Infection

Question 1

Bacteria

Answer 1

Unicellular, prokaryotes, no nuclear-categorized by shape (spherical is cocci, rods is bacilli, spirals)
Pilus, flagella, cell wall phospholipid and protein are important for drug interventions, capsule-keeps from getting engulfed by phagocytes, nucleoid enzymes promote infection and damage, biofilms-matrix secreted by bacteria to protect them

Question 2

Clinical stages of infection

Answer 2

Incubation period: 1st exposure to infectious period hours to years, no symptoms, low pathogen load but growing
Prodrome period- vague mild symptoms, pathogen continues to grow
Period of illness-severity worsens, both immune and inflammatory response triggered, growth toward peak
Period of decline- decrease if tx or immune wins, peak decline
Period of convalesce-decrease until resolved

Question 3

Stages of infection

Answer 3

Invasion/penetration (transmission)-infectious agent/antigen invades the body, avoids immune detection, triggers inflammatory response
Multiplication- time of rapid cellular growth and division, occurs before the immune system can respond
Spread/tissue damage- local or disseminated presence of disease causing agents
Colonization- presence of infectious agents on a body surface without causing disease to the person

Question 4

Outbreak

Answer 4

Greater than anticipated increase in number of endemic cases, single case in a new area, if not quickly controlled and outbreak can become an epidemic

Question 5

Endemic

Answer 5

Disease or condition regularly found among particular people or in a certain area

Question 6

Epidemic

Answer 6

Disease that affects large number of people in a community, population, region
Includes obesity, opioids

Question 7

Pandemic

Answer 7

Epidemic that has spread to a different countries and continents

Question 8

Communicability

Answer 8

Time an infectious agent can be transferred directly or indirectly to another person

Question 9

Infectivity

Answer 9

Ability to produce or transmit infection

Question 10

Immunogenicity

Answer 10

Ability of a foreign substances to provoke an immune response in the body

Question 11

Toxigenicity

Answer 11

Ability of an microorganism to produce a toxin that contributes to the development of the disease

Question 12

Pathogenicity

Answer 12

Ability of an organism to cause disease or harm to the host

Question 13

Virulence

Answer 13

Degree of pathology caused by the organism, usually correlated with the ability of the pathogen to multiply within the host but may be affected by other factors

Question 14

Portal of entry

Answer 14

How pathogen enters

Question 15

Viruses

Answer 15

Capsid coating protects the nucleic core, can not survive without a host, simple microorganism
Pathogenic properties: binds to cell membranes, inserts into host cells, matures, new virions, bud release from plasma membrane, multiple steps in replication, may have viral latency-remain dormant for various periods of time, may invade immune response by antigen variation (drift and shift)

Question 16

Fungi/yeast

Answer 16

Molds and yeast, large eukaryotic microorganisms, mold is aerobic yeast are facultative anaerobes, infection cause by fungi are mycoses, fungi in skin, hair, nails are dematophytes
Many are part of natural biome, cell wall is polysaccharide, highly opportunistic, phagocytes an T cells are important to limit, adapt to host by producing immunosuppressant, damage tissues with enzyme toxin secretion

Question 17

Gram negative bacteria

Answer 17

Negative for stain, cell wall thin but duplicate, release ENDOtoxins from cell wall, causing cell lysis, lipopolysaccharide wall, ENDOtoxins can cause fever, DIC, septic shock

Question 18

Gram positive bacteria

Answer 18

Positive for stain, single wall teichoitic acid and peptioglycan, release EXOtoxin, type 1 produces pro inflammatory cytokines, type 2 damages cell membranes, type 3 enters ell and causes damage
Listeria monocyogenes only gram + bacteria that makes ENDOtoxin

Question 19

Acid fast bacilli

Answer 19

TB, mycobacterium, THICK cellular wall, slowing growing as nutrients have a hard time penetrating wall, long time to grow out cultures, long time to teat

Question 20

Aerobic bacteria

Answer 20

Pseudomonas, anthrax, must have o2

Question 21

Anaerobic

Answer 21

Do not grow when o2 is present

Question 22

Facultative anaerobes

Answer 22

Ecology, can grin with or without o2

Question 23

Staph aureus

Answer 23

Develop protective capsules, that delay immune response, resistance to intracellular oxidative lysis, on skin, nose adheres to surface proteins, connective tissues, endothelium, manifestations in community and hospital acquired, potential to be DRUG RESISTANT

Question 24

E. coli

Answer 24

May exist as biofilms, normal GI flora, multipl strains, cause UTIs, travelers diarrhea, may be DRUG RESISTANT

Question 25

Mycobacterium

Answer 25

Survives and grows within macrophages and phagolysomes, contagious, and opportunistic, resistance and can be active or latent, Develop a capsule that prevents phagocytosis, suppresses host response forms granulomas-tubercles-caseales-collagen scar-immune system response is dormant

Question 26

Coronavirus

Answer 26

Lots of strains, droplet transmission, infectious 2-3 days before symptoms, up to 10 days after more risk if multi morbid and infection, ARB/ACE protective

Question 27

Influenza

Answer 27

RNA virus: A, B, C, 2 surface protein, causes fever, ache, fatigue, pro inflammatory cytokines and chemokines, TNF and interferon, produced by viral cells, hemagglutinin binds to receptors on epithelia cells of throat and lungs, incubation short, long shedding time

Question 28

Herpes simplex

Answer 28

She’d from point of infection, HS 1 oral via saliva, infection of epithelia cells, virus moves along axon of dorsal root ganglia, HS 2 genital with mucous membranes contact

Question 29

Varicella/herpes zoster

Answer 29

Chicken pox/shingles, initial is varicella, zoster is reactivating of earlier acquired appears as vesicles along dermatone, can be transmitted mother to neonate post herpatic neuralgia, vaccine

Question 30

Rubeola (classic measles)

Answer 30

RNA virus, resp tract amplifies in local lymphatic tissues and disseminates, very contagious, incubation 6-19 days (5 days before and 14 days after rash develops), droplet spread, hangs around for 2 hours after carrier is out of area, Maculopapular rash, head, trunk, and extremities, Koplic spots, buccaneers mucosa, RNA virus

Question 31

Rubella (3 day German)

Answer 31

can cause congenital rubella syndrome, sensorineural deafness, congenital heart disease, pulmonary artery stenosis, retinopathy, cataract

Question 32

Candida albicans

Answer 32

Yeast normal micro biome, opportunistic, antibiotics, immunocompromised, can be local or disseminated, resistance has developed, biofilms, cell wall adherence

Question 33

Antigenic shift

Answer 33

2 strands of the same sort of virus come together and form a second very virulent virus such as covid 19

Question 34

Antigenic drift

Answer 34

Small mutation over time such as the flu

Question 35

Antibiogram

Answer 35

Published organizations list infective organisms-numbers of infections, resistance and antibiotics that organism was susceptible to

Question 36

Goal of anti microbial stewardship programs

Answer 36

Decrease microbial resistance to abx therapy, use guidelines and antibiograms to help prescribe right drug to right bug, use upturns to change or stop abx, intentional with duration, monitor for c. Diff

Question 37

Hospital acquired infection

Answer 37

Can be same organism as community required, but hospital usually worse hospital develops within 14 days of DC, greater than 4 days after admission, any infection in LTC, CLABSI, CAUTI, VAP, SSI, different type of pathogen, duration of tx

Question 38

HIV

Answer 38

Types 1 and 2, 1 more common in US, blood borne pathogen via IVDU, blood products, blood, sex, mother to baby, viral envelope, proteins protruding GP120, enzymes on inside of virus, reverse transcriptase, targets CD4 cells virus binds with CD4 cells inject RNA into cytoplasm, integrates with host DNA transcription and translation results in new viral proteins production virus buds through cell membranes and infects more cells overtime infected CD4 cells eventually rupture or are killed by other cells,

Question 39

HIV acute infection

Answer 39

Syndrome after initial infection (40-90% of infected persons) flu like symptoms, fever, lymphadenopathy, pharyngitis, rash, myalgia, n/v/d, HA, weight loss, thrush, hepatosplenomegaly, time 1-6 weeks after exposure , if known exposure antivirals should be started!

Question 40

HIV testing

Answer 40

Gold standard combo HIV AB/AG, designed to detect early infection If AG (-) unlikely for acute infection If Ag(+) then HIV 1-HIV2 AB to be done If Ag(+), HIV1/HIV2 AB differentiation immunoassay is (-), or indeterminate then viral load test should be done (CD4 test)

Question 41

HIV vs. AIDS

Answer 41

HIV CD4 count greater than or equal to 200, no AIDS illness or history of AIDS CD4 count less than 200, even if its once, and or presence of AIDS illness

Question 42

AIDS illness

Answer 42

Pneumocystis jiroveci PNA (PJP), lymphoma, kaposi, toxoplasmosis, progressive multi focal leukoencephalopathy, TB, disseminated mycobacterium avian complex (MAC), oral candida infection CMV, invasive cervical CA, histoplasmosis

Question 43

HIV/AIDS in kids

Answer 43

Baby test at 2-4 weeks if viral load (-) retest at 4 months If no tx s/s will occur at 6 months, opportunistic infections 1st year of life, life expectancy 3 years, mm decreased by 76% if antivirals started ASAP

Question 44

Fulminant

Answer 44

Little or no prodromal period, subclinical, brewing, difficult to treat, evolved into chronicity, individuals get very ill very quick

Question 45

Antibiotic resistance

Answer 45

Due to inappropriate use or farming animals receiving antibiotics

Question 46

Mechanisms of resistance

Answer 46

Inactive antibiotic Modify the antibiotic molecule Change the metabolic pathways to be less sensitive Multi drug transporters prevent entrance of increase efflux of antibiotics