Because I know your weekend won't be complete without it...

Here is the study guide from my most recent medical microbiology exam. And yes, it's 12 pages long. :)

Chapter 19 - Mechanisms of Bacterial Pathogenesis

1. Define each of the following terms: pathology, etiology, etiological agent, pathogenesis, colonization, disease, infection, pathogen, pathogenic, bacteremia, septicemia, toxemia, viremia, and reservoir.
Pathology – study of disease
Etiology – the cause of the disease (eg. The organism)
Colonization – bacteria growing in the body
Disease – change from a state of health
Infection – colonization with a pathogenic bacterium
Pathogen – disease-causing agent
Pathogenic – adj. for pathogen
Bacteremia – bacteria in the blood
Septicemia – bacteria growing in the blood
Toxemia – toxins in the blood
Viremia – viruses in the blood
Reservoir – where the pathogen “hangs out” naturally.

2. What is normal flora? Explain how normal flora could be categorized as: mutualistic, commensal, or opportunistic. What is a parasite?
Normal flora is the colonization of bacteria in out body that is normal and not harmful. They contribute to microbial antagonism, and may synthesize nutrients such as vitamins that help us.
Mutualistic – both benefit
Commensal – one benefits
Opportunistic – NF takes advantage of suppressed immune system to cause infection in an unusual location
Parasite – one benefits, other is harmed

3. What is the germ theory of disease? What are Koch’s Postulates? What are they used for?
Germ theory – germs cause disease. One germ, one disease.
Koch – to prove which microorganism is the causative agent of the disease
Isolate sample from infected individual
Culture
Infect new individual
When signs and symptoms develop that are the same as the first infected individual, the organism is the same, and can be concluded to be the causative agent.

4. Describe how each of the following is used to describe a disease (and explain what the term means): communicable, contagious, noncommunicable, endemic, epidemic, pandemic, acute, chronic, and latent.
Communicable – can spread from person to person (HIV)
Contagious – spreads easily from person to person (rhinovirus)
Non-communicable – cannot be spread from person to person (tetanus)
Endemic – at a consistent rate of infection
Epidemic – spike of infection rate in a given area
Pandemic – disease is worldwide
Acute – rapid onset, severe, then finishes
Chronic – slow onset, prolonged illness
Latent – person is a carrier, but shows no symptoms. Can flare up (varicella)

5. What is the difference between a local infection and a systemic infection?
Local – confined to one area
Systemic – whole body

6. What is the difference between a primary infection and a secondary infection? What is a subclinical infection?
1ary – first infection
2ary – infection after the 1ary, more susceptible to it bc of weakened immune system
Subclinical – no symptoms

7. Describe the following mechanisms of disease transmission: contact transmission (direct, indirect, and droplet), vehicle transmission, and vector transmission.
Contact:
Direct – person-to-person
Indirect – through an inanimate object
Droplet – cough, sneeze
Vehicle – food and water
Vector – insect bite

8. What is a fomite? What is a nosocomial infection?
Fomite – for indirect transmission
Nosocomial – acquired in a healthcare setting

9. What is epidemiology?
Study of frequency and distribution of disease.

10. What is the Center for Disease Control and Prevention (CDC)? What types of things does this agency do?
National Epidemiology Center (USA). Tracks infectious diseases, helps local health agencies during outbreaks. Publishes monthly reports.

11. Describe the sequence of events successful pathogens carry out.
Transmission to host, entry into tissue, adherence to target tissue, invasion/evasion, host damage, exit, transmission.

12. What are portals of entry? What are the possible portals of entry for pathogens?
PofE are where the pathogen gains entry to the host. Usually: mucous membranes (GI, GU, respiratory), parenteral, skin.

13. What are virulence factors? How does each of the following function as a virulence factor: adhesions, fimbriae, biofilms, capsule, cell walls of mycobacteria, toxins, and enzymes?
Adhesins – help bacteria stick to host tissue. Fimbriae and pili.
Fimbrie – “ “
Biofilms – glue to surfaces
Capsule – evade phagocytosis, poorly antigenic
Mycolic acid – evade phagocytosis
Toxins – host damage, direct (exo) and indirect (endo)
Enzymes – kinase, coagulase, hyaluronidase, collagenase, IgA protease.

14. Give the function of each of the following enzymes and explain how they can aid pathogens in causing disease: hemolysins (both α and β hemolysins), leukocidins, streptokinase, staphylokinase, coagulase, collagenase, proteases, hyaluronidase, and phospholipase C.
Hemolysins – lyse RBCs
α – complete lysis
β – partial lysis
Leukocidins – lyse WBCs
Strepto/staphylokinase – break down blood clots, gain entry
Coagulase – formation of blood clots, wall off from WBCs
Collagenase – break collagen, get deeper into tissues
Protease – break down specific proteins, eg. IgA protease.
Hyaluronidase – break down hyaluronic acid, get deeper into tissues
Phospholipase C – hydrolyses lecithin (in tissues)

15. What are exotoxins? List the examples of the following types of exotoxins discussed in class and explain how they affect the host: cytotoxins, enterotoxins, and neurotoxins.
Exotoxins – released by the cell. Usually G(+), but can be G(-).
Cytotoxins – damage cells
Erythrotoxins – damage to capillary cells, cause blood to leak out (S. pyogenes)
Enterotoxins – damage to GI -> diarrhea, vomiting, etc. (Cholera, S. food poisoning, bacterial dystentery)
Neurotoxins – inhibit normal NT flow (Tetanus, Botulinum)

16. What is endotoxin? How does it affect humans?
Made by G(-) cells, is the LPS in the outer membrane. Once ingested by phagocytes, LPS is relased, stimulating cell to release cytokine IL-1, which reaches hypothalamus. Resets the “thermostat”, h-thal. Releases prostaglandins to initiate the fever response (vasodilation, vasopermeability, high temp.). Can lead to shock due to decrease in BP from vasodilation.

17. How do the following help bacteria evade the immune system: antigenic variation and inactivation of antibodies or complement?
AV – evade immune system’s antibodies
Inactivation – cascade/signaling system is disrupted

18. What are cross-reactive antibodies? How are they involved in damage to host cells?
Antibodies produced in response to an antigen, that undergo slight variation in the final differentiation process, that are similar enough to our own proteins to elicit an inflammatory response against our own tissues. Strep throat -> rheumatic fever, glomerulonephritis. Heart valves & strep. Antibiotics are prescribed with Strep. Infections not to help clear up the infection (which will subside in a few days), but to prevent the formation of antibodies that could attack our own cells.

19. What are superantigens? How are they involved in damage to host cells?
Antigens that are repeating polysaccharide units, stimulate non-T-cell-specific activation of the immune system, large cytokine release -> shock. Can get out of hand quickly, lead to death. Toxic shock syndrome (S. aureus).

Chapter 20 - Antibacterial Agents

1. Briefly describe the history of the antibacterial agents Protosil (sulfanilamide) and penicillin.
Protosil (sulfas) – 1935, used first in mice to treat systemic strep. Protosil is cleaved in the body to produce sulfanilamide, the active agent.
Penicillin – Alexander Fleming – Penicillium mold prevented bacterial growth on a plate.

2. Are all antibacterial agents antibiotics? Why or why not?
No – antibiotics are, by definition, made by other microorganisms. Some antibacterial agents, like the sulfa drugs, are made in the lab.

3. Describe the property of selective toxicity. Why is this an important property of antibacterial agents?
Selective toxicity means that the drug is selectively harmful toward the pathogen, and not our own cells. This is important because we want to maximize damage to pathogens while minimizing damage to our cells.

4. What is the difference between broad-spectrum and narrow-spectrum drugs? Under what conditions would each type of drug be used?
Broad – affects all, used when ID in unknown
Narrow – affects some, used when ID known, to protect NF

5. List the various targets of antimicrobial drugs and give which types of drugs have each type of target. (Those listed in Figure 20-1 and those discussed in class).
Cell wall synthesis
Penicillins
Cephalosporins
Beta-lactams
Isoniazid
Ethambutol
Cycloserine
Ethionamide
Bacitracin
Polymixin
Protein Synthesis
30S:
Aminoglycosides
Tetracyclines
50S:
Chloramphenicol
Macrolides
Clindamycin
Linezolid
Quinupristindalfopristin
DNA replication
Quinolones
Metronidazole
Clofazimine
RNA synthesis
Rifampin
Rifabutin
Antimetabolites
Sulfanamides
Dapsone
Trimethoprim
Para-aminosalycylic acid

6. What are Beta-lactams? What do they do to kill bacterial cells?
Β-lactams are rings in the structure of antibiotics in the penicillin and cephalosporin families. They inactivate bacterial enzymes used in the synthesis of peptidoglycan. Without p-glycan, the cells cannot replicate.

7. What would be a problem with drugs used to fight fungal infections?
How about those used to fight viral infections?
Fungal – harder to crate drugs with selective toxicity as fungi are eukaryotic cells. More in common structurally, so harder to target.
Viruses – spend little time outside of host cells, hard to detect and target. Don’t carry out metabolism, so not “cell” processes to target.

8. List and describe the mechanisms of antibiotic resistance. What are beta-lactamases?
Destroy the drug (lactamases)
Altering drug target site
Increase drug elimination from cell, host
Alter permeability to drug (more impermeable)
β-lactamases are enzymes that break the β-lactam ring of antibiotics in the penicillin and cephalosporin families.

9. How is resistance to a drug acquired?
Begins with spontaneous mutation, and spreads through plasmid transfer (pili, phage conversion).

10. What human practices lead to antibiotic resistance in bacteria?
Overuse of antibiotics
Use by immunosuppressed individuals
Patient noncompliance
Animal feed

Chapter 22 –

Staphylococcus organisms

G(+) coccus. Facultative anaerobes. Tolerate high salt (resistance to osmotic pressure).
S. AUREUS – COAGULASE+

Virulence – capsule, peptidoglycan, teichoic acid, protein A, cytoplasmic membrane, toxins – exfolitoxins, enterotoxins, TSS superantigen, cytotoxins; enzymes: coagulase, catalase, hyalurondiase, fibrinolysin, lipases, nucleases, penicillinase

Epidemiology – NF skin, nares. Survive on dry surfaces, fomite spread.

Diseases
Staph. Scalded Skin Syndrome (Ritter’s) (destroy connective tissue between dermis and epidermis, epidermis falls off. Exfolitoxins).
Bullous Impetigo – blisters on skin
Food Poisoning – heat stable toxin
TSS – high mortality
Folliculitis – hair follicles infected (“ingrown hairs”?)
Furuncle (boil) (site of draining pus, must be drained (will not clear up))
Carbuncle (several sites of draining pus)
Pustular Impetigo
Bacteremia
Endocarditis
Pneumonia
Osteomyelitis – infection in bone, from bacteremia or spread of wound
Septic Arthritis

ID: Gram stain, catalase, coagulase, mannitol fermentation.
Treatment – penicillin resistance is common


Chapter 23 – Streptococcus
G(+), chains, fac. Anaerobes, some are aerotolerants. Produce lactic acid. Catalase (-). Complex nutritional requirements.

Virulence –
Capsule – mimics hyaluronic acid
M proteins
Heart valve protein (rheumatic fever protein)
Blocks C3B
Toxins – erythrogenic
Streptolysin
Type S – aerobic conditions
Type O – anaerobic conditions
Streptokinase
Breaks down blood clots

Epidemiology
Oropharynx and skin – children and Young adults
Transmitted through direct contact (infected mucus, body secretions)
Asymptomatic patients, pts on antibiotics are less contagious
Noninvasive disease is common
Over 10 million cases, underreported
Most common : pharyngitis, pyoderma

Diseases –
Suppurative (development of pus)
Pharyngitis (strep throat)
2-4/365 incubation
cannot diagnose visually
Complication : Scarlet fever
Pyoderma (Impetigo)
S. aureus
Erysipelas
Acute skin infection
Systemis signs (fever, chills…)
Cellulitis
Inflammation of connective tissue
Bacteremia
40% mortality
Necrotizing Fasciitis
Streptococcal gangrene
Destroy muscle, fat, skin
25% mortality
Streptococcal toxic shock syndrome (STSS)
Superantigens
Often accompanies NF
45% mortality

Non-suppurative (no pus)
Rheumatic Fever
Complication of pharyngitis or skin infections, may have had asymptomatic infection
Prevented with antibiotics
Cross-reactive antibodies
Inflammation in heart, joints, blood vessels, skin
Affected individuals are more susceptible to further infection/damage
Actue glomerulonephritis – damage to glomerulus, causes blood in the urine

ID –
S.pyogenes :
Group A
G(+)
blood agar
PYR enzymes (differentiate b/t S. pyogenes, S. anginosus)
Antigen detection – rapid strep test

Treatment –
Penicillin
Macrolides
NF – surgery
Rheumatic Fever – preventative antibiotics
Wash hands, etc.

Ch 23 b

Strep. agalactiae

Group B strep

Characteristics-
G(+) streptococci
Facultative anaerobe
Beta-hemolytic (Small percentage non-hemolytic)
B antigen

Virulence –

Epidemiology –
Site : lower GI tract, GU tract
10-30% of pregnant women are carriers
60% of infants born to infected mothers become infected
In men and non-pregnant women :
Skin and soft tissue
Bacteremia
UTI/urosepsis
Pneumonia
Predisposing factors :
Diabetes mellitus
Cancer
Alcoholism

Diseases –
Puerperal sepsis (childbed fever)
In newborns : Septicemia, Pneumonia, Meningitis
Early-onset neonatal disease (1/52)
Acquired in utero or at birth
Bacteremia, pneumonia, meningitis
Must examine CSF
5% mortality
15-30% of survivors have permanent neurological damage –
blindness, deafness, severe mental retardation
Late Onset Neonatal disease(1-12/52)
Source : mother, other infants
Bacteremia, meningitis
Pregnant Women – UTIs
Men and non-pregnant women
In immunocompromised individuals
Bacteremia
Pneumonia
Bone and joint infections
Skin and soft tissue infection
15-32% mortality

ID –
Culture
Antigen detection
PCR

Treatment –
Penicillin G
Pregnant women – IV of antibiotics before delivery, can cross placenta, offers defense if colonized by bacteria

Viridans Streptococci

Characteristics –
Heterogenous collection of alpha-hemolytic and non-hemolytic strep. Spp.
20 spp. In 6 groups
Req. complex media, blood products, 5-10% CO2

Colonize
Oropharynx (NF)
GI (NF), GU

Diseases
Dental caries
Subacute endocarditis
Not from Ig, but from bacteria. The viridans bind to damaged (congenital, superantigen) heart valves. Transmitted during dental work.
Suppurative intraabdominal infections

Treatment
Penicillin
Some resistant strains

Strep. pnuemoniae

Characteristics -
G(+) coccus, large cells, oval/lancet shape
Also called diplococcus, pneumococcus
Fastidious requirements
Alpha-hemolytic in aerobic
Beta-hemolytic in anaerobic
Catalase (-)
Poor growth in high glucose
Prominent capsule

Virulence factors
CAPSULE

Epidemiology
Enodgenous (NF)
Direct transmission is rare
Often a SECONDARY infection
Young and old at higher risk (meningitis)
More common in cool months

Diseases
Sinusitis & Otitis media
Over 7 million cases/year
Paranasal sinuses and middle ear
2ary to viral infection in upper respiratory tract
Sinus – all ages
Otitis media – young children
Eustacian tube is shorter, bacteria can travel more easily to middle ear. Opening more narrow, closes off more easily. Closes off, fluid accumulates, puts pressure on tympanic memrane, can rupture eardrum (can heal), break malleus/incus/stapes -> hearing loss.
Meningitis
6000 cases/year
Mostly in children
More damage than other types of meningitis

Bacteremia
55000 cases/year
Endocarditis, even with previously undamaged heart valves

Identification

Treatment
Penicillins and others
Immunization


Ch 24 – Enterococcus

Characteristics
Originally group D strep
E. faecalis
E. faecium
Catalase (-)
Fermentation
Tolerates high salt, bile salts
Commensal organism in large intestine
High antibiotic resistance
Infections : endogenous source

Transmission
Person-to-person
Contaminated food

Virulence Factors:
Multi-drug resistance
Colonization
Secreted factors

Diseases
Risk factors:
Catheterization
Long-term hospitalization
UTI (especially w/ catheter)
10% of all nosocomial infections
Vancomycin- Resistant Enterococcus (VRE) 35-50% mortality
Peritonitis (after surgery)
Endocarditis (5-15%)
Bacteremia
Wound infections, abcesses

Treatment
Highly resistant
25% resist aminoglycoside
50% resist ampicillin
25% resist vancomycin