ALL BACTERIA! Flashcards
Salmonella (general): Similar to
Shigella, E coli (Enterobacteriaceae Family)
Enteroaggregative E. coli (EAEC): Similar to
EPEC
Acinetobacter baumanii: At Risk
Hospitals
Acinetobacter baumanii: Disease
OPPORTUNIST!
Nosocomial infections
Acinetobacter baumanii: Gram stain
-
Acinetobacter baumanii: Negative for: (2)
Oxidase
Sugar fermentation
Acinetobacter baumanii: Oxygen
aerobe
Acinetobacter baumanii: Reservoir
Hospital
Acinetobacter baumanii: Shape
short rod
Acinetobacter baumanii: Transmission/vector/ habitat
Indwelling medical devices
Acinetobacter baumanii: Treatment
Multidrug resistant
Acinetobacter baumanii: Virulence Factors (4)
Capsular polysaccharides
Adhesins
Proteolytic/lipolytic enzymes
LPS
Bordetella pertussis: At Risk
Infants more likely to die
Bordetella pertussis: Diagnosis (3)
Contact history, classic cough, lymphocytosis
**Requires fresh, Bordetella-optimized media for growth (not typically used)
PCR for repeat insertion sequences
Bordetella pertussis: Disease
Pertussis (whooping cough)
Bordetella pertussis: Epidemiology
Major childhood killer pre-1940
–Highest fatality of all among children before vaccine!
Re-emerging now: waning immunity, Agic divergence, decreased vaccination
Bordetella pertussis: Gram stain
-
Bordetella pertussis: Incubation Period
7-10 days
Bordetella pertussis: Oxygen
Obligate aerobe
Bordetella pertussis: Pathogenesis (6 steps)
- intro via water droplets
- interact w/ciliated epithelial cells (trachea/nasopharynx)
- adherence
- multiplication/toxin production -> local inflammation, mucous secretion, patchy ulcers, cyanosis, pneumonia
- host evasion
- spread
Bordetella pertussis: Reservoir
NONE - only infects humans
Bordetella pertussis: Shape
coccobacilli
Bordetella pertussis: Symptoms
[Catarrhal stage] runny nose, sneezing, low-grade fever, mild cough
[Paroxysmal stage] whooping cough, vomiting, cyanosis
Bordetella pertussis: Transmission/vector/habitat
Aerosol
Bordetella pertussis: Treatment
Treat for hypoxia
Erythromycin (alt: tetracycline or chloramphenicol)
–Resistant to penicillin and ampicillin
Treat household contacts prophylactically
Bordetella pertussis: Vaccine
DTP (trivalent): side-effects - encephalopathy and permanent neurologic sequelae (not used anymore)
DTaP (acellular trivalent component) introduced mid-90s
-> contains pertussis toxin, FHA, pertactin, and fimbrae
NO lifelong immunity
Bordetella pertussis: Virulence Factors (6)
PERTUSSIS TOXIN (inhibits Gi for adenylate cyclase -> adenylate cyclase activated -> cAMP accumulation -> lymphocytosis, histamine-sensitivity, enhanced insulin secretion)
ADENYLATE CYCLASE toxin (catalyzes cAMP from ATP -> impaired leukocyte function and apoptosis)
DERMONECROTIC toxin (VSM contraction => ischemic necrosis of lung tissue)
TRACHEAL CYTOTOXIN (CILIOSTASIS, kills tracheal epithelial cells, proinflammatory)
Endotoxin (LPS)
Several adhesins: pili, Filamentous hemagglutinin, Pertactin, Tracheal colonization factor (-> colonization)
Campylobacter (jejuni): At Risk (3)
Infants to young adults in developed
Infants in developing
Immunocompromised, esp. with humoral immunodeficiency (severe)
Campylobacter (jejuni): Diagnosis (4)
Gm stain stool specimen
Enrich with filters (very small)
Hippurate positive (very diagnostic)
Culture at 42C in microaerophilic conditions (body temp of poultry)
Campylobacter (jejuni): Disease (2)
Diarrhea from inflammatory enteritis
Bacteremia (rare)
Campylobacter (jejuni): Epidemiology (3)
MOST COMMON cause of diarrhea in the world
Typically sporadic cases
Multiple simultaneous cases usually point to common contaminated source
Campylobacter (jejuni): Gram stain
-
Campylobacter (jejuni): Incubation Period
3-5 days
Campylobacter (jejuni): Infectious dose
Low infectious dose (500 = 1 drop of raw chicken juice)
Campylobacter (jejuni): Oxygen
microaerophilic
Campylobacter (jejuni): Pathogenesis (3 steps)
- survive gastric barrier
- arrive in small/large bowel - inflammation
- bloodstream (rare)
Campylobacter (jejuni): Prevention (2)
Pasteurization of milk, cooking meat (esp. poultry)
Campylobacter (jejuni): Reservoir
Animals (esp. poultry -does not make animals sick)
Campylobacter (jejuni): Shape
curved or comma with uni or bipolar flagellum
Campylobacter (jejuni): Symptoms
Prodrome (fever, malaise, headache)
fever; abd. pain; diarrhea (few days to a week)
Complications = autoimmunity to nerves (Guilliam-Barre syndrome)
Campylobacter (jejuni): Transmission/vector/ habitat (3)
Food (esp. raw chicken), milk, or water
Campylobacter (jejuni): Treatment
Oral rehydration therapy
Antimicrobial therapy as indicated (erythromycin; alt - cipro)
Chlamydophilia (general): Diagnosis (4)
General Diagnosis
- Check for group antigen
- Compare acute and convalescent Ab titers
- Direct fluorescent Ab exam of appropriate clinical specimens
- PCR
Chlamydophilia (general): Gram stain
Gm- (by phylogeny)
Chlamydophilia (general): Life Cycle (forms, 3 steps)
Elementary Bodies (EB): small, non-multiplying, with a rigid bacterial-like cell wall -> transmits infection
Initial Bodies (IB) [aka reticulate bodies (RB)]: larger, actively multiplying, lack rigid wall, non-infectious
Intracellular growth
- EB enter by inducing host phagocytosis (even in non-phagocytotic cells)
- EB lose cell wall during first 24h, double in diameter, and synthesize RNA to yield IB
- IB divide by binary fission -> some progeny converted back to EB
Chlamydophilia (general): Shape
pleomorphic
Chlamydophilia (general): Special growth conditions
OBLIGATE intracellular (canNOT make ATP => depends on host ATP)
EB -> IB (RB) in host cell -> divide -> host cell dies and release EBs
Chlamydophilia (general): Treatment
Tetracyclines are effective but single high dose azithromycin may be more indicated
Any antibiotic used must enter cells
Chlamydophilia pneumoniae: Diagnosis
Antibody assay
Chlamydophilia pneumoniae: Disease
Atypical (diffuse) pneumonia
Chlamydophilia pneumoniae: Epidemiology (2)
Causes 10% of pneumonia in adults
May play a role in coronary atherosclerosis
Chlamydophilia pneumoniae: Number of serotypes
1 serotype
Chlamydophilia pneumoniae: Symptoms (3)
Pneumonia/bronchitis
Gradual onset of cough
Little/no fever
Chlamydophilia pneumoniae: Transmission/vector/ habitat
Person-to-person via aersol
Chlamydophilia psittaci: At Risk
Contact w/birds
Chlamydophilia psittaci: Diagnosis (2)
Pathogen in blood or sputum
Antibody assay
Chlamydophilia psittaci: Disease
Psittacosis (parrot fever)
Chlamydophilia psittaci: Number of serotypes
1 serotype
Chlamydophilia psittaci: Pathogenesis
Disseminated infection that targets epithelial cells, endothelial cells, Mos
Chlamydophilia psittaci: Reservoir
Birds (induces chronic subclinical infection with constant fecal excretion)
Chlamydophilia psittaci: Symptoms (3)
Fever and headache
Severe -> interstitial pneumonia
Chlamydophilia psittaci: Transmission/vector/ habitat
Inhalation of bird feces
Chlamydia trachomatis, serotypes L1-3: Diagnosis
Ag testing to differentiate between C. trachomatis serotypes
Chlamydia trachomatis, serotypes L1-3: Disease
Lymphogranuloma venereum
Chlamydia trachomatis, serotypes L1-3: Symptoms (2)
Painless papule progresses to ulcerating vesicle (2 weeks post-exposure)
Can -> painful suppurating disease of regional lymph nodes
Chlamydia trachomatis, serotypes L1-3: Transmission/vector/ habitat
STD
Chlamydia trachomatis, serotypes A-C: At Risk (2)
Poor hygiene
Asia and Africa
Chlamydia trachomatis, serotypes A-C: Diagnosis (1)
Ag testing to differentiate between C. trachomatis serotypes
Chlamydia trachomatis, serotypes A-C: Disease
Trachoma (chronic conjunctivitis)
Chlamydia trachomatis, serotypes A-C: Epidemiology (1)
World’s leading cause of preventable blindness
Chlamydia trachomatis, serotypes A-C: Pathogenesis
Chronic conjunctival reinfection causes infolding of eyelashes => corneal scarring and blindness
Chlamydia trachomatis, serotypes A-C: Prevention (4)
Surgery, prophylactic antibiotics, facial cleanliness, environmental improvements/sanitation
Chlamydia trachomatis, serotypes A-C: Special Features: Intra vs extracellular, presence of capsule, invasive or not
More invasive serotypes
Chlamydia trachomatis, serotypes A-C: Symptoms (5)
Cloudy cornea Discharge from eye Swelling of lymph nodes in front of ears Swollen eyelids Turned-in eyelashes
Chlamydia trachomatis, serotypes A-C: Transmission/vector/ habitat (2)
Mechanical (finger to eye)
Flies
Chlamydia trachomatis, serotypes A-C: Treatment
Annual universal treatment with azithromycin
Chlamydia trachomatis, serotypes D-K (perinatal): At Risk
Neonates
Chlamydia trachomatis, serotypes D-K (perinatal): Diagnosis (1)
Ag testing to differentiate between C. trachomatis serotypes
Chlamydia trachomatis, serotypes D-K (perinatal): Disease (2)
Inclusion conjunctivitis Infant pneumonia (usually an extension of ocular disease)
Chlamydia trachomatis, serotypes D-K (perinatal): Epidemiology (2)
Inclusion conjunctivitis - most common vertically transmitted neonatal disease
Occasionally seen beyond neonatal age where environ. contamination (swimming pools, etc.) is involved
Chlamydia trachomatis, serotypes D-K (perinatal): Symptoms (3)
Large lymphoid follicles
Papillary hyperplasia of the conjunctiva
Red, irritable eye with sticky discharge
Chlamydia trachomatis, serotypes D-K (perinatal): Transmission/vector/ habitat (3)
Perinatal
Swimming pools
STD
Chlamydia trachomatis, serotypes D-K: Diagnosis (2)
Yearly rapid PCR test of urine for sexually active women
Ag testing to differentiate between C. trachomatis serotypes
Chlamydia trachomatis, serotypes D-K: Disease (2)
Non-gonoccocal urethritis
More severe -> epididymytis, salpingitis -> infertility
Chlamydia trachomatis, serotypes D-K: Epidemiology (2)
Possibly most common venereal disease
Infection increases chance of HIV transmission
Chlamydia trachomatis, serotypes D-K: Symptoms (2)
Males: usually asymptomatic (purulent urethral discharge)
Females: frequently asymptomatic
Chlyamydia trachomatis, serotypes D-K: Transmission/vector/habitat
STD
Chlamydia trachomatis, serotypes D-K: Treatment (1)
Single high dose azithromycin for BOTH sexual partners
Corynebacterium diphtheriae: At Risk (2)
Developing countries w/inadequate pediatric immunization and medical care
Travelers (need booster DTaP)
Corynebacterium diphtheriae: Diagnosis (4)
Tentative: tellurite agar, Tinsdale’s medium, and Leoffler media (+ for METACHROMATIC GRANULES)
Definitive:
- -Toxin production (Elek test)
- -PCR for toxin gene
- -Immunoassay of serum
Corynebacterium diphtheriae: Disease (1)
Diphtheria: infection of skin and/or throat
Corynebacterium diphtheriae: Epidemiology (3)
Once a major cause of death in US -> in pre-immunization era, major fraction of pop. were carriers
Epidemics in poorly immunized pop. w/inadequate medical care
Presents as necrotizing skin infection in the tropics -> spread by contact
Corynebacterium diphtheriae: Gram stain
!!+++++++!!
Corynebacterium diphtheriae: Incubation Period
2-5 days
Corynebacterium diphtheriae: Life Cycle
Do NOT form spores!
Corynebacterium diphtheriae: Other
All other corynebacteria (diptheroids) are normal inhabitants of our skin/throat
Corynebacterium diphtheriae: Oxygen
aerobe
Corynebacterium diphtheriae: Prevention (2)
Immunity depends on presence of Ab against toxin (antitoxin)
Give DTaP booster to travelers
Corynebacterium diphtheriae: Reservoir
NONE - only infects humans
Corynebacterium diphtheriae: Shape
rod
club-shaped
(pleomorphic)
Corynebacterium diphtheriae: Symptoms (3)
Fever, cough, sore throat
Gray PSEUDOMEMBRANE formation in severe cases (thrush)
Inflammation of lymph nodes
Corynebacterium diphtheriae: Transmission/vector/habitat
Aerosol
Corynebacterium diphtheriae: Treatment (2)
Horse antitoxin immediately (hypersensitivity and anaphylactic shock common)
Penicillin prophylactically or as treatment
Corynebacterium diphtheriae: Vaccine
Toxoid - DTaP good for 10 years
Corynebacterium diphtheriae: Virulence Factors (1)
DIPHTHERIA EXOTOXIN - blocks eukaryotic cell protein synthesis (inactivates EF2) => produces systemic symptoms)
- -Lethal to eukaryotic cells
- -Targets heart, kidney, nervous system
- -Exotoxin has 2 domains which dissociate within endosome - cell surface receptor (B, promotes endocytosis) and toxin domain (A)
Coxiella burnetii: At Risk (2)
Exposure to barn animals, especially birth of barn animals
Cardiac vascular disease can increase risk of endocarditis
Coxiella burnetii: Diagnosis (3)
Serologic testing for C. burnetii Ags
Indirect immunofluorescence assay (most dependable)
Immunohistochemical staining and DNA detection methods of infected tissues
Coxiella burnetii: Disease (2)
Q fever
Can progress to chronic endocarditis
Coxiella burnetii: Gram stain
-
Coxiella burnetii: Prevention (4)
Dispose of birth products of sheep and goats
Restrict access to barns/labs housing potentially infected animals
Vaccination
Counseling
Coxiella burnetii: Reservoir
Sheep and cattle -> tick and so on
Coxiella burnetii: Special growth conditions
Obligate intracellular
Coxiella burnetii: Symptoms (5)
Intersitital pneumonia, fever, headache, rash (some patients), elevated LFTs
Coxiella burnetii: Transmission/vector/ habitat (2)
Inhaling Coxiella from placental tissue (carcass) of sheep or cattle
Spore-like stage transmits the infection
Coxiella burnetii: Treatment (3)
Doxycycline
Quinolone Abx
Chronic endocarditis -> aggressive therapy, surgery
Diffuse adhering E. coli (DAEC): At Risk
Older children in developing countries
Diffuse adhering E. coli (DAEC): Diagnosis (2)
PCR for virulence genes
Tissue culture -> diffuse adherence
Diffuse adhering E. coli (DAEC): Disease
Diarrhea
E. coli (general): Diagnosis (7)
Stool samples Enrich in Gm- broth PCR -> virulence factors Toxin analysis Antigen testing Tissue culture assay for adherence Lac +!
E. coli (general): Gram stain
-
E. coli (general): Negative for: (1)
Oxidase
E. coli (general): Oxygen
fac. Anaerobe
E. coli (general): Positive for: (3)
Lactose
Glucose (+gas)
Nitrate
E. coli (general): Prevention (2)
Grain fed cattle harbor more acid shock resistant E. coli
–Hay feeding leads to a higher pH => lack of adaptation of pathogenic E. coli
Hygiene
E. coli (general): Shape
rod
Ehrlichioses: At Risk (1)
Exposure to ticks
Ehrlichioses: Disease (2)
Monocytic Ehrlichiosis
Granulocytic Ehrlichiosis
Ehrlichioses: Epidemiology (1)
Found in southern US
Ehrlichioses: Gram stain
-
Ehrlichioses: Pathogenesis (1)
Infects monocytes and granulocytes
Ehrlichioses: Special growth conditions (1)
Obligate intracellular
Ehrlichioses: Symptoms (3)
Fever, lymphocytopenia, elevated LFTs
Ehrlichioses: Transmission/vector/ habitat
Ticks
Ehrlichioses: Treatment (1)
Tetracyclines
Enteroaggregative E. coli (EAEC): At Risk
Children in developing countries
Enteroaggregative E. coli (EAEC): Diagnosis (2)
PCR for virulence genes
Tissue culture -> aggregative adherence
Enteroaggregative E. coli (EAEC): Disease (1)
Chronic Diarrhea
Enteroaggregative E. coli (EAEC): Epidemiology (2)
Common in developing countries
2012 outbreak in Germany of O104:H4 due to strain that expressed STX
Enteroaggregative E. coli (EAEC): Pathogenesis (1)
Aggressive epithelial cell attachment
Enteroaggregative E. coli (EAEC): Special Features: Intra vs extracellular, presence of capsule, invasive or not
No A/E lesions
Enteroaggregative E. coli (EAEC): Symptoms (2)
Persistent diarrhea
Weight loss
Enteroaggregative E. coli (EAEC): Treatment (1)
Fluoroquinolones (travelers and HIV+)
Enteroaggregative E. coli (EAEC): Virulence Factors (3)
Heat stable-like toxin (EnteroAggregative stable toxin; EAST)
Plasmid encoded toxin (Pet)
Hemolysin
Enterobacter cloacae: At Risk (1)
Hospital setting following antibiotic treatment
Enterobacter cloacae: Disease (4)
OPPORTUNIST!
Infections of burns, wounds, respiratory, UT
Enterobacter cloacae: Gram stain
-
Enterobacter cloacae: Oxygen
fac. Anaerobe
Enterobacter cloacae: Pathogenesis
Forms biofilms
Enterobacter cloacae: Positive for: (1)
Lactose
Enterobacter cloacae: Shape
rod
Enterohemorrhagic E. coli (EHEC): At Risk (2)
HUS in ~7% of cases (due to RBC destruction and damage to BV wall lining)
–Acute renal failure (via HUS) in severe cases (children <10; elderly)
Enterohemorrhagic E. coli (EHEC): Diagnosis (3)
Sorbitol negative growth (RED on Sorbitol MacConkey Agar)
H7 serology and toxin analysis
PCR/Immunoassay for Shiga-like toxins
Enterohemorrhagic E. coli (EHEC): Disease (2)
Bloody diarrhea
Hemolytic uremic syndrome (HUS) if toxin spreads -> due to Shiga-like toxin
Enterohemorrhagic E. coli (EHEC): Incubation Period
3 days
Enterohemorrhagic E. coli (EHEC): Infectious dose
Low infectious dose (~100)
Enterohemorrhagic E. coli (EHEC): Negative for: (1)
Sorbitol**
Enterohemorrhagic E. coli (EHEC): Number of serotypes
O157:H7 = most important
Enterohemorrhagic E. coli (EHEC): Pathogenesis (5)
- COMMON pili-mediated attacment (weak)
- T3SS induced formation of attach/efface lesions
- other E. coli proteins recruit host cell actin (alter morphology and impact signal transduction pathways in host cell to form A/E lesions)
- lesions lead to effacement retraction of host cell microvilli)
- interaction of other virulence factors to attach (Tir-intimin) and produce pedestals (actin polymerization; role unclear)
Enterohemorrhagic E. coli (EHEC): Reservoir
Cattle (immune - lack host glycolipid for Shiga-toxin binding) but 28% shed EHEC
Enterohemorrhagic E. coli (EHEC): Similar to
Shigella
Enterohemorrhagic E. coli (EHEC): Special Features: Intra vs extracellular, presence of capsule, invasive or not
Mostly extracellular
Enterohemorrhagic E. coli (EHEC): Symptoms (3)
Abd. Pain, bloody diarrhea,
NEVER systemic
HUS
Enterohemorrhagic E. coli (EHEC): Transmission/vector/ habitat (3)
Food/water
Animals in petting zoos
Person-to-person
Enterohemorrhagic E. coli (EHEC): Treatment (2)
Supportive care
Antibiotics and antimotility agents are contraindicated
Enterohemorrhagic E. coli (EHEC): Virulence Factors (8)
T3SS (LEE pathogenicity island)
TIR: T3SS secreted protein delivered to epithelial cell surface for E. coli attachment
INTIMIN: Tir binding protein on E. coli surface
–Facilitates strong attachment
SHIGA-LIKE TOXIN (STX): gene on phage, disrupts euk. protein synthesis (cytotoxic) via RNA cleavage (subunit A), binds to cell (subunit B)
HEMOLYSIN: pore forming protein
Capsule (K-antigen)
LPS
Common pilus
Enteroinvasive E. coli (EIEC): Diagnosis (1)
PCR for virulence genes
Enteroinvasive E. coli (EIEC): Disease (1)
Diarrhea
Enteroinvasive E. coli (EIEC): Epidemiology (1)
Less common in industrialized nations
Enteroinvasive E. coli (EIEC): Pathogenesis (3)
- attaches to cells of colon via non-fimbrial adhesins
- invades mucosal cells
- multiplies within cell but does not become systemic.
Enteroinvasive E. coli (EIEC): Similar to
Shigella dysentery
Enteroinvasive E. coli (EIEC): Special Features: Intra vs extracellular, presence of capsule, invasive or not
Highly invasive
Enteroinvasive E. coli (EIEC): Symptoms (1)
Watery diarrhea that can contain blood and mucus (similar to Shigella)
Enteroinvasive E. coli (EIEC): Transmission/vector/habitat (1)
Food
Enteroinvasive E. coli (EIEC): Virulence Factors (2)
Plasmid encoded genes for invasion, replication, and survival (similar to Shigella)
Attaches via non-fimbrial adhesins
Enteropathogenic E. coli (EPEC): Diagnosis (2)
PCR for virulence genes
Tissue culture -> localized adherence
Enteropathogenic E. coli (EPEC): Disease (1)
Childhood Diarrhea
Enteropathogenic E. coli (EPEC): Epidemiology (1)
Leading cause of childhood diarrhea (developing countries)
Enteropathogenic E. coli (EPEC): Pathogenesis
Localized adherence by bundle-forming pili -> A/E lesions -> malabsorption -> diarrhea
Enteropathogenic E. coli (EPEC): Symptoms
Diarrhea
Enteropathogenic E. coli (EPEC): Transmission/vector/habitat
Person-to-person
Enteropathogenic E. coli (EPEC): Treatment
Antibiotics guided by susceptibility testing for severe or protracted cases
Enteropathogenic E. coli (EPEC): Virulence Factors (3)
Attaching/Effacing (A/E) lesions
Bundle-forming pili (Bfp)
NO toxins
Enterotoxigenic E. coli (ETEC): At Risk (2)
Travelers, infants in developing countries
Enterotoxigenic E. coli (ETEC): Diagnosis (1)
PCR for virulence genes
Enterotoxigenic E. coli (ETEC): Disease
Traveler’s Diarrhea
Enterotoxigenic E. coli (ETEC): Pathogenesis (3)
- fimbriae adhere to receptors on enterocytes in SI
- net loss of fluid and electrolytes into lumen of gut (LT/ST)
- watery diarrhea (LT/ST)
Enterotoxigenic E. coli (ETEC): Symptoms
Watery diarrhea
Enterotoxigenic E. coli (ETEC): Transmission/vector/ habitat (2)
Food/water
Person-to-person
Enterotoxigenic E. coli (ETEC): Treatment
Loperamide (+fluoroquinolone)
Azithromycin or rifaximin (for travelers)
Enterotoxigenic E. coli (ETEC): Virulence Factors (2)
Heat-labile toxin (LT): targets adenylate cyclase => increased cAMP levels => excess Cl- secretion and blocked Na+ uptake
Heat-stable toxin (ST): alters cGMP levels -> same effects as LT
Haemophilus influenzae (type B and other encapsulated, typeable, systemic): At Risk (3)
6-12 months of age (no more passive immunity)
Complement deficiencies
Developing countries