micro Flashcards
Bacillus anthracis
Morphology
Transmission and Reservoir
Virulence Factors
Pathogenesis
Diseases
Diagnosis
Treatment and Prevention
Gram+ spore-forming rod
extracellular
aerobic
non-hemolytic
———————–
- cattle, sheep, goats
- no person-to-person transmission
cutaneous
- spores enter cutaneous abrasion
inhalation
- inhalation of spores
GI
- ingestion of uncooked meat
———————–
- poly-D glutamic acid capsule: anti-phagocytic
- protective antigen (PA): binds to host cell receptors and LF and EF
- lethal factor (LF): toxin that is a protease
- edema factor (EF): toxin that activates adenylate cyclase to increase cAMP in host cells
- capsule encoded by pXO2 plasmid
- exotoxins (LF and EF) encoded by pXO1 plasmid
———————–
1) germination of the spore
2) multiplication and toxin production
3) may stay contained in the skin or spread through the
bloodstream and lymphatics
3) causes inflammation of lymph nodes
———————–
cutaneous anthrax:
- 1-7 day incubation
- pruritic papule vesicle black eschar
- enlarged lymph nodes
inhalation anthrax (Woolsorter’s Disease):
- 4-6 day incubation
- flu symptoms w/o runny nose
- bloody pleural effusions
- mediastinal widening due to enlarged lymph nodes
- hemorrhagic meningitis “Cardinal’s cap”
- 45% fatality if recognized and treated early
GI anthrax:
- 1-5 day incubation
- GI symptoms
- 40% mortality
———————–
- medusa’s head/comet tail colonies on blood agar
- box car appearance on Gram stain
- Doxycycline
- Ciprofloxacin
- Raxibacumab
Clostridium botulinum
Morphology
Transmission and Reservoir
Virulence Factors
Pathogenesis
Diseases
Treatment and Prevention
Gram + spore-forming rod
anaerobic
tennis racket appearance of Gram stain
extracellular
———————–
- ingestion of contaminated food (e.g. honey, home-cooked food)
- colonization of GI tract or wound
- no person-to-person transmission
———————–
- botulinum toxin: prevents release of ACh by cleaving neuronal proteins involved in synaptic vesicle docking; acts at neuromuscular junction
- serotype A is most serious because it persists longest in the neuron
- serotype E also causes vomiting
———————–
- usually a bacterial intoxication
- infant botulism and adult infant botulism are caused by C. botulinum that colonizes the GI tract and produces toxins in vivo
- wound botulism: C. botulinum enters wound and produces toxin in vivo
- toxin spreads to CNS
———————–
botulism
- 12-72 hour incubation
- double vision
- swallowing difficulties
- descending flaccid paralysis
- breathing problems
- infants first present with constipation
- 70% fatality if untreated; 10% fatality if treated
———————–
- anti-toxin
Clostridium perfringens
Morphology
Transmission and Reservoir
Virulence Factors
Pathogenesis
Diseases
Gram + spore-forming rod
anaerobic
extracellular
———————–
- found in soil, GI tract, & contaminated food
- puncture wound or ingestion of contaminated food
———————–
- alpha toxin: phospholipase C that disrupts plasma membranes
- β toxin: forms pores
- heat-labile enterotoxin: damages membranes
———————–
- toxin production in vivo
———————–
gas gangrene,
anaerobic cellulitis
wound infections
organ infections
bacteremia
food poisoning
- 12 hour incubation
- diarrhea, cramps
Clostridium septicum
Morphology
Transmission and Reservoir
Diseases
Gram + spore-forming rod
anaerobic
extracellular
———————–
- found in GI tract
———————–
infections in patients with cancer of the GI tract
Clostridium difficile
Morphology
Transmission and Reservoir
Virulence Factors
Pathogenesis
Diseases
Diagnosis
Treatment and Prevention
Gram + spore-forming rod
anaerobic
extracellular
———————–
- GI tract
- ingestion
———————–
- toxin A: monoglucosyltransferase; interferes with actin cytoskeleton to make intestinal epithelial cells leaky; attracts neutrophils and stimulates the release of cytokines; causes inflammation
- toxin B: same mechanism as toxin A; also induces cytopathic effect in tissue culture cells
- binary toxin: disrupts actin cytoskeleton; only found in some isolates; more frequent in patients w/ more severe disease
———————–
1) use of antibiotics disrupts the gut flora
2) ingestion
3) colonization in gut
4) toxin production leads to diarrhea
5) pseudomembranous inflammation
———————–
diarrhea in hospitalized patients; spectrum from asymptomatic carriage to toxic megacolon and death; relapse may occur
———————–
- detection of toxins is gold standard for diagnosis
———————–
“Very Fun Medications”
1) Vancomycin
2) Fidaxomicin
3) Metronidazole
- use soap and water, not alcohol, to remove spores
Clostridium tetani
Morphology
Transmission and Reservoir
Virulence Factors
Pathogenesis
Diseases
Treatment and Prevention
Gram+ spore-forming rod
anaerobic
extracellular
———————–
- soil
- puncture wound or contaminated umbilical stump
———————–
- tetanus neurotoxin/tetanospasmin: inhibits release of inhibitory neurotransmitter glycine by cleaving neuronal proteins involved in synaptic vesicle docking; works on CNS in spinal cord
———————–
toxin migrates
along motor neurons into CNS
———————–
tetanus
- incubation time up to months
- spastic paralysis
- death by respiratory failure
neonatal tetanus
———————–
- tetanus antitoxin
Salmonella typhi
Enterobacteriaceae
Morphology
Transmission and Reservoir
Virulence Factors
Pathogenesis
Diseases
Diagnosis
Treatment and Prevention
Gram- enteric rod
———————–
- reservoir: human carriers (often with gallstones)
- transmission: fecal-oral contamination
- India subcontinent, Central & South America, Asia, Africa
———————–
- same virulence factors as non-typhoid Salmonella
- polysaccharide capsule containing Vi antigen
———————–
1) similar to non-typhoid Salmonella, except it disseminates quickly once it reaches the lamina propria
2) moves through the blood and/or lymph to reticuloendothelial tissue (liver, spleen, bone marrow)
3) multiplies in those tissues
4) suddenly emerge 1-2 weeks later in the blood and bile
———————–
typhoid fever
initial symptoms:
- low grade fever
- constipation
after 1-2 weeks:
- septic shock
- high fever
- diarrhea
- hemorrhaging and perforation of the intestine, which can lead to peritonitis
- abdominal rose spots
- 10-20% mortality w/o treatment
———————–
- blood cultures
———————–
- Ciprofloxacin
- Ceftriaxone
Proteus mirabilis
Enterobacteriaceae
Morphology
Diseases
Treatment and Prevention
Gram- enteric rod
———————–
catheter-associated UTI
———————–
- Aminopenicillins +/- B-lactamase inhibitors
Enterobacter cloacae
Enterobacteriaceae
Morphology
Diseases
Treatment and Prevention
Gram- enteric rod
———————–
hospital-acquired pneumonia
———————–
- Nitrofurantoin
Campylobacter jejuni
Morphology
Transmission and Reservoir
Virulence Factors
Pathogenesis
Diseases
Treatment and Prevention
Gram- enteric
rod
curved
motile
microaerophilic
grows best at 42C
———————–
- reservoir: animals, including pets
- ingestion of contaminated food (poultry) or water
- contact with sick pets
———————–
- adhesins
- LPS
- enterotoxin: causes ADP-ribosylation of Gs, resulting in activation of adenylate cyclase and accumulation of intestinal cAMP; not required for pathogenesis
- gangliosides sugars mimic neuronal tissue and are associated with Guillain-Barre syndrome
———————–
invades lower small intestine or upper large intestine and induces inflammation
———————–
- 3-5 day incubation
- cramps, diarrhea (sometimes with fecal leucocytes), fever
- Guillain-Barre syndrome
- arthritis
- macrolides
- tetracyclines
Bacteroides fragilis
Morphology
Transmission and Reservoir
Virulence Factors
Diseases
Treatment and Prevention
Gram- enteric rod
anaerobic
———————–
- found in colon
-endogenous infection
———————–
- capsule
- enterotoxin (some species)
- proteases & enzymes
- LPS (not endotoxic)
———————–
intra-abdominal infections (peritonitis followed by abscess formation) & bacteremia
———————–
These Many Medications Can Confidently Cover Bacteroides
1) Tigecycline
2) Metronidazole
3) Moxifloxacin
4) Clindamycin
5) Cefoxitin
6) Carbapenems
7) B-lactams + B-lactamase inhibitors
Porphyromonas gingivalis
Morphology
Transmission and Reservoir
Virulence Factors
Diseases
Gram- rod
anaerobic
bile-sensitive
———————–
- found in mouth
- endogenous infection
———————–
- endotoxic LPS
- proteases and other enzymes
———————–
respiratory tract infections
Prevotella melaninogenica
Morphology
Transmission and Reservoir
Virulence Factors
Diseases
Gram- rod
anaerobic
bile-sensitive
———————–
- found in mouth
- endogenous infection
———————–
- capsule
- endotoxic LPS
- proteases and other enzymes
———————–
respiratory tract infections
Prevotella bivia
Morphology
Transmission and Reservoir
Virulence Factors
Diseases
Gram- rod
anaerobic
bile-sensitive
———————–
- found in female genital tract
- endogenous infection
———————–
- endotoxic LPS
- proteases and other enzymes
———————–
pelvic inflammatory disease; infertility
Francisella tularensis
Morphology
Transmission and Reservoir
Virulence Factors
Diseases
Treatment and Prevention
Gram- rod
———————–
reservoir:
- various animals
infectious material:
- tick saliva or
feces
- contaminated
animal products
- water
- dust
- hay
transmission
- tick bite
- inoculation into wound
- contact
- inhalation
- ingestion
- not transmissible between people
very virulent
found in Martha’s vineyard
———————–
- capsule
- FPI pathogenicity island: cluster of genes that are responsible for intracellular survival
———————–
tularemia
- 3-5 day incubation
- fever, chills, headache, malaise, anorexia, fatigue
- ulceroglandular (lesion + lymphadenopathy)
- oculoglandular
- pharyngeal
- glandular
- pneumonic
- typhoidal: disseminated infection that does not fall into other categories
- 4% fatality
———————–
- Streptomycin or Gentamicin
- Doxycycline or Ciprofloxacin for PEP
- alert microbiology lab, b/c very virulent
Yersinia pestis
Enterobacteriaceae
Morphology
Transmission and Reservoir
Virulence Factors
Diseases
Treatment and Prevention
Gram- enteric rod
safety pin morphology
———————–
- rodent reservoir
- flea vector
- contagious
- SW US
———————–
- plasminogen activator - causes fleas to regurgitate it
- Yersinia outer protein (YOP): inhibits phagocytosis & lymphocyte proliferation
- LPS: endotoxic
- polypeptide capsule
———————–
acute febrile lymphadenitis (bubonic plague)
- most common form
- fevers, chills, weakness, headache, pain and swelling in lymph nodes
pneumonic
- 2-4 day incubation
- pneumonia w/ bloody sputum
- 50% mortality
septicemic
- bacteremia after escape from lymph nodes
———————–
- Streptomycin or Gentamicin
- Doxycycline or ciprofloxacin for PEP
- contact isolation
- droplet precautions for 72 hours after starting antibiotics
Rickettsia rickettsii
Morphology
Transmission and Reservoir
Virulence Factors
Pathogenesis
Diseases
Diagnosis
Treatment and Prevention
atypical; Gram- structure; pleomorphic
obligate intracellular
energy parasite ticks (transmitted to offspring; ticks can become infected after feeding off of an infected animal)
———————–
- ability to direct actin reorganization resulting in the formation of filopodia that enhance spread between cells
- phospholipases, proteases, and membrane peroxidation result in host cell damage
———————–
1) enters through tick bite
2) spread via lymph and blood
2) grows inside vascular endothelial cells and causes lysis and rash
- escapes phagosome to live in cytoplasm
———————–
Rocky Mountain spotted fever
1) spotted rash 2-4 days after onset (not always seen)
2) fever, malaise, headache, myalgias, vomiting, abdominal pain, diarrhea, conjunctivitis, mental confusion, meningitis, respiratory difficulties, renal dysfunction, myocarditis
3) 25% fatality if untreated; 4% fatality if treated
———————–
- can be non-specifically detected by Weil-Felix test (not currently used clinically)
———————–
- Doxycycline
