Bugs and Drugs Flashcards
Streptococcus pneumonia (pneumococcus) is the most common cause of what 4 diseases?
Pneumococcus MOPS pneumonic 1) Meningitis 2) Otitis Media (in children) 3) Pneumonia 4 Sinusitis
- “rusty sputum”
- sepsis in sickle cell anemia/asplenia
S. Pneumoniae Gram stain? capsule? Shape? Catalase +/- ? Hemolysis? Optochin/Bacitracin sensitive/resistant?
S. Pneumoniae Gram positive encapsulated cocci catalase negative alpha (partial/green) hemolytic optochin sensitive (differentiate from S. Viridans)
OVRPS pneumonic (Optochin-Viridans is Resistant; Pneumoniae is Sensitive)
Viridans streptococci Gram stain? capsule? shape? catalase +/- Hemolysis? Optochin/Bacitracin sensitive/resistant?
Viridans streptococci Gram positive nonencapsulated cocci catalase negative alpha hemolytic optochin resistant (differentiate from S. Pneumoniae)
OVRPS pneumonic (Optochin-Viridans is Resistant; Pneumoniae is Sensitive)
Also, bacitracin resistant (vs. S. Pyogenes which is succeptible to bacitracin.
S. Viridans
Colonization locations (normally and pathologically?)
Disease?
S. Viridans is part of the normal flora of the mouth. S. Mutans causes dental carries.
Also (S. Sanguis) causes subacute bacterial endocarditis of previously damaged valves. Classically after dental procedures.
S. Pyogenes (Group A Strep)
Causes what diseases?
Pyogenic- pharyngitis (strep throat), cellulitis, impetigo, endocarditis (uncommon)
Toxigenic- Scarlet fever, Toxic Shock-like syndrome, necrotizing fasciitis
Immunologic- Rheumatic fever, acute glomerulonephritis
Streptococcus Bovis (Nonenterococcus Gama hemolysis) If found in blood culture or as cause of subacute endocarditis, what do you need to check for?
S. Bovis bacteremia highly associated with GI malignancy (it is a normal comensal flora of gut)
Major virulance factor of Group A strep?
Group A strep = S. Pyogenes
M protein is the major virulance factor (prevents phagocytosis). Antibody to M protein causes resistance to organism. But antibodies to different M (3 and 18) proteins can lead to rheumatic fever (Always pharynx infection) or autoimmune complex deposition -> glomerulonephritis (PSGN, more commonly skin but can be pharynx)
N terminus is the variable region that Ab’s are created for.
Over 80 M protein serotypes
Streptolysin O?
Streptolysin O is virulence factor of S. Pyogenes. Binds to lipid/cholesterol -> polymerizes -> forms a pore -> hemolysis.
Antibody increases to Streptolysin O post infection (especially of pharynx)
ASO titer
Toxic Shock syndrome
A superantigen produced by Staph A. and Strep Pyogenes. The toxin binds MHC-II and TCR indiscriminately resulting in polyclonal T-cell activation -> cytokines/immune response. Fever, vomiting, rash, desquamation, shock, end organ failure.
Acute Rheumatic fever typically presents how long after S. Pyogenes infection?
PSGN?
ARF = 3-6 weeks (prevented by treatment)
PSGN = 2-4 wks (probably not prevented by treatment)
Group B Strep (S. Agalactiae)
Gram, catalase, hemolysis, differentiation
Colonize where?
Disease whom?
Gram + cocci, catalase -, Beta hemolysis, Bacitracin resistant (vs group A sensitive, B-BRAS)
Group B for Babies
Colonize 25% of women vagina
Causes pneumonia, meningitis, sepsis in babies
Tx; Prophylactic with PCN antibiotics prior to delivery.
Enterococci (Group D strep)
Gram stain, catalase, oxygen use?
Colonize where? Infections?
Hemolysis?
Normal colonic flora. Gram positive, Catalase negative, facultative anaerobe.
UTI, Biliary tract, subacute endocarditis, 4% meningitis
VRE (nosocomial)
Hemolysis (none/gamma)
Staph Aureus Gram Stain? Shape? chains/clusters? Catalase +/- Coagulase +/-
Gram Positive catalase positive Cocci in clusters
Coagulase positive
Differentiate S. epidermidis from S. saprophyticus
both these staphs are catalase +, coagulase negative
S. epidermidis is sensitive to novobiocin
S. Saprophyticus is Resistant
At staph retreat. NO StRESs
Novobiocin - saprophyticus is resistant, epidermitis is sensitive
Staphylococcus aureus
Virulence factors?
All in the Cell Wall
Protein A is the major virulence factor for S. aureus. Binds Fc-IgG, which inhibits complement fixation and phagocytosis.
clumping factor- (like coagulase) but binds fibrinogen to cell and clumps bacteria together
techoic acid- attach to human cells
Staphylococcus aureus
Colonization
Diseases?
Colonize anterior nares, some skin/nose/vagina
Inflammatory- skin infections, organ abscess, pneumonia, osteomyelitis, acute endocarditis
Toxin mediated-
1) Toxic Shock syndrome (TSST-1, superantigen, stimulates broad, nonspecific immune response)–> IL1,2,interferon, ect.
2) Scalded skin syndrome (exfoliative toxin A/B slough at desmosomes of granular skin layer),
3) rapid food poisoning (preformed enterotoxin ingestion)
-MRSA- resistant to B-lactams bc altered pcn binding protein
Staph epidermidis
Colonization?
Disease?
Normal skin flora. Often contaminates blood cultures. Can infect prosthetic devices and IV caths by making adherent biofilms
What does coagulase do?
It coagulates fibrinogen/fibrin. Can help microorginism form abscess
Macconkey agar
when negative?
Negative with catalase +
MacConkey is selective for gram negative organisms because GPs can’t grow in the presence of bile salts.
Gram negative organisms that ferment lactose will produce acid which lowers the pH and causes the medium to turn red.
GNRs that can’t ferment lactose, ferment peptone which creates ammonia –> raising pH. This produces clear colonies.
Staph Aureus resistance
Has plasmids, mostly transfers by transduction (bacteriophages)
PCN -> MRSA -> VISA/VRSA
Also 15% resistant clindamycin
Job’s Syndrome
Hyper IgE, poor neutrophil chemotaxis,
afflicted by boils (cold abscesses), like staph A.
FATED Mnemonic Facies (coarse) Abscesses (cold) Teeth (retain primary "baby" teeth) E -> Hyper IgE Dermatologic problems (eczema)
Catalase Positive Organisms
SLAP NECKS for catalase pos orgs.
S – S. aureus, L – Listeria, A – Aspergillus, P – Pseudomonas, N – Nocardia, E – E. coli, C – Candida, K – Klebsiella, S – Serratia
Encapsulated Bacteria
+
Vaccines for asplenic patients
SHiNE SKiS mnemonic for encapsulated bacteria – S. pneumonia, H. influenza type B, N. meningitides, E. coli, Salmonella, K. pneumonia, Group B Strep
+ vaccines
S. Pneumoniae, H. Flu, N. Meningitidis
Endocarditis
Acute organisms?
Subacute organisms?
S/S?
Acute Endocarditis usually: S. Aureus, B-hemolytic strep, pneumococcus
Subacute: Viridians strep > Enterococci > CoNS (coag negative staph, HACEK organisms
Community Prevalence: Nongroup A strep (40%) > Staph A. (28%) > Enterococci > others
Hospital Acquired: Staph A. (53%) > Enterococci (13%)
S/S Fever, chills, night sweats, myalgia, heart murmers, anemia, ESR, CRP, CHF (develops most often from valvular dysfunction), Osler’s Nodes (painful red immune complex depositions causing inflammation), splinter hemorrhage (vertical bleeding under nails), Roth’s spots (retinal hemorrhage)
FROM JANE Fever Roth's Spots (Retinal) Osler's Nodes (ouch) Murmur
Janeway Lesion (on palms and soles of feet)
Anemia
Night sweats
ESR increased/Emboli
Most common isolated nosocomial bacterial infection
2nd?
1) S. Aureus
2) Enterococcus (E. Faecalis and faecium predominantly)
Difficulty treating enterococci?
What two common Enterococci?
Resistances?
Prevalence Hosp. Aq. infections: E. Faecalis > E. faecium, but E. faecium is increasing
Both are resistant to PCN G
E. faecium is by far the most resistant and challenging enterococcal species to treat; indeed,
>80% of E. faecium resistant to vancomycin
>90% are resistant to ampicillin (historically the most effective β-lactam drug against enterococci)
Resistance to vancomycin and ampicillin in E. faecalis isolates is much less common (∼7% and ∼4%, respectively).
Factors increasing VRE colonization
The most important factors associated with VRE colonization and persistence in the gut include
prolonged hospitalization; long courses of antibiotic therapy; hospitalization in long-term-care facilities, surgical units, and/or intensive care units;
organ transplantation; renal failure (particularly in patients undergoing hemodialysis) and/or diabetes
VRE found on many inanimate objects in hospital. VRE can survive exposure to heat and certain disinfectants
Most common Bacterial causes of central line associated bacteremia
1st?
2nd?
1) S. Epidermidis (Coag neg. Staph)
2) Enterococci
Bacteria found in the intestine (7+4)
Gram Negative
Shigella
Salmonella
E. Coli
Yersinia
Campylobacter
Vibrio
Helicobacter
Gram positive
E. faecalis/faecium
Listeria
Clostridium
Enterobacteriaceae Gram stain? Morphology? oxidase +/-? ferment? Bugs with main causes of enteric infection?
Gram negative oxidase negative bacilli
All ferment glucose
Salmonella, Shigella, E. coli, Yersinia
“Shit Stink’s EspeCially Yours”
***campylobacter is distantly related and is top 3 cause of bacterial diarrhea
**others in enterbacteriaceae family include Klebsiella, Serratia, enterobacter, citrobacter, proteus….
Antigenic structures (3) of enteric bacteria (enterobacteriaceae)
All Gram negatives have LPS: consists of Lipid A, core polysaccharides, and O antigens (Lipid A portion is toxic). O for oligosacharide!!
H antigen (flagellar protein): Not all enterics have it
K antigen (polysaccharide capsule. Not all enterics have it, usually associated with increased virulence especially with bacteremias.
Vibrio Cholera S/S? mechanism of S/S? transmission/reservoir? Infectious dose? Treatment?
Abrupt onset diarrhea, abdominal cramps, some vomit. 15-20L/day diarrhea, High mortality if untreated.
Mechanism = Enterotoxin (A-B) B subunit binds cell surface receptor and injects subunit A. A ultimately constitutively activates Adenylyl cyclase which leads to cAMP concentrations and Cl- secretion and decreased Na+ absorption. Cytotonic.
Transmitted fecal/oral, reservoir aquatic environments
High infectious dose: 10/\8
Treatment:
1) Fluid replacement
2) Antibiotics (shorten course)
* *requires phage to transfer enterotoxin before virulent.
E. Coli Stain? shape? Oxygen? capsule? Colonize? Strains? Why? COMMON TO ALL Virulence factors?
Gram negative encapsulated bacilli, facultative anaerobe,
Colonize as normal small intestine flora: most abundant fac. anaerobe/GNBacilli in feces.
EIEC, ETEC, EPEC, EHEC (plasmid/phage differences)
general Virulence factors:
Fimbriae (adhesins): allow attachment to overcome peristalsis-> cystitis, pyelonephritis.
K capsule: virulence factor, antigenic -> pneumonia, neonatal meningitis
LPS - septic shock
ETEC (enterotoxigenic)
S/S
mechanism
Tx
S/S travelers diarrhea (70%), watery/secretory,
Toxin-noninvasive:
- Heat labile: similar to cholera (same mechanism cAMP by Ad. Cyclase)
- Heat stable: peptide toxin activates Guanylate cyclase -> cGMP -> fluid secretion
Tx; Fluid replacement. Bismuth. Generally don’t recommend antibiotics.
EPEC (enteropathogenic)
S/S
mechanism
Tx
common Pediatric and Persistent (can be weeks)
S/S watery diarrhea
Mechanism: Small intestine. noninvasive. no toxin. Adhere to enterocyte, TYPE III secretion, attach and efface/flatten villi -> poor absorption -> osmotic diarrhea
Tx; fluid replacement, rapid response to antibiotics
EHEC (O157:H7 most common) S/S mechanism Transmission Tx
Noninvasive but cytotoxic
Watery progress to Bloody diarrhea, hemorrhagic colitis, fever in severe cases, HUS (thrombocytopenia, hemolytic anemia, renal failure)
Mechanism: Shiga-like toxin. Stx-I and II. Encoded by phage. STx binds sphingolipid. Stx-I subunit A binds rRNA and cleaves (60s subunit) -> inhibit protein synthesis -> cell death. Stx-II subunit A inactivates Bcl-2 –> Apoptosis.
+ Otherwise also attach/efface enterocytes.
Transmission: Classically ground beef (cattle as reservoir), also fresh produce through manure runoff (spinach/lettuce/sprouts ect.)
Tx; Supportive. No proven benefit of antibiotics.
**Fecal leukocytes uncommon
LAB: does not ferment sorbitol, the rest of E. Coli do.
Shigella S/S Mechanism Transmission Tx;
4 groups (A-D) INVASIVE! but not systemic. NOT NORMAL FLORA!
S/S All can cause dysentery.
Fever/malaise/vomit/watery diarrhea –» Frank dysentery, cramps/tenesmus/up to 20stools/day
Mechanism: Large intestine.
Only type 1 dysenteriae makes Shiga toxin.
Otherwise M cell entry, Macrophage uptake -> induce apoptosis -> invade basal side epithelia -> break from vacuoles -> spread cell to cell. Immune response facilitates spread but ultimately can overcome infection.
Transmission: Low infectious does (10-100 organisms), acid resistant, Fecal/oral. Four F’s: Food, fingers, feces, flies.
Tx; fluid replacement, antibiotics for severe cases
Gastroenteritis definition
Infectious disease with some combination of diarrhea watery or bloody, vomiting, and abdominal pain and cramping +- Fever.
Dysentery is a type of gastroenteritis.
Salmonella S/S Mechanism Transmission Tx;
G - bacilli, facultative anaerobe, facultative intracellular parasite. produces H2S, Vi capsule
Invasive can become systemic. NOT PART OF NORMAL FLORA!
Clinical manifestations #Salmonella enteritidis: Gastroenteritis = N/V/D headache, chills, fever, watery diarrhea (2nd most common bacterial cause to campylobacter), little to no blood.
#Salmonella cholerasuis: Septicemia: prolonged fever without diarrhea dx w/blood cultures. Salmonella cholerasuis, no GI involved. **Salmonella osteomyelitis in sickle cell patients
#Salmonella typhi -Typhoid fever: constipation/inflammatory diarrhea, increasing fever, 6-8 week course. Colonization of gall bladder can lead to carrier or intestinal perforation.
Mechanism: Invasion of M cells (Ilium/colon).
Typhoid: Uptake by phagocytes -> Once phagocytosed, typhoidal salmonellae disseminate throughout the body in macrophages via the lymphatics and colonize reticuloendothelial tissues (liver, spleen, lymph nodes, and bone marrow).
Transmission: Oral. Typhoid is transmitted only by humans S. Typhi and S. Paratyphi. Non-typhoidal = animal reservoirs (poultry, eggs, contaminated fresh produce)
Tx: supportive for gastroenteritis (Ab actually increase shedding time)
For Typhoid: ->
Antibiotics (ciprofloxacin or ceftriaxone), prevent typhoid with vaccine. Immunity in general hard bc 2500 “serovars”
Yersina enterocolitica S/S Mechanism Transmission Tx;
Yersina pestis -> bubonic plague
Invasive. Can be serious and systemic.
S/S low fever, watery diarrhea +- blood, fecal leukocytes. Mimic appendicitis. One Complication is Reiters syndrome
Mechanism: Infects terminal ileum (mimic appendicitis)
Transmission: pet feces, undercooked pork, dairy products
(remember lobacter also transmitted from young pets)
Tx; supportive, antibiotics used but not proven
Campylobacter jejuni/coli Gram stain, catalase? oxidase? shape? S/S Mechanism Transmission Tx;
Gram negative comma shaped rods, catalase and oxidase positive. Invasive
S/S diarrhea/fever/abdominal cramping, 1/2pts have bloody diarrhea. +- Fecal leukocytes
Complication:
- Guillain-Barre (demyelination, hands/feet-> proximal; paresis/paresthesia-> paralysis)
- Reiters syndrome: HLAB27+ (autoimmune reactive arthropy/arthritis)
Mechanism: Invasive, enterotoxin, cytotoxin. small intestine -> Terminal ileum/proximal colon.
Transmission: warm months. milk or water. sporatic cases with young pets. Undercooked poultry!!
Tx; Fluid replacement. Antibiotics (erythromycin/quinolones)
H. Pylori Colonization? S/S Mechanism Tx;
Gram negative comma shaped bacilli
Noninvasive, high urease activity
Colonization: Gastric mucosa, highly mobile rapid penetration into mucous (less acidic), urease-> ammonia to raise pH. 50% world colonized (most common human pathogen), but projected to decrease.
S/S Gastritis, nearly all duodenal ulcers, 70% gastric, + gastric cancer (may regress with antibiotic tx)
Mechanism: decreases acidity, gastric atrophy
Dx; with histology, rapid urease biopsy, or breath test (C13)
tx; triple/quadruple therapy only for symptomatic
3) PPI, clarithromycin, and amoxicillin, or metronidazole
4) PPI, bismuth, metronidazole, and tetracycline
Dysentery
Syndrome: Fever, abdominal cramps, bloody/mucosal diarrhea
Type III secretion system
Bacterial (gram negative) protein that some organisms have that sense eukaryotic cells, attach, and secrete proteins into the eukaryotic cell that causes changes and “helps the bacteria survive”. Such as evading immune response.
May also help invade into cells
Infectious dose — The infectious dose of E. coli O157:H7 for humans is only 10 to 100 organisms, which is low compared with that of most other enteric pathogens:
●Shigella – 10 to 100 organisms
●Campylobacter jejuni – 10(4) to 10(6) organisms
●Salmonella – 10(5) to 10(8) organisms
●Vibrio cholerae – 10(5) to 10(8) organisms
●Enterotoxigenic E. coli (ETEC) – 10(8) organisms
●Yersinia enterocolitica – 10(9) organisms
Just to see
Definition of inflammatory diarrhea
The presence of gross or occult blood, fecal leukocytes, or elevation in fecal calprotectin (a protein found in leukocytes) indicates an inflammatory diarrhea. However, if the diarrhea has caused skin breakdown (eg, infants with marked diaper rash) or anal fissures, then a positive test for occult blood may not reflect an inflammatory diarrhea.
Lactose Fermenters GNR
E. Coli Klebsiella Enterobacter Citrobacter Arizona (Salm.) Serratia
Cows Sleep and Eat entirely Kale
EIEC (Enterinvasive)
S/S
mechanism
Tx
INVASIVE (only invasive E. Coli I know of)
S/S Dysentery (similar to shigella)
Mechanism: Invades intestinal mucosa, causes necrosis/inflammation. No toxin produced.
Tx; ?
Listeria
Gram stain
Structure
S/S (3 infections)
Transmission
Mechanism/virulence factor
Tx:
Gram +, nonspore forming, facultative intracellular bacilli
S/S
1) Pregnant women: 3rd trimester (spread to fetus -> death/premature labor with infection)
2) Fetus/neonate: acquired from mother (in utero/vagina) -> two weeks postpartum neonatal meningitis.
3) Elderly/immunocompromised: meningitis
Transmission: unpasteurized milk/cheese, deli meat, vaginal transmission childbirth. Don’t eat soft cheese/cold cuts.
Mechanism: Listeria Lyses (with listeriolysin O) phagocytic vacuole to escape into cytosol. Polymerizes actin (actin rockets), allows movement and invasion of neighboring cells.
Tx; If LP confirms meningitis, cover empirically for >50y/o and neonates. TMP or ampicillin
Meningitis within most 3 months (3 organisms)
Meningitis post maternal antibodies (2)
Neonatal (acquired exiting vagina): Listeria, E. Coli, Group B Strep
Post maternal antibodies: N. Meningitides, H. Flu
S. pneumoinae is also significant 6mo on.
How to confirm meningitis
bacterial
fungal/TB
viral
LP: All can have high opening pressure
Bacterial: high neutrophils (PMN), high protein, low glucose
Fungal/TB: lymphs, high protein, low glucose
Viral: lymphs, normal->increased protein, normal glucose
viral gastroenteritis epidemiology Transmission: Incubation? S/S vaccine?
epidemiology: >75% cause of gastroenteritis of known.
Top 2 in children are #1 Rotavirus (Except where vaccinated), #2 Norovirus
etiology, many serotypes
Transmission: Fecal- oral,
Incubation: 1-2 days, resolves 4-7 days.
S/S: watery diarrhea without blood/mucous, +-nausea/vomit, intestinal cramping, +-muscle ache, +- low grade fever
Vaccines: rotavirus available. Norovirus in dvlp.
Norovirus Describe structure ect. epidemiology? Transmission: Immunity:
Small non-enveloped (+) ssRNA with cup/chalice-like indentations
Epidemiology: Most common cause of diarrheal outbreaks older children and adults. (cruise ships, hospitals, nursing homes)
Transmission: Fecal oral, also surfaces, water, food (shellfish)
Immunity: 6mo
Rotavirus Describe structure ect. epidemiology? Genetic Diversity Transmission Invasion: S/S Tx: Immunity:
nonenveloped (with 3 protein shells) 11 genome segments of dsRNA that code for single strand mRNA that make 1 protein, contains enzymes as well (like RNA-dependent RNA polymerase).
Epidemiology: most common cause childhood diarrhea (severe infantile gastroenteritis)
Genetic diversity: if 1 cell infected by multiple virions, exchange genome segments. Virus assembled in RER
Transmission: Mostly fecal-oral and surfaces
Invasion: Protein must be cleaved by Trypsin in gut to be infective (must supply trypsin in cultures)
S/S: Up to 50% asymptomatic
-fever, vomiting, diarrhea (explosive)
Tx; oral rehydration therapy
Immunity: vaccination can reduce severity and incidence. breast feeding is protective. IgM, IgG, IgA, and cellular responses occur. Immunity is not complete but results in milder infections
Enteric Adenovirus
virology
S/S
Non-enveloped, icosahedral dsDNA.Humans only reservoir.
Incubation 4-10days
S/S Most infections are asymptomatic
Serotype 40, 41 gastroenteritis (diarrhea with vomit later, symptoms lasts 5-12 days which is LONG for a virus)
Common: URI, conjunctivitis “pink eye”, pharyngitis, pneumonia (4-5% of viral caused resp illness), hemorrhagic cystitis.
**No association with human tumors
Astrovirus
Epidemiology:
Transmission:
Invasion:
small non-enveloped virus, ss + sense RNA genome, star shaped capsomer
Epidemiology: associated with 2-8% diarrhea, but associated with outbreaks.
Transmission: fecal-oral, food
Protein must be cleaved by Trypsin in gut to be infective (must supply trypsin in cultures)
Positive vs negative ssRNA viruses action upon infection
+ strand = mRNA = translated directly
- strand must be translated to + by RNA-dependent RNA polymerase (they must carry the enzyme in their capsid)
6 DNA viruses
ssDNA vs dsDNA?
Enveloped?
HHAPPPy
Herpes Hepadna Adeno Papova = Papilloma (HPV) Parvo = B19 Pox
- All DNA viruses EXCEPT Parvoviridae have dsDNA, parvo is ssDNA (- sense)
- *Poxviridae is the only DNA virus NOT in icosahedral symmetry. POX in a BOX, replicates in cytoplasm (has own DNA dependent RNA polymerase
PAP smear are naked.
-PApilloma, Adeno, PArvo
Neisseria meningitidis structure/morphology? metabolism: epidemiology reservoir Transmission toxin Clinical manifestations (2) Treatment
Gram negative encapsulated kidney shaped diplococci
Metabolism: Facultative anaerobe, ferments Maltose and Glucose
High Risk: Infants 6mo-2yr, Army recruits, College Freshman
Reservoir: Nasopharynx (5% of population, can impart immunity), strict human colonization.
Transmission: Respiratory
Toxin: LPS, no exotoxin
Clinical:
1) Meningitis: Fever, nuchal rigidity, vomit, lethargy/AMS, petechial rash (especially with septicemia)
2) Septicemia: Fever, petechial rash, septic shock, Waterhouse-Friderichsen Syndrome: Adrenal hemorrhage with septic shock/rash
Treatment:
Vaccine not available <2y/o, lasts 2-4yrs.
PCN G or Ceftriaxone
Neisseria Gonorrhoeae structure/morphology? metabolism: epidemiology toxin Clinical manifestations (Men/women/both) & neonates Treatment
Gram negative kidney shaped diplococci (no capsule)
Metabolism: Facultative anaerobe, ferments Glucose ONLY, gram stain where Gonorrhoeae will be inside WBC’s
Epidemiology: Humans only, sexually transmitted (2nd most common to Chlamydia) . Often co-infected with Chlamydia trachomatis. Increase risk for other STD.
Toxin: LOS (similar to LPS), no exotoxin
Clinical: May be asymptomatic (major public health obstacle) but still infectious
Men: Urethritis, prostatitis, epidydimitis
Women: urethritis, Cervical gonorrhea -> PID
Both: Gonococcal bateremia, septic arthritis, proctitis
Neonates: Opthalmia neonatorum conjunctivitis (prophylactic erythromycin or silver nitrate eye drops at birth). Fitz-hugh-Curtis Syndrome: (liver capsule infection. RUQ pain.
Tx; Ceftriaxone IM + Azithromycin PO both x1 (substitute azithro with doxy if needed). No immunity from vaccinations nor following infections (large antigenic heterogeneity). TREAT SEXUAL CONTACTS. Resistance is developing!!
The azithromycin has activity at a different target and also is used to tx chlamydia
What virulence factors help Neisseria avoid immune damage on mucosal surfaces?
IgA protease
Pili: To adhere (closely to host cell) which is protective from gut motility AND phagocytic detection/attack
Pelvic Inflammatory Disease What is it? S/S complications? Tx;
Imprecise description of infection of uterus, fallopian tubes, and/or ovaries. Often purulent.
S/S fever, LOWER ABDOMINAL PAIN, abnormal menstrual bleeding, cervical motion tenderness (doctors fingers or guys penis). Nausea, Vomiting. Menstruation spreads disease.
Complications: Sterility (up to 25%?), ectopic pregnancy, abscess, peritonitis, perihepatitis. SCARRING causes a lot of this. Recurrent infection increases complications
Tx; Ceftriaxone (gonnorhea)+ Doxycycline (Chlamydia)
Otitis media incidence in children by 3
what bacteria?
80% of children by 3 have had otitis media
Strep pneumoniae, H. Flu, Moraxella
“Stop Having Media”
Moraxella
Reservoir
Clinical manifestations
Treatment
Reservoir: Normal respiratory flora
Clinical manifestations
1) Otitis Media
2) Can cause sinusitis, bronchitis, pneumonia
3) COPD exacerbation
Tx; Resistant PCN, treat with azithromycin or clarithromycin
Phase variation in bacteria
Ability of single bacteria to turn on and off protein expression, notably antigenic proteins.
Chlamydia trachomatis structure/morphology parasite pump Transmission Life Cycle (basic to all chlamydia)
Clinical manifestations
tx;
Gram negative obligate intracellular. atypical cell wall. Cannot be visualized except as a clump of inclusion inside cell. May need Nucleic Acid Amplification Test (PCR). Infection increases risk for other STD’s.
PUMP: ATP/ADP translocator. No mechanism to create ATP
Transmission: THE most common STI. Coinfection with Gonorrheae common (discovered if PCN doesn’t work)
Life cycle: Biphasic
1) Elementary Body (EB) is infectious (temporarily stable extracellularly) and enters cells by endocytosis. Prefers columnar cells that line mucous membranes (think conjunctivitis, cervicitis, pneumonia). EB inhibits phagosome-lysosome fusion once endocytosed -> transform to RB
2) Reticulate Bodies (also called initial body): Binary fission. More EB and RB’s made. Cell lyses -> infection spread.
Clinical manifestations: Often asymptomatic 75%female, 50%male)
1) Urethritis: purulence, dysuria, PMN’s without bacteria on microscopic exam (vs. gonorrhea)
2) Epididymitis/PID: Infection can extend to cevix/salpingitis
3) Inclusion conjunctivitis: mostly neonates but also adults. 4)Also infant pneumonia
5) Trachoma: Chronic keratoconjunctivitis -> begins scarring/blindness. (TRANSMISSION from hand-hand contact)
6) Lymphogranuloma venereum: ulceration that heals but travels to inguinal lymph nodes -> may ulcerate/purulent -> may disseminate/systemic/peritonitis
7) Reiter’s Syndrome
8) Fitz-hugh-Curtis Syndrome: (liver capsule infection. RUQ pain.
Tx;
Adults Azithromycin PO generally works.
Children: Prevent inclusion conjunctivitis with erythromycin eye drops at birth, but if develops requires systemic therapy. In infants use erythromycin instead of azithromycin for everything. Pneumonia also use erythro. **infection associated with mild/moderate eosinophelia
Most common cause of neonatal conjunctivitis in the USA
tx;
Inclusion conjunctivitis from Chlamydia trachomatis (vagina acquired)
7-12 days incubation. May disseminate and cause pneumonia
Chlamydia psittaci
Transmission
Clinical manifestation
Transmitted from 130+ bird species dust/feces
Atypical pneumonia
Chlamydia pneumoniae
Transmission
Clinical manifestation
Transmission: person to person, typically younger adults
Atypical pneumonia
Leading cause of preventable blindness
tx;
Trachoma from Chlamydia trachomatis
Blindness develops over 10-15 yrs. Disease of poverty
Scarring causes contraction of eyelids inward -> eyelashes scratch/further damage cornea/sclera
Tx; Topical DOES NOT WORK. Use oral azithromycin
Fitz-hugh-Curtis Syndrome:
(liver capsule infection. RUQ pain.) Associated with Chlamydia Trachomatis and Neisseria Gonorrhea
Treponema pallidum subspecies pallidum structure/morphology? Transmission toxin (none) Clinical manifestations (3.5) Treatment
Gram-negative spirochete lacking LPS and containing axial filaments that run along the inner side of outer membrane. Difficult to culture, ID with darkfield microscopy, immunoflourescence, or silver stain.
Transmission:STI that causes Syphilis. Skin-skin, even intact skin can be invaded.
Untreated it progresses through 3 stages (latent period btw 2 and 3)
Primary Syphilis #PAINLESS Chancre (ulcer) with regional nontender lymph swelling 3-6wks after infection, resolves without scar. HIGHLY INFECTIOUS VACATION RESORT FOR Treponema
Secondary hematologic spread (often 6 wks after primary chancre heals) # Rash on palms/soles, also diffuse and mucosal (macular, sometimes papular/pustular) (bronze colored) # Generalized lymphadenopathy # Condyloma latum (painless wartlike lesion often warm/moist places like vulva/scrotum) -> ulcerates -> INFECTIOUS!!!! # CNS, eyes, bones, kidneys, joints or almost any organ may be involved
Latent (resolves 2nd stage): +- relapse to secondary, after 4 years disease is considered noninfectious except pregnant woman -> fetus
Tertiary (1/3 of latent will progress, 15% of untreated pts)
# 3-10yrs postinfection => GUMMAS of skin/bone (granulomatous lesions -> necrotic/fibrous). If bone = deep gnawing pain.
# 10+yrs post => Cardiovascular (aortic aneurism) -> dissections. caused from destruction of supplying vasa vasorum
# Neurosyphilis:
-Asymptomatic
-Subacute meningitis (high lymphs vs usual PMN’s)
-Meningovascular Syphilis circle of willis dmg/infarct
-Tabes Dorsalis: Posterior column/dorsal ganglia dmg
Tx; PCN is effective. Watch out for Jarisch-Herxheimer Phenomenon, which is worsening symptoms likely due to release of spirochete cell contents.
Herpesviruses
Structure
Replication
Common clinical features
Linear dsDNA Enveloped with icosohedral capsid
Replication: Genome is delivered to NUCLEUS and forms an episome (circle) upon infection. This is where virus is replicated and capsid formed. Envelope is from Golgi.
Clinical Features:
- All Herpes establish latent infection
- primary infection often different than reactivation
- Disease of reactivation usually less severe
- Herpesvirus more severe with Tcell defects
Acyclovir and Ganciclovir similarity/difference
MOA
Which treats; HSV, CMV, VZV?
Acyclovir and Ganciclovir are nucleoside analogues given as prodrugs that must be activated by viral enzymes.
Acyclovir (tx HSV and VZV) @ by thymidine kinase
Ganciclovir (tx CMV) @ by UL97 protein kinase
The different viruses contain different enzymes
HSV-1 and HSV-2
Invasion
Transmission
S/S and progression
-Primary
-reactivationInvasion: Labile virus. Invades direct contact break in skin/mucosa.
Transmission: Shedding, periodic and can be when asymptomatic
Progression: Genital Herpes/Oral Herpes
Primary: papule -> vesicle -> pustule -> scab (= primary disease resolution)
Other
Gingivostomatitis: Fever, malaise, multiple vesicles
Herpetic keratitis -> corneal blindness
Neonatal Herpes -> stillborn/congenital defects
Herpetic Whitlow -> Wear a glove Dr.Whitlow!
Disseminated Herpes -> Immune compromised hosts, includes organ involvement
Encephalitis-> Most common cause viral encephalitis in US. Fever and focal neurologic abnormalities, necrosis of brain
Reactivation comes from latent virus in sensory basal ganglia
What infectious organisms can cross the blood-placental barrier?
S/S?
Others related to vertical transmissino
TORCHES
TOxoplasmosis Rubella Cytomegalocirus HErpes and HIV Syphilis
S/S hepatosplenomegaly, jaundice, thrombocytopenia, growth retardation
Others:
Meningitis: E. Coli, Listeria, Group B strep
Parvovirus B19 -> hydrops fetalis
Varicella-Zoster Virus
Varicella?
Zoster
Varicella (Chickenpox)
Highly contagious, fever, malaise, headache followed by rash. Rash is “dew on a rose petal.” = vesicle on erythematous based.
-Crops of lesions show up at different times -> different stages of dvlpment.
Vaccine exists now for Varicella
Zoster (shingles)
reactivation from sensory ganglia migrates to skin in dermatomal pattern (not that this doesn’t cross midline)
-> Burning, painful skin lesions.
Zoster vaccine recommended above 60y/o (reduces incidence by 50%)
Cytomegalovirus
Prevalence
Clinical manifestations:
Prevalence: 80% adults
Clinical manifestations:
#Asymptomatic (most)
#Congenital: vertical transmission. stillbirth, mental retardation, microcephaly, deafness
#mononucleosis syndrome: Fever, chills, sweats, headache, pharyngitis, lymphadenopathy, enlarged spleen. Atyptical lymphocytes (T cells). Negative monospot
#Reactivation:any and everywhere. especially immunocompromised.
(Marrow transplant ) Viremia, retinitis, colitis,
pneumonia (marrow transplant)
EBV Prevalence Clinical manifestations: Dx; Malignancies
90% adults, latent in B cells
Clinical manifestations: #Mononucleosis: Feer, malaise, pharyngitis, lymphadenopathy, splenomegaly, hepatomegaly/hepatitis, rash with antibiotics (ampicillin/amoxicillin)
Dx; Heterophil antibody test (monospot)…cardiolipin and shit
EBV specific antibodies
Malignancies: (activates c-myc among other TF’s)
Burkitt Lymphoma (8:22, 2:8, 8:14)
Hodgkins lymphoma
nasopharyngeal carcinoma
LESS associated I think \/
gastric adenocarcinoma
Leiomyosarcoma
Herpes viruses with multinucleated giant cells (syncytial cells)
HSV 1,2
VZV
4 exudative pharyngitis infections
EBV, Strep pyogenes, adenovirus, HSV in adolescents
In general IgM vs IgG antibodies are associated with acute vs past infection?
IgM is acute
IgG can be acute/chronic/past
HHV8
Latent in B cells, pretty much causes/promotes Kaposi Sarcoma in immunodeficient patients, especially AIDS
KS = angioproliferative inflammatory lesion
Infection with low grade fever, headache, malaise, upper respiratory symptoms followed by sudden appearance of erythematous malar rash (may includ nasolabial fold) is caused by what?
This is 5th disease, caused by parvovirus B19
5 common causes of Orchitis
# Chlamydia trachomatis, Neisseria gonorrhaeae # Mumps (usually parotid involvement first) # Tuberculosis # Treponema Pallidum (Syphilis)
Usually these diseases travel
Epydidimitis -> Orchitis
In thinking about UTI’s
Leukocyte esterase in urine tells you what?
Nitrite test tells you what?
WBC casts tell you what?
Urease = ?
Polymicorbial urine culture tells you what?
Leukocyte esterase = likely bacterial etiology
Nitrite test = gram negative UTI
WBC casts = ascent to kidneys = pyelonephritis
Urease = proteus, klebsiella. A clue would be an alkaline urine. IF neg: E coli, enterococcus
Polymicrobial culture = poor urine catch, contamination
Top 3 causes of UTI
# Leading cause = E. Coli # 2nd in comm acquired sexually active women = Staph Saprophyticus # 3rd = Klebsiella pneumoniae
Top 2 infectious causes Cellulitis and Impetigo
Staph Aureus and S. Pyogenes
Reiter’s Syndrome
Description and bugs
HLA-B27+ genetics
Urethritis, conjunctivitis, arthritis (reactive)
Autoimmune trigger, initial offending agent often gone before symptoms occur
“Can’t see, can’t pee, can’t climb a tree”
Bugs:
Shigella, salmonella, Yersinia, campylobacter, chlamydia
“SSYCC”
2 most common causes of GRAM NEGATIVE sepsis
1st E. Coli
2nd Klebsiella pneumoniae
Enterobacter
Gram stain
colonization
Highly motile, gram negative rod. Lactose fermenter. Normal flora of GI tract. Occasionally responsible hospital acquired infections
