Bacillus and Clostridium Flashcards
How are pathogens (Bacteria) transmitted to host?
-Animal food products
-Vectors: ie animal vectors
- P to P
-Fecal oral
-aerosol
-hand to hand
What are portals or entry into host>
-cuts in skin
-resp tract
-GI tract
-genital tract
-urinary tract
What are physiological host defenses?
skin, mucous, ciliated epithelium, cell secretions
What are virulence factors? examples? (4)
-Stuff the pathogen uses to get into the cell
-Adhesins: proteins that help attachement
-pili
-lipoteichoic acid: also help with attachment
-toxins
What are the three steps of biofilm formation?
1)attachment: forms microcolonies
2) growth: of mature biofilm
3) detachment: in chunks
What are exotoxins and endotoxins? Give examples (2 ea)
-Proteins that the pathogen uses to harm the host cell
-exotoxins: released by bacteria cell and are taken up by host cell
-endotoxins (EG LPS, peptidoglycan): on the surface of the bacteria that release upon cell lysis. when the endotoxins reach cell surface they harm it.
What are four tissue-degrading enzymes?
Lecithinase, collagenase, coagulase (for blood degradation), hyaluronidase
What do bacteria secretion systems do?
Inject bacterial proteins into the host cell from the bacteria surface
What are commensal organisms?
organisms that work in a symbiotic relationships with their host
What are the two classes of pathogens?
-Strict pathogens: organism that are always associated with disease
-opportunistic: organisms that are apart of normal flora, but can establish disease under certain conditions
What are normal flora on the skin?
-aerobic and anaerobic ditheroid bacilli (irregular, non-spore rods)
-non-hemo aerobic and anerobic staph
-gram-pos aerobic spore-forming bacilli
-fungi and yeast
-acid-fast
What are normal flora on the ear (1 group)? what are the pathogens (3)?
-Norm: coag-neg staph
-Pathogen: S.pneuomoniae, Pseudomonas aeruginosa, Enterobacteriaceae
What are normal flora on the mouth/throat/nose(5)? what are the pathogens(6)?
-Norm: Corynebacteria, Staph, Strep, pneumococci, haemophili
-Pathogen: Strep pyrogenes, strep pneumoniae, staph aureus, neisseria meningitidis, Haemophilus influenzae, Moraxella catarrhalis, enterobacteriaceae
What are normal flora on the eye(4)? what are the pathogens(7)?
-Norm: coag-negative staph, Haemophilus, Neisseria, Viridans strep
-Pathogen: S.pneumonia, S.auerus, H.influenzae, N.gonorrhoeae, Chlamydia trachomatis, P.aeruginosa, Bacillus cereus
What are the normal flora of the lower resp trac (1)t? what are the pathogens (5)?
-Norm: sterile-ish
-Pathogen: S.pneumoniae, S.aureus, Enterobacteriaceae (Klebsiella), anaerobic cocci ssp (Peptostreptococcus), gram-negative rods
What are the normal flora on the Esophagus(2)? what are the pathogens(2)?
-Norm: Anything in the saliva and food
-Pathogen: Candida and visuses
What are normal flora on the stomach (5)? what are the pathogens (2)?
-Norm: Lactobacillus, streptococcus, helicobacter pylori, acid-tolerant and lactic acid producing bacteria
-Pathogen: H.pylori, enteric bacteria
What are the normal flora in the small and large intestines(2)? what are the pathogens (2)?
-Norm: anaerobic bacteria, fungi, viruses
-Pathogen: Salmonella and Campylobacter (anything that can cause gastroenteritis)
What are normal flora on the cervix(1)? what are the pathogens(3)?
-Norm: sterile
-Pathogen: N.gonorrhoeae, C.trachomatis, actinomyces
What are the 5 classes of antibiotics?
1)beta-lactams: targets bacterial cell wall synthesis
2)Cell wall/peptidoglycan synth inhibitors
3) Cell membrane disruptors
4)Protein synthesis inhibitors
5) Quinolines: inhibits DNA synthesis
What are the normal flora on the vagina(4)? what are the pathogens(5)?
-Norm: Lactobacilli, staph, strep, Enterobacteriaceae
-Pathogen: N.gonorrhoeae, Tricoomonas vaginalis, C.albicans, herpes, papillomavirus
What are normal flora on the urethra(3)? what are the pathogens(5)?
-Norm: lactobacilli, strept, coag-neg straph.
-Pathogen: Enterococcus, enterobacteriaceae, Candida, N.gonorrhoeae, C.trichomatis
What are Beta-lactams? give four examples
-targets cell wall synthesis (bacterial)
-includes penicillin, cephalosporin, monobactams, carbapenems
-can be broken down by beta-lactamase
What are Glycopeptides, Bacitracins MOA?
cell wall inhibitors(
What is a cell membrane disruptor antibiotic?
Polymyxins
What are five protein synthesis inhibitors?
The -cyclines (tetracyline, Doxycycline, Minocyline), Chloramphenicol, Macrolides, Clindamycin/lincomycin, Aminoglycosides
Why might one person use one antibiotic over another?
-Poor penetration into tissue
-not effective on organism
-bacteriostatic verus cidial
-EG) Tetracyline is bacteriostatic and doesn’t penetrate into the CSF very well. Chloramphenicol can be distributed to CNS and CSF
What are quinolines?
antibiotics that inhibits bacterial DNA synthesis
What type of bacteria is Bacillus?
-Spore forming
-gram-pos
What type of bacteria is clostridium
-spore forming
-gram-pos
What are the general characteristics of bacillus? (7) Hemo?
-ubiquitous in nature (everywhere)
-spore forming
-aerobic
-found in soil
-saprophytic
-Gram positive
-rod-shaped
-Can be hemo, but not nessisary
What is bacillus morphology? (6) Hemo?
-Rods, with boxy ends
-chains
-spores in the middle
-non-motile
-round colonies on agar
-can be hemolytic, but not necessary
What are the two special characteristics of bacillus?
-Saphrophytic
-spores –> can be sterilized via autoclaving
What is cutaneous anthrax? Where does it dome from? what does it do?
When injured skin gets infected with anthrax.
-Spores from contaminated soil or animals, germinate at entry site. Vegetative cells form gelatinous edema
-Can get into lymphatic system, blood stream, other tissue
-can be fatal, but treatable and aparent
-black scab (eschar)
What is GI anthrax? What does it causes
-When one eats anthrax
-causes intestinal inflammation, vomitting, fever
-rarely fatal, but you would wish you were dead (20 to 60% fatal)
What is inhalation anthrax?
-Spores inhalled into lungs
-when spore germinate into the lungs, they start to form toxins in the lymph nodes and lungs
-leads to hmorrhaging and sepsis
What is sepsis (measured)
1e7 bacterial cells per mL of blood
What is the capsule of B.anthracis made of? what does it do?
-Avirulent strains do not have capsules (capsules = virulent)
- made of poly-D-glutamic acid
-prevents phagocytosis
What are the three anthrax toxins? are they endo or exotoxins?
-PA: protective antigen: binds to membrane and one of the other toxins
-EF (edema factor): activates a signaling cascade that results in fluid formation
-LF (lethal factor): activates a signaling cascade that results in cell death
-are all exotoxins
What makes a host susceptible to B.anthracis(5)? what makes them resistant(4)?
Susceptible: proliferation at the site of entry, capsule is intact, large amounts of proteinaceous fluid, few leukocytes, rapid dissemination into bloodstream
Resistant: proliferation of a few hours, large accumulation of leukocyte, capsules disintegrate, localized
What is the most common type of anthrax infection?
cutaneous
What is the development of cutaneous anthrax at 1-7 days? how about 7- 10 post infection? What antibiotics help?
1-7: insect bite leads to necrotic ulcer with black eschar and marked edema. Lymphangitis, lymphadenopathy and normal fever symptoms
7-10 (post-infection): fully developed eschar eventually dries and separates. Leaves a scar
-Antibiotics do not stop disease progression, just prevent dissemination. Use Ciprofloxacin (a quinolone), or Penicillin G and gentamycin/streptomycin
What is the incubation period of inhalation anthrax?
6 weeks
What are the early and later manifestations of inhalation anthrax?
Early: marked hemorraging necrosis, edema of mediastinum. Subpleural pain, mediastinal widening on chest radiograph
Later: hemorrhagic pleural effusions, sepsis
Where do you get specimens from for inhalation, cutaneous and GI anthrax? (for testing and from environment)
-Inhalation: Fluid from pus, lesion, blood, CSF, and pleural fluid.
-GI: Stool or other intestinal contents
-Found in contaminated soil
How does B.anthracis look on agar(3)?
-BAP: non-hemo, grey to white, rough/ground glass texture
-Medusa head: leaves a mark when you try to pull or spread it. It doesn’t want to leave the plate
-Increase capsules on bicarbonate agar
What does a B.anthracis gram stain look like
looong gram positive rod chains
What is the ID test for B.anthracis
-Lysis by anthrax gamma-bacteriophage
- Detection of capsule by florescent antibody
-ID of toxin genes by PCR
Why don’t we use anthrax vaccines
-lots of intramuscular boosters. followed by annual boosters
-Thee vaccine sucks ass+
What antibiotics do we use to treat anthrax (2)?
-Ciprofloxacin: a quinolone that prevents the unwinding and duplicating of bacterial DNA
-Penicillin G + gentamycin/streptomycin
Where is B.anthracis found?
-soil
-grazing animals -> infected via injured mucous membrane
What does B.cereus cause? what causes it?
-causes food posioning: vomiting, diarrhea
-produces toxins that causes the infections
-happens quickly, but leaves quickly (24 hr flu/food posioning)
Where does B.cereus come from? how does it get into us?
Found in soil. Contaiminated plants have spores on them, which can germinate when cooked (rice)
how much B.cereus needed to have an illness?
Unlike antrax, B.cereus is normally found in 1e5 bacteria per a gram of food. This makes it hard to test via fecals
What else can B.cereus infect (3)?
Skin, eye (forgein body, trauma), systemic infections due to medical devices (typically due to medical device/drug use)
What antimicrobial agents can you use against B.cecrus (2.5)?
-Vancomycin
-Clindamycin (+ aminogylcosides)
Which bacillus has hemolysis? Which bacillus has long thin chains?
(Bacillus cereus versus anthrax)
Thin long chains: anthracis
Hemolysis: cereus
What are the general characteristics of Clostridium (6)? where does it live? what does it cause(4)? hemo?
-Anaerobic
-large, gram pos rods
-no big chains
-motile -> flagella
-live in soil or instinal tracts
-saprophytes
-Causes botulism, teanus, gas ganrene, and pseudomembrane colitis
-spores have larger diameter than rodes
-B-hemo
What can Clostridium ssp cause?
Tetanus, botulism
Grow me some Clostridium ssp: What are the growth characteristics and colony formation of Clostridium on agar? what environment does it need? hemo?
-Growing: saccharolytic or proteolytic (sugar and protein). Needs anaerobic conditions (some aerotolerant). Likes BAP
- Looks like: large raised round colonies. Produce a zone of beta hemo
What are characteristics of Clostridium ssp under a microscope?
-gram positive rods
-spores have a large dia than rods
How do you get botulism? what causes botulism?
get it thru ingesting bad food, but found in soil and feces. Caused by C.botulinum
Is the C.botulinum toxin an endotoxin or an exotoxin? how many antigenic varieties are known and how many are pathogenic?
Endotoxin. Seven different types A thru G. only four (A, B, E, and F) are pathenogenic
E: seafood botulism
F: infant botulism
What does the C.botulinum toxin do? What neurotransmitter does it affect
It breaks down the SNARE proteins that allow synaptic vessicles to release their Ach
How do you neutralize anthrax toxin? how about botulism toxin?
Botulism: 20 min at 100 C
Anthrax: raxibacumab or obiltoxaximab (bind to PA)
What are common sources of botulism?
Likes anerobic environments it can eat stuff in
-spiced, smoked, vacuum-packed, or canned foods
-honey, jarred baby food
What is the clinical presentation of botulism
-Progressive paralysis
- Eventually resp paralysis or cardiac arrest
-starts with incoordination of small muscles: Visual disturbances, inability to swallow, speech difficulty
-No post-infection anti-toxin
How do you test for C.botulinum?(sample recovery, test)
-recover bacteria from feces, gastric secetrion, or serum
-Mouse-bio assay, ELISA, or PCR
-can be grown from the infected food
What is a mouse bio-assay
-mouse is injected IP with specimen
-if C.bot is present, mouse dies rapidly
What are some treatments for botulism
-Antitoxins for A, B and E
-Supportive care: respiration aid (for infant botulism)
Where does C.botulinum come from?
-Starts in the soil
-veg, fruit or other plant material contain it
-canned/preserved food provide an anaerobic environment for spores
Where is C.tetani come from?
-Found in soil and feces
What is the clinical pathology of teteus (incubation period, characteristics, mortality rate)
-Incu period: 4-5
-Causes tonic contractions of voluntary muscles: lock jaw. Starts are area of injury
-death from interference with respiration process
How does C.tetani invade the body?
-localized to area where spores are introduced (injury)
-Toxin from vegetative cells reach CNS –> Causes hyperreflexia and paralysis
How do you diagnose tetus?
-culture tissues
-antitoxin tests
How to stop tetani (prevention (4) and treatment):
Prevention: Immunization with toxoid, proper wound care, antitoxin, penicillin
Treatment: IM administraiton of anti-toxin, muscle relaxants, sedation, ventilation, large dose IV anti-toxin, additional doeses of toxoid
What does C.tetani look like under a microscope:
Same of other Clostrium ssp, but has a flaggella
How can C.tetani can be IDed?
specific flagellar antigen. Common O antigen
What toxin does C.tetani produce? what does it do?
tetanospasmin. Binds to pre-synaptic inhibitory cells, stopping them from down regulating Ach excitatory signals
what class of antibiotics is B.cereus resistent against?
beta-lactams. They produces beta-lactamases
