Microbiology Flashcards
1
Q
intravascular sources of bacteremia
A
- transient: MCC teeth brushing
-
continuous: IE and other endovascular infections where there is a constant low level of bacteria being seeded over time→ biofilm
- mycotic aneurysm: damage to endothelial cells lining arteries→ seeding
- suppurative thrombophlebitis: damage to endothelial cells lining vein→ clot and seeding of clot by organisms
2
Q
extravascular sources of bacteremia
A
bacteria enter blood stream through lymphatic sysmte from another side of infection
-
intermittent: MCC of sepsis; often associated with extravascular infection that provides portal of entry for bacteria
- usually coagulase(-) staph, S. aureus, candida
3
Q
how much bacteria/mL can lead to septic shock?
A
1 bacterium/10mL of blood can lead to septic shock
- 3 cultures/24 hrs increases liklihood of picking up organism
- kids: tolerate more bacteria so it will probably show up with less culturing
4
Q
sepsis
A
bacteremia with associated clinical manifestations:
- fever and shaking chills OR v. low temp
- decreased urination
- rapid pulse and RR
- N/V/D
- confusion esp. in elderly
5
Q
severe sepsis
A
sepsis and associated organ dysfunction with:
- hypotension (systolic <90, MAP <70 that can be reversed with volume or vasopressors)
- confusion
- oliguria
- hypoxia not explained by respiratory disease
- met. acidosis
- DIC: protein C inhibits plasminogen activor inhibitor→decreased coagulation cascade
- hepatic dysfunction not explained by liver disease
6
Q
septic shock
A
sepsis and hypotension requiring vasopressors despite fluid resuscitation
- perfusion abnormalities may include lactic acidosis, oliuria, AMS, acute lung injury
7
Q
SIRS
A
whole body inflammatory state without proven source of infection
- TLR4 recognizes gram(-) LPS→ cytokine storm (TNFa, IL-1, IL-6)
- variation in number of acyl chains in lipid A can impact signaling through TLR4 and dramatically alter the host response
8
Q
procalcitonin
A
differentiates infectious vs. noninfectious SIRS
- <0.5ng/mL: low risk for progression to severe sepsis/shock
- 0.5-2ng/mL: sepsis should be considered
- >2ng/mL: high risk for pression to severe sepsis/shock
9
Q
malaria
A
- caused by 4 distinct species of protozoans
- p. falciparum is most lethal and MC strain in africa
- p. vivax: MC strain worldwide
- Duffy antigen on RBCs in erythrocyte receor for p. vivax (absence prevents p. vivax malaria)
- HbS, HbC, and thalassemias provide protection
10
Q
cyclic pattern of malaria symptoms
A
- cold stage: lysis of RBC→ feeling of intesne cold for 15-60 mins
- hot stage: circulating merozoites and immune response→ intense heat, dry burning skin, throbbing headage for 2-6 hours
- sweating stage: merozoates are infecting other RBCs→ produse sweating, decling temp, exhaustion for 2-4 hours
11
Q
recrudescence of malaria
A
parasitemia falls below detectable levels and then later increases to a detectible parasitemia
12
Q
relapse of malaria
A
sporozoites invade hepatocytes, develop into schizonts and may or may not be observed in circulation; individual may be asymptomatic
13
Q
p. falciparum
A
more acute and severe than malaria caused by other plasmodium species
-
PfEMP-1: receptor on 100% of RBCs enabling infection of all RBCs (other parasites have less access)
- cerebral malaria: sticking of RBCs along BBB→ poor oxygenation
- placental malaria: infected RBCs sequester in maternal circulation of placenta
14
Q
trypanosome cruzi
A
chronic parasitic infection transmitted by reduviid bug→ chagas disease
- not intracellular; chronically can infect heart, colon, esophagus
- romana sign (inflammed eye)
15
Q
leishmaniasis
A
sand fly regurgitation→ multiplication in histocytes; comes in cutaneous (MC), mucocutanous, and visceral forms
16
Q
toxoplasmosis gondii
A
leading cause of death attributed to foodborne illness in US; 60 million carry parasite but few are symptomatic
- detection with toxo-specific antibodies, inteprete whether it is new or reccurant infection
- in newborn: chorioretinitis, hydrocephalus, intracranial calcifications; highest risk of transmission in 3rd trimester; most babies do not initially show signs but develop disabilities later
- in immunocompromised: leading cause of focal CNS disease in AIDS; eye disease (retinochoroiditis) can result rom congenital infection or infection after birth→ white fluffy patches on fundoscopy
17
Q
borrelia
A
- spirochetes that are large enough to see with microscope
- b. burgdorferi (lyme dsease)
- relapsing fever
18
Q
borrelia burgdorferi
A
- lyme disease; vectored by deer ticks, requires 24 hours to transmit
- serolog: confirms exposure but not disease and not promptly
- stage 1: flulike with erythema migrans
- stage 2: musculoskeletal and/or neurologic symptoms
- stage 3: additional neurologic symptons, post-lyme syndrome with lingering neurological sequlae
- treat: amoxicillin or doxy for 10-30 days (lingering symptoms are due to damage, not bacteria)
- potential for jarisch-herxheimer rxn
19
Q
relapsing fever
A
- louse or tick borne (louse is more severe, tick is more likely in US)
- borrelia immediately enter bloodstream→ repeated rounds of bacteremia and clean up by IL-10→ spirochetes vary surface antigens
- repeated high fevers with wellperiods between
- diagnosis: peripheral blood smear (spirochetes visible during febrile periods)
- treatment: tetracycline (Jarisch-Herxheimer rxn)
20
Q
rickettsia
A
- small cocci to short-rods transferred by arthropod vectors
- obligate intracellular parasite (grown in vitro in tissue culture)
- reproduce by binary fission
- Omp A&B, T4SS, phospholipase A1, ActA
- diagnose with immunochemical staining
- rocky mountain spotted fever
- typhus
- treat: doxy (even kids); chloramphenicol for pregnany and allergic patients
21
Q
rocky mountain spotted fever
A
- rickettsial disease spread by dog ticks and mice
- eschar at tick site (mediterranean spotted fever also has this)
- pitecheal rash on extremities that spreads towards trunk
- treatment: doxy
22
Q
typhus
A
- humans are normal host and reservoir; body louse as vector
- abrupt onset of fever/chills and unremitting headache
- Brill-Zinsser Disease: recrudescent form of epidemic typhus (maay be seen in geriatrics who had typhus in WWII)
- treatment: doxy (even for small children)
23
Q
ehrlichia
A
- human monocytic ehrlichiosis: tiny gram (-) obligcate intracellular parasite that replicate in WBC
- severe headache, fever/shaking, chills one week after tick bite
- morulae on blood smear
- treatment: doxy (even for children)
24
Q
anaplasmosis
A
causes human monocytic anapalsmosis (similar to erlichiosis, obligate intracellular parasite that survives and mulltiplies in early endosome of WBC)
25
S. aureus
* gram+ coagulase+ (doesn't spread)
* virulence factors: protein A, capsule, toxins (exfoliatin, TSS)
* surface lesions
* **impetigo:** due to mix of s. aureus and s. pyrogenes; mupiricin ointment
* exfoliating rash of TSS
* scalded skin syndrome due to exfolatin (no infection at site just circulating toxin)
* **furunculitis:** bacterial infection of hair follicles and sweat glands; abcess drainage and antibiotics
26
s. epidermidis
* gram+ coagulase(-) novobiocin sensitive
* surface lesions: infection piercings→ biofilm with chronic low grade infection (Au, Ag less likely to cause infection)
* no treatment except for removal of piercing/catheter (organism is protected in biofilm)
27
streptococci
* subcutaneous infection: **cellulitis/erysipelas:** usually due to s. pyogenes, can spread (coagulase -) and break down tissues
* deep skin: **necrotizing fascitis:** usually group A strep with high proteases; mysterious etiology (infects healthy individuals), rapidly spreading
* **post strep glomerulonephritis:** 3-4 wks s/p strep skin infection with specific M protein-types; lesions are sterile (no treatment)
28
scabies
* mites→ scabies: itching due to delayed hypersensitivity reaction
* treat with topical steroids (itch) and malathion (antimite)
29
cutaneous mycoses
* **dermatophytosis:** epidermophyton, trichophyton, or microsporum
* **tinea versicolor:** malassezia (normal flora)
* **tinea nigra:** wernecki (soil organism)
30
dermatophyosis
* v. common, caused by epidermophyton, trichophyton, or microsporum
* infect **superficial keratinized structures** (produce keratinases)
* symptoms are called tinea (jock itch, athlete's foot, ringworm)
* transmitted by fomites or autoinoculation
* dianosis: **KOH mount, culture, PPD, wood's lamp**
* treat all sites simultaneously with OTC topical antifungal
31
tinea versicolor
* **common hypo/hyperpigmented areas on trunk caused by overgrowth of normal flora malassezia**
* diagnosis: KOH mount of skin scrapings
* treat: **selenium sulfide cream**
32
tinea nigra
* uncommon **infection of injured extremity by soil organism wernicki**
* **dark brown spot (rule out melanoma)**
* diagnosis: KOH mount for **thick septate (branching hyphae with dark pigment in their walls)**
* culture on **sabouraud's agar at room temp for _shiny black colonies_**
* treat: topical salicylic acid and topical azole
33
subcutaneous mycoses
* **sporotrichosis:** sporothrix (vegetation)
* **chromomycosis:** tropical soil fungi
* **mycetoma:** petrillidium or madurella (soil)
34
sporotrichosis
* **"rose picker's disease" caused by sporothrix (thermally dimorphic fungi of vegetation that enters skin through small injuries)**
* **painless ulcer at site→ lymphatic spread over years**
* if COPD→pulmonary
* if immunosuppressed→ disseminated, meningitis
* diagnosis: punch biopsy **(round or cigar-shaped yeast)**
* culture at room temp from **pus (hyphae and conidia resemble daisies)**
* treat: **oral azoles (amphotericin B for 3-6 mo if serious)**
35
chromomycosis
* **tropical soil fungi** that enter by injuries with thorns/splinters
* **gradually spreading wartlie or plague lesions with _scattered black dots_**
* diagnosis: KOH mount for **gray or black septate hyphae or conidia**
* **biopsy of spots: dark brown, round fungal cells inside leukocytes or giant cells******
36
mycetoma
* **rare infection of wounds on extremities** by petriellidium or madurella from soil
* **forms abcesses, granulomas, pus with granules**
* **differentiate from actinomycosis by staining (fungal cells are bigger)**
* diagnosis: **needle biopsy, xray**
* treat: **combo of surgery, IV amphotericin B, oral azole**
37
candida
* gram+, multimorphic (yeastlike, pseudohyphae, hypae)
* virulence factors, no particular tissue tropism
* neutropenia is major predisposition
* **c. albicans:** thrush, vaginitis, diaper rash
* less common: hand infection, folliculitis, full-GI infections (leukemia)
* **chronic mucocutaneous candidiasis with impaired CMI, genetically low IFN-g, IL-2, 17, and/or 22**
* candidemia and disseminated disease (organ abscesses): potentially lethal and on the rise (those with v. impaired CMI survive long enough to develop)
* diagnosis: exam, biopsy, culture, and/or CT
* treatment: **topical azoles and polyenes (superficial), oral azoles (more serious), + amphotericin B if life-threatening**
* **echinocandins and/or voriconazole if drug-resistant**
38
herpesvirus species
* large enveloped DNA virus, treat with acyclovirs and derivatives
* HSV1: oral herpies
* HSV2: genital herpes
* HSV3 (VZV): chicken pox, herpes zoster
* HSV4 (EBV): mono
* HSV5 (CMV)
* HHV6b, HH7: Roseola
* HHV8 (KSHV): Kaposi's Sarcoma
39
HSV 1
* above the waist; 50-80% seropositivity
* recurrent disease: cold sores, **exogenous rash latency in dorsal root ganglia**; 20% of seropositive have recurrent lesions
* **herpetic whitlow:** HSV1/2 of nonmucosal sites acquired by direct contact
40
HSV2
* vesiclar letions on labia, penis, anus, mouth
* lesions are contagious but shedding and transmission can occur without symptoms
* primary infection can occur in eye at birth from vagina→corneal scarring and vision loss mediated by T cells that destroy cornea
41
HSV 3 (VZV)
* **endogenous rash (aerosol transmission)**→ vesicular rash "dew drops on rose petals" on face and trunk
* **latency in dorsal root ganglia**
* **herpes zoster:**"shingles" outbreak along single dermatome
* **herpes zoster ophthalmicus:** 30% of zosters affect face; can involve retina→ blindness
* vaccine: live, attenuated virus
42
EBV
* mono; infects B cells and epithelia of oropharynx
* restricted to humans (90% is infected by adulthood); **no rash**
* **oral hairy leukoplakia:** overgrowth of oral epithelial cells in immunocompromised
43
CMV
primary infection is usually asymptomatic; when symptoms occur it is **similar to EBV except no sore throat and presence of petecial rask and jaundice**
44
roseola
* infects CD4+ T cells; transmissted in saliva
* by 2 yrs \>90% of children have had it twice
* 3 days of high fever, fever breaks→ faint rash on trunk
* mistakenly given antibiotics, rash attributed to drug allergy
45
kaposi's sarcoma
* found in B cells and endothelial cells
* no known disease in primary infection
* recurrences linked to cancers and AIDS
* treat underlying immunodeficiency
46
coxsackie virus
* enterviridae; small naked ssRNA
* herpangina: throat infection with red-ringed blisters and ulcers on tonsils and soft palate
* hemorrhagic conjunctivitis: eye pain→ red, watery eyes with swelling, light sensitivity and blurred vision
* **hand, foot, mouth:** painful red blisters on throat, tongue, guns, hard palate, inside cheeks, palms and soles
* highly contagious, spread on hands and surfaces contaminated by feces and saliva, aerosol spread
* no treatment
47
HPV
* small, naked DNA virus; warts infecting skin, genitals, cervix, anus, and mucosa
* spread by direct contact, **differentiate from lesions caused by molluscum contagiosum**
* treat with chemical or surgical removal
* vaccine available (recombinant HSV)
48
pox virus
* large enveloped DNA virus
* **molluscum cotagiosum virus:** pearly, pink, papules, umbilicated
* transmission: skin-skin contact or fomites
* treatment: surgery, cryotherapy or chemicals
* **monkey pox:** indistinguishable from small pox; fatality rate 10-15%
* **small pox:** variola virus eradicated with live attenuated vaccinia vaccine; carries risk for immunocompromised→ papular, vesicular then pustular, scabs leave pitted scars
49
measles
* paramyxovirus, enveloped negative strand RNA
* **most contagious virus known**
* **koplik spots:** small red sports with bluish centers on buccal mucosa
50
rubella virus (german measles)
* toga virus, enveloped +RNA
* respiratory virus, aerosol spread
* maculopapular rash, lymphadenopathy, arthralgia
* congential infections are severe and cause defects
* no treatment, prevent with MMR vaccine
51
how do tumors differ antigenically from normal cells?
most tumors do not express MHC class II or costimulatory proteins; immune response gets started when dendritic cells or other APCs present digested tumor antigens
52
immunotherapies to direct the immune system to treat cancer
* **non specific stimulation of tumor immunity (check point inhibitors)**
* ****anti PD1/PD1-L (usually down regulate immune system by preventing activation of T-cells→ reduced autoimmunity, promotes self-tolerance)
* antibodies to CTLA4 that block inhibition of activated T cells
* **adoptive T cell therapies**
* **T cells engineering (e.g., CARTs)**
53
type I HSR
* immediate hypersensitivity
* mediated by IgE (normal response to worms)
* allergic rhinitis, systemic anaphylaxis, food allergies, wheel and flare, asthma
* first exposure: allergens contain peptides presented by MHC II→ activate TH2 cytokines (IL4→ IgE→ mast cell)
* second exposure: mast cell degranulation
* histamines: vascular leaking
* lipid mediators (PAF, PGD2, LTC4): bronchoconstriction and intestinal hypermotility
* cytokines (TNF): inflammation
* enzymes (tryptase): tissue damage
* treatment: avoid allergen, desensitization (controlled exposure→ IgA and IgG which block binding of allergen to IgE of mast cells)
54
type II HSR
* antibodies bind to cell-associated antigen/cell surface receptors and fix complement→ new epitopes→ lysis
* cytotoxic: autoimmune **hemolytic anemia (IgG),** acute rheumatic fever, transfusion reactions
* noncytotoxic: **myasthenia gravis (antagonist Ab), grave's disease (agonist Ab)**, type II diabetes (non-insulin dependent)
55
type III HSR
* mediated by immune complex formation→ deposit in tissues→cellular damage and loss of function
* **SLE,** RA, post-step glomerulonephritis, serum sickness, arthus reaction
56
type IV HSR
* mediated by antigen specific effector T cells (CD4+ TH1)
* delayed type (ppd): proteins→ local skin swelling
* contact hypersensitivity (poison ivy)→ haptens or small metal ions→ local epidermal reaction
* tuberculin test, **MS,** contact dermatitis, hashimoto's, **insulin dependent diabetes (type I), celiac disease**
57
how is the breakdown in B cell tolerance involved in pathogenesis of autoimmune disease?
* **central B cell tolerance:** clonal deletion of self-reactive B cells in bone marrow
* **peripheral B cell tolerance:** without cognate T cell help, antigen-activated B cells in T cell zome of lymph die by apoptosis
58
how is the breakdown in T cell tolerance involved in pathogenesis of autoimmune diseases?
* negative selection: normally T cells that bind to self peptides presented by MHC on thymic cells are deleted
* **defects in AIRE gene→ production of variety of autoimmune B and T cells responses**
* peripheral selection: insufficient control of T cell costimulation: activation of naive T cells requires both antigen presentaiton and costimulation
* **Th17 (helper CD4+ cells that secret IL17):** pro-inflammatory
59
treatment options for autoimmune diseases
* plasmapheresis/splenectomy: removes antigen, antibody, complexes
* IVIG: FcR effects, Ig suppression
* anti-inflammatory drugs: NSAIDs, steroids
* depletion of immune cells: cyclophosphamide, methotrexate, rituximab
* block interaction/activation of immune cells: anti-TNFs
* replacement therapy: insulin for diabetes, synthroid for hashimoto's
60
c. tetani
* infection is usually transient
* AB toxin→ synaptobrevin II protease→ stimulates **inhibitory CNS**→ failure of **GABA** **and glycine** release→ **spastic paralysis**
* diagnosis by exam (few tests because symptoms are toxigenic)
* treatment: antitoxin to bind and inactivate
* prevent: toxoid vaccine
61
c. botulinum
* contaminated food: heat inactivates toxin, terminating bacteria die in GI but exotoxin absorbed from gut
* kids: spores can germinate in GI and secrete exotoxin
* wounds: IVDA or immunosuppression
* synaptobrevin II protease activity→ **stimulates PNS→ failure of ACh release→ flaccid paralysis**
* treat: human-derived antitoxin for baby to bind and inactive NT
62
c. perfringens
* environmental and normal flora, relatively aerotolerant (unlike other clostridia)
* produces exotoxin A (necrotizing, hemolytic, cardiotoxic)
* infectious process, not just toxigenic
* **gas gangrene: myonecrosis** due to vegetative cells in deep tissue→ degradative enzymes produce gas in tissue
* food poisoning: GI enterotoxin
* symptomatic treatment
63
c. difficile
* normal flora
* pseudomembranous colitis after antibiotic use or chemo; often nosocomial
* nonbloody cramping diarrhea; mucoid, greenish, malodorous
* exotoxin A (necrotizing, hemolytic, cardiotoxic) and exotoxin B (disrupts cytoskeleton by depolymerizing actin, kills surrounding cells)
* treatment: change antibiotic (cures 20%), intervene surgically if needed
64
gram negative anaerobic bacteria
* **bacteriodes, prevotella:** tissue degrading enzymes
* diagnosis: anaerobic culture and gas chromotography
* treatment: antibiotics plus surgical care
* lethal exotoxemia, gas gangrene: must be resolved ASAP
* **actinomyces:** pus containin nodules with sulfur franules near mouth or colon
* treatment: penicillin , surgical care usually necessary
65
bacillus anthracis
* spores in dirt→ cows→kills cows→ blood/meat/feces→ soil (no vector)
* **cutaneous:** small sore→ blister→ skin ulcer + eschar and major swelling but no pain
* **GI:** N/V/bloody D
* **inhalation:** cold or flu→most serious form
* treat: cipro/doxy
66
francisella tularemia
* US/canada: rabbit; more virulent
* europe/asia: rabbit, beaver
* **ulceroglandular: MC,** following tick/deer fly bite or after handling infected animal
* **glandular:** similar but with no ulcer
* **oculoglandular**
* **oropharyngeal**: ulcer (from eating or drinking)
* **pneumonic:** by inhaling dust or aerosols
67
brucella
* undulant fever
* osteoarticular complications ar eMC
* treatment: doxy
68
yersinia pestis
* spread by rodents or fleas
* 1-6 day incubation period
* **bubonic: \>80%**; rapid onset of fever, painful swollen tender lymph nodes
* pneumonic: potential for person to person spread
* septicemia→ **accral necrosis**
* **treatment: streptomycin**
69
leptospira
* contaminated water or food enter **abraded skin or mucous membranes→ cross to lymphatics→ leptospiremia**
* acute febrile illness followed by more mild, self-limiting multiorgan involvement
* treat: **penicillin G (jarisch-herxheimer reaction possible)**
70
bartonella henselae
* **"cat scratch fever"**
* transmitted by **fleas; infects kittens**
* fever, enlarged tender lymph nodes 1-2 weeks after exposure
* self-limited in a healthy person; usually granulomatous conjunctivitis
* **in HIV: bacillary angiomatosis and peiosis hepatis**
71
animal bites
* **dog→ capnocytophaga canimorus:** facultatively anaerobic gram (-) rod, part of normal flora of dogs, treat with penicillin G
* **cat→ pasteurella multicida:** clinical evidence of wound infection within a few hours, treat: amoxicillin
