone infection/bacteremia Oct 4, 2024 Transmission: Contact with pseudomonas contaminated material (potted plants=> soil) ○ Fomites Treatment: Antibiotics ○ Requires combination therapy => due to the amount of resistance Intrinically resistant to many antibiotics Poor uptake of many antibiotics=> bacteria must take up antibiotics Regulated resistance genes=> provide antibiotic resistance Additional resistance Plasmids transduction=>resistance genes Prevention Hygiene ○ Sterilizing equipment Gram-negative curves (vibrios, commas) Many uses capsules Endotoxins (sepsis especially with bacteremia) Secreation systems Many have flagellas (motile) 3 major antigens ○ O, K, H Genus: Vibrio Campylobacter Helicobacter Vibrio Cholera Epidemiology: Found in water and shellfish ○ Grow in water=> doesn’t need a host, reproduces by itself (becoming a problem) ○ Grows from 14℃- 40℃ (wide range of temp) Flagella positive (able to move around in natural habitat, when get into us, it can migrate into us) Requires high dose to infect Facultative anaerobe (presence and absence of O2) Virulence factor: Pilus (move and release things to extracellular environment) ○ Pathogenicity island => cluster of genes ○ Toxin regulated expression => isn’t always expressed, not much intoxication Exotoxin (cholera toxin) ○ Transduction acquires=> make things go from bad to worse Other toxins (can cause diseases in the absence of Cholera toxin) Exotoxin (cholera toxin) ○ Results in cell releasing Na, H2O, Cl- ○ Loss of material that results in diarrhea Disease: Without vibrio toxin ○ Diarrhea, vomiting With vibrio toxin ○ Diarrhea, vomiting ○ Severe dehydration, metabolic acidosis hypokalemia (low K) and hypovolemic shock (blood/fluid loss resulting in lack of blood flow) Transmission: Fecal-oral ○ Water contamination Treatment: Fluid and electrolyte replacement antibiotics Prevention: Sanitation (water quality) Campylobacter Jejuni Epidemiology Normal flora ○ Poultry => doesn’t do anything in poultry, dangerous in us ○ Zoonotic infection=> severe disease is from our immune response to bacteria Disease Usually ○ Diarrhea, abdominal pain Rare (immune-mediated) ○ Reactive arthritis ○ Guillian-barre syndrome=> autoimmune response Affects neuronal tissues Virulence factor Molecular mimicry: (idea that the antigen from pathogen look a lot like our own: immune system can do nothing (bacteria win) or immune system attack self (specifically nerve cells) ) ○ Guillian-barre syndrome  Immune system attacks peripheral nerves Transmission Contaminated food ○ In slaughtering, there's contamination from Gi tract to muscle Treatment GI infection ○ Self-limiting ○ Fluid and electrolyte prevention Cooking food Helicobacter Pylori Epidemiology Restricted to humans Disease: Asymptomatic infection (~90%)=> can still spread, bacteria will not go away Symtomatic (~10%) ○ Chronic infection ○ Gastritis, ulcers Immune-mediated? Don’t know if it is from bacteria or the immune system (acidic stomach) Virulence factor Motility => make small ulcers and burry itself in the ulcers to thrive and neutralize pH Urease activity (increase localized pH) Adhesion proteins => staying on cell Exotoxin O antigen look like human blood type O sugar => molecular mimicry; our system won’t attack this bacteria because it doesn’t attack O type Transmission Fecal-oral Treatment: Proton pump inhibitors (falling out of favor) Antibiotics ○ Resistance Prevention: Hygiene Oct 7, 2024 Spirochetes (cork screw pasta) Stain gram (-) but lack many LPS ○ Gram (-) or gram neutral Pink from thin pepti. Genus: Borrelia Treponema Borrelia: Burdorferi ○ Lyme disease Epidemiology Endemic in mice and deer in the US => utilizing ticks to move from one host to another (us) ○ Northwest- mid Atlantic ○ Upper midwest - not a lot in Iowa Different insect species in different areas of the US Zoonotic infection (humans dead end host) Insect vector: replicate in both mammals and insects Different genes expressed in different hosts/ different with host **Bullseye rash occur for Lyme disease*** Virulence factor: ??? don’t no why it causes that disease No identifiable toxin Antigenic (phase) variation of outer proteins => ○ Immune evasion Immune system recognize outer proteins and create antibodies but antigen changes the outer membrane (epitope) (cat and mouse effect) Disease: Erythema migrans (bullseye rash) 60% joint arthritis (esp. knee) => replication, harder to get antibodies to penetrate 10-20% neurological manifestations (palsy) 5% cardiac complication Transmission: Ticks, infected animals ○ Usually in the summer (tick feeding) Treatment: Antibiotics ○ Challenge to completely clear Prevention: Tick control Treponema Pallidum ○ Syphillus Epidemiology Only found in humans Virulence factor: Adhesions (stick to things) Most damage immune mediated Disease tertiary: tissue/ organ destruction => come from immune response creating damage ○ Blindness, dementia ○ Neurosyphilis, cardiovascular syphilis Transmission: Sexual transmission In utero => able to cross placental barrier ○ Birth defects or lethal to fetus Prevention Safe sex Education STD: Multiple infections ○ Treatment Not dealing with a single entity Obligate intracellular bacteria replication can ONLY take place inside a host cell ○ Not environment Gram (-) rods Rod like shape Have LPS Genus: Chlamydia Rickettsia Chlamydia Trachomatis Epidemiology Human host ○ Infected mucosal epithelial cell Virulence factor: Cell lysis => breaking down cell membrane to release contents ○ Trigger damaging immune response Forms to replicate and transmit ○ EB= elementary body (spore like)- inert form, stable in the environment  The spread of new cells and other individuals ○ RB= reticulate body (replicating) Disease Asymptomatic ○ May become symptomatic later Men are more likely to be asymptomatic ○ Ping pong effect Epithelial damage ○ Vaginal tract ○ Other mucosal areas (can occur during childbirth) Memory response => worse disease (gets progressively worse the number of times an individual gets infected) Transmission: Sex transmission Birth Treatment: Antibiotics Prevention: Safe sex education Rickettsia Rickettsii ○ Rocky mountain spotted fever Epidemiology Natural host: rodents (asymptomatic) and hard ticks Noonotic infection (humans dead end host) Virulence factor: Adhesions Cell lysis (causes disease) Disease: Rash, (very high) fever, headaches, malaise, nausea Destruction of infected endothelial cells (cells that make up blood vessels) ○ Leaky blood vessels (lack of oxygen being carried) Organ failure from lack of blood Rare: neurological problems, pulmonary and renal failure, and cardiac abnormalities ○ Come from blood loss Transmission Hard ticks Treatment Antibiotics Prevention: rodent/tick control