Microbiology- studyguide

Gram positive/negative cocci

1. S. aureus

   1. Enzyme: Coagulase, Lipase, Penicillinase

   2. Toxin: Enterotoxin, Exfoliative, Toxic shock syndrome

   3. Diseases- Localized infections; Folliculitis & Hidradenitis, Furuncle, Carbuncle, Impetigo/ Systemic infections; Osteomyelitis & Bacteremia/ Toxigenic diseases; Food intoxication, Staph. scalded skin syndrome, Toxic shock syndrome

   4. MRSA: Methicillian-resistant S. aureus; vancomycin, needs multi. Drugs

   5. Coagulase: coagulates blood plasma

2. Streptococci

   1. Pyogenes:

      1. Blood hemolysis: Beta  

         1. Toxin: Streptolysins, Erythrogenic (pyrogenic), Superantigens

         2. Virulence factor: C-carbohydrate, Fimbriae, M-protein, Capsule, C5a protease

   2. Pneumoniae

      1. Blood hemolysis: Alpha

      2. Toxins: pneumonlysin; can dmg host tissues & trigger inflammation

      3. Virulence factors: large capsules (polysaccharide)

   3. Neisseria (gram rxn, Gonorrhea pathogenesis, virulence factors)

      1. Gram reaction: negative

      2. Gonorrhea pathogenesis: Fimbriae; slows phagocytosis, IgA protease

      3. Virulence factors: lg capsule, adhesive fimbriae, IgA protease, Endotoxins

Gram positive rods

1. Endospore forming bacteria

2. Bacillus food poisoning:

   1. Bacillus cereus (antibiotics source)

      1. Airborne/dustborne

      2. Grows in food; spores survive cooking & reheating

      3. Symptoms: nausea, vomiting, abdominal cramps, diarrhea (24hrs)

      4. No treatment

   2. Botulism: Bacillus botulinum

      1. Inhabits soil & water

      2. Caused by improper home canning/ Temp & pressure not achieved, air evacs but spores stay; favors anaerobic conditionsà spore germination & vege growth

      3. Toxin—neuromuscular; blocks release of acetylcholine for muscle contraction to occur

      4. Symptoms: double/blurred vision, difficulty swallowing, neuromuscular symptoms

      5. Infant botulism— consumption of honey; ingested spores germinate & release toxin (floppy baby syndrome)

      6. Wound botulism— spores enter wound —> cause food poisoning symptoms (injecting drug users)

      7. Treatment— 1^st: determine presence of toxin in food, intestinal contents, feces; Administer antitoxin (cardiac & respiratory support)/ infectious —> penicillin

      8.   Prevention—proper preserving & canning foods; additional preservatives

   3. Anthrax: Bacillus anthracis

      1. Virulence factor: polypeptide capsule, exotoxin (edema; fluid leaking out of blood vessels & building up in spaces between cells or inside body cavities, cell death)

      2. From livestock (Africa, Asia, Middle East)

      3. 3 types:

         1. Cutaneous- spores enter skin, black sore

         2. Pulmonary- inhalation of spores from animal products/soil

         3. Gastrointestinal- ingested spores (rare & lethal)

      4. Treatment: wombo/combo ciprofloxacin & clindamycin, Vax-Purified toxoid (BioThrax) w/ annual boosters

   4. Gas gangrene and clostridium

      1. Clostridium

         1. Characteristics: Gram +ve, spore-forming rods, Anaerobic, catalase -ve

      2. Gas gangrene (Clostridium perfringens/Myonecrosis)

         1. Soft tissue & wounds

         2. Spores: soil, human skin, intestine, vagina

         3. Virulence factor: Alpha toxin, collagenase, Hyaluronidase, DNase

         4. Treatment: no vax, cephalosporin/penicillin, hyperbaric O2 therapy

         5. Prevention: cleansing wounds, compound fractures, infected incisions

         6. Clostridial Gastroenteritis: Mild intestinal illness; improper storage of poultry & meat; Rapid recovery/resolved on own

   5. Tetanus (lockjaw): Clostridium tetani

      1. Neuromuscular; effects the jaw muscle (tetanospasmin- neurotoxin causes paralysis; muscles contract uncontrollably, affects lungs —> death)

      2. Soil & GI tract of animals

      3. Enters body through spores, accidental puncture of wounds, burns, umbilicus, frostbite, crushed body parts

      4. Treatment: vax w. boosters every 10 yrs; control- metronidazole & muscle relaxants

   6. c-diff infection/CDI: Clostridioides difficile

      1. intestinal disease; normal resident of intestine (low numbers)

      2. Cause of diarrhea in hospitals; Antibiotic-associated colitis- too many antibiotics cause overgrowth of bacterium in the colon

      3. Treatment: Mild cases- fluids & electrolyte replacement, w/drawls of antimicrobials; Severe cases- oral vancomycin/metronidazole

1. Mycobacterium

   1. Cell wall and acid-fast staining: cord factor- waxy coat that helps the bacteria stick together in rope-like clusters; reason why acid-fast staining works & why its so virulent (too many together to fight at once

   2. Growth pattern: cluster/clumps  

   3. Tuberculosis

      1. General Characteristics

         1.   Acid-fast bacillus due to mycolic acid in the cell wall

         2. Strict aerobe; slow-growing

         3. Non-motile, non-spore-forming, no capsules or flagella

         4. Produces catalase

      2. Transmission and Epidemiology

         1. Spread via airborne respiratory droplets

         2. Infectious dose: 10 bacterial cells

         3. One-third of the world population is infected

         4. High prevalence in areas with poor healthcare, malnutrition, and immunosuppression

         5. Most U.S. cases occur in recent immigrants

      3. Pathogenesis

         1. Bacilli are phagocytosed by alveolar macrophages

         2. Multiply intracellularly, triggering immune response

         3. Formation of tubercles (granulomas) with central caseous necrosis

         4. May remain latent or progress to active disease

      4. Stages of TB:

         1. Primary Tuberculosis

            1. Occurs after initial infection

            2. Formation of tubercles in lungs

            3. May heal by calcification or progress

         2. Latent Tuberculosis

            1. Non-contagious, asymptomatic phase

            2. Bacilli remain dormant in tubercles

         3. Secondary (Reactivation) Tuberculosis

            1.   Reactivation in immunocompromised individuals

            2. Severe symptoms: coughing, blood in sputum, fever, weight loss

            3. High mortality if untreated

         4. Disseminated (Extrapulmonary) Tuberculosis

            1. Spread to lymph nodes, kidneys, bones, brain, genital tract

            2.  Serious complications

            3. Virulence factors: complex waxes & cord factors that prevent destruction by lysosomes (cell’s digestive system) & macrophages (maid cells)

            4. Factors:

            5. Inadequate nutrition, debilitation of the immune system= immune system army is getting weaker, poor access to medical care, lung dmg, genetics

            6. Lung droplets (airborne transmission)

      5. Diagnosis

         1. Tuberculin skin test (Mantoux test)

         2. Interferon-gamma release assays (QuantiFERON-TB Gold, T-SPOT)

         3. Chest radiograph (to detect lung lesions)

         4. Acid-fast staining (Ziehl-Neelsen or fluorescent)

         5. Culture and biochemical identification (definitive)

      6. Treatment

         1. Initial 2-month phase: Rifampin, Isoniazid, Pyrazinamide, Ethambutol (RIPE)

         2. Continuation phase: Isoniazid and Rifampin for 18 weeks

         3. Drug resistance is common; multiple-drug therapy is essential

         4. Directly Observed Therapy (DOT) used to improve compliance

      7. Prevention

         1. Bacille Calmette-Guérin (BCG) vaccine (used outside the United States)

   4. Leprosy introduction

      1. Myobacterium leprae (Hansen’s Disease)

      2. Strict parasite; slow growing

      3. Multiplies in globi (host cells in Lg packets)

      4. Skin & mucous membrane —> nerves

Gram negative rods

1. Pseudomonas

   1. Pigments: Pesdomonas aeruginosa —> pyocyanin (greenish blue), grape odor

   2. Nosocomial infection- hospital/healthcare associated infections (HAI); acquired while receiving treatment at a healthcare facility (usually after 48hrs of admission)

2. Brucella and undulating fever, potential for bioweapon

   1. Brucellosis- undulant fever (rising & falling)

   2. Bioweapon: can be aerosolized, leading to respiratory infections for prolonged periods

3. Legionella and Pontiac fever:

   1. Legionella: Causes Legionnaires’ disease and Pontiac fever

   2. Found in warm water systems such as air conditioners, hot tubs, fountains

   3. Legionnaires’ Disease:

      1. Severe atypical pneumonia with fever, cough, and multi-lobar infiltrates

      2. Risk groups: older adults, smokers, immunocompromised

      3. Diagnosis: urinary antigen test, culture on buffered charcoal yeast extract agar

   4. Pontiac fever: mild, flu like illness

4. Enterobacteriaceae

   1. Coliform vs no coliform: gram -ve in environment & lactose fermenters; hygiene indicators vs non-lactose fermenters & true pathogens (don’t belong to coliform)

   2. MA and lactose fermentation:

   3. Different types of E coli, traveler’s diarrhea, 0157:H7, UTI and other coliforms

   4. Types of Ecoli

      1. Enterohemorrhagic (EHEC): hemorrhagic colitis à hemolytic uremic syndrome & kidney

      2. Enterotoxigenic (ETEC): severe diarrhea from heat-labile toxin & heat-stable toxin; stimulate secretion & fluid loss; fimbriae

      3. Enteroinvasive (EIEC): inflammatory disease (Lg intestine)

      4. Enteropathogenic (EPEC): infantile diarrhea (weight loss)

      5. Enteroaggregative (EAEC): pediatric diarrhea

      6. Diffusely adherent (DAEC): minor cause of pediatric diarrhea

   5. Traveler’s diarrhea: travelers consume contaminated food/water; loose stools, stomach cramps, nausea & vomiting; hydration & good hygiene

   6. O157:H7: foodborne illness (fast food hamburgers; reservoir=cow intestine); Workers no wash hands, undercooked beef & unpasteurized milk

   7. Virulence factor: Shiga toxin (toxic gene from Shigella); dmg blood vessels, hemorrhagic colitis & hemolytic uremic syndrome

   8. UTI

   9. Others

      1. Klebsiella pneumoniae: Lungs; Lg capsules; causes nosocomial pneumonia, meningitis, bacteremia, wound infections, & UTI’s

      2. Enterobacter sp.: UTI’s, surgical wounds

      3. Citrobacter sp.: opportunistic UTI’s & bacteremia

      4. Serratia marcescens: red pigment; pneumonia, burn, wound infections, septicemia, meningitis

Non LF, Salmonella and shigella. Plague and Yersinia

1. Non-lactose fermenters

   1. Opportunistic: Proteus, Morganella,Providencia

   2. True Enteric Pathogens: Salmonella & Shigella

2. Salmonella

   1. Salmonella bongori

   2. Salmonella enterica (6 subsp.)

      1. Enterica

      2. Salamae 

      3. Arizonae

      4. Diarizonae

      5. Houtenae

      6. Indica

   3. Typhoid fever= unclean hands & “Typhoid Mary”

   4. Ingestion of food/water contaminated w. feces & close personal contact

   5. Asymptomatic carriers & chronic carriers shed bacilli gallbalder

   6. Bacilli like small intestine → invasive diarrhea → septicemia

   7. Treatment: ciprofloxacin/ceftriaxone

3. Shigella

   1. Diarrhea; invades villus Lg intestine

   2. Symptoms: fever, nausea, painful cramps, watery stool filled w. mucous & blood

   3. Treatment: fluids, ciprofloxacin & sulfatrimethoprim

4. Plague: Yersinia pestis:

   1. Virulence: capsule & envelope proteins protect against phagocytes & intracellular growth

   2. Coagulase, endotoxin, murine toxin

   3. Transmission: wild & domestic animals/ infected humans

   4. Vector: flea; bacteria in gut → coagulase= blood clotting → blocking esophagus = ravenous flea

   5. Pathology:

      1. Bubonic: necrosis & swelling of lymph nodes; groin/armpit

      2. Septicemic (black death): virulence- intravascular coagulation, hemorrhage, & purpura (red/brown spots)

      3. Pneumonic: lungs

   6. Treatment: ciprofloxacin

   7. Prevention: Hygiene, rat population control, quarantine

5. Yersinia

   1. Yersinia enterocolitica: domestic & wild animals, fish, veggies, water

   2. Enters small intestine mucosa, survive phagocytes, inflame ileum & can mimic appendicitis

   3. Y. pseudotuberculosis: similar to enterocolitica w. lymph node inflammation

Haemophilis and blood agar growth

1. Haemophilus: blood loving; hemin (factor X)/ nicotinamid adenine dinucleotide (NAD/factor V)

   1. Gram -ve rods

   2. Pleomorphic

   3. Fastidious (picky bacteria)

   4. Resistant to temp. extremes, disinfectant, sensitive to drying

2. H. influenzae: acute bacterial meningitis, bacteremia, pneumonia

   1. Symptoms: fever, vomiting, stiff neck, neurological impairment

   2. Treatment: ceftriaxone w. dexamethasone

3. H. ducreyi: agent chancroid STD

   1. Treatment: azithromycin

4. H. parainfluenzae: normal oral & nasopharyngeal microbes; infective endocarditis

5. Blood agar: a nutrient-rich growth medium that supports the growth of a wide range of microorganisms, particularly fastidious organisms such as streptococci.

6. Spirochetes and endoflagella

   1. Spirochetes: helical, gram negative

   2. Endoflagella: flexing propels cells by rotation & crawling motions

7. Syphilis stages and latency, diagnosis microscopy and serological tests

   1. Stages, diagnosis, serological tests

      1. Incubation; asymptomatic

      2. Primary: chancre at inoculation site (mouth & genitals); dark-field microscope

      3. Primary latency: healed chancre; little scarring & few symptoms if any; serological tests

      4. Secondary: multiplies in bloodstream; rash on skin (no pain), fever, headache, sore throat; serological tests & dark-field microscope

      5.  Latency: disappears, but not gone; seropositive blood test

      6. Tertiary: if left untreated, returns; DNA analysis of tissue

8. Borrelia and relapsing fever cycle

   1. Borrelia hermsii

   2. Transmission- ticks

   3. 2-15 days —> high fever, shaking, chills headache, fatigue

   4. Treatment: doxycycline w. erythromycin

   5. Cycle:

      1. Initial infection

      2. Antibody response → reduce fever, then reinfection of mutant strain → relapse fever → second time, slows symptoms till another relapse happens

9. Lyme disease causative agent and borrelia

   1. Borrelia burgdorferi

      1. Tick bites

      2. Non-fatal, slowly progressive mimicking neuromuscular & rheumatoid conditions

      3. Treatment: early-doxycycline/amoxicillin; late- ceftriaxone & azithromycin

10. Cholera and gastric ulcer by helicobacter

    1. Vibrio cholerae

       1. Warm, monsoon, alkaline, saline conditions

       2. El tor – more infectious

       3. Spread by ingestion of contaminate food/water; mucous membranes of small intestine

    2. Helicobacter pylori

       1. Produce urease, converts urea into ammonium & bicarbonate which causes gastric ulcers

11. Rocky mountain spotted fever

    1. Rickettsia rickettsii

       1. Tick bite

       2. Symptoms: fever, chills, headache, spotted rash; CNS fatal if involved

       3. Cell wall less bacteria and mycoplasma

    2. Mycoplasma= cell-wall-deficient bacteria; pleomorphic (shapeshifters)

       1. M. pneumoniae- slowly spreads over interior lungsl; fever, chest pain, sore throat

       2. M. genitalium & Ureaplasma urealyticum- weak sexually transmitted diseases

Fungi

1. Fungi morphological identification, opportunistic vs true pathogens

   1. Fungi morphological identification: A method to identify fungi based on their physical characteristics, such as structure, color, and type of growth form.

   2. Opportunistic pathogens- little → no virulence; host defenses must be already compromised

   3. True pathogens- invade & grow in healthy, non-compromised host

2. Fungal thermal dimorphism- Switch from Hyphal cells (mycelial/mold phase) to yeast cells (parasitic phase); Temps to grow: molds= 30C, yeasts= 37C

3. Dermatophytes and ringworm/location. Oral thrush and candidiasis. Opportunistic diseases from fungi

   1. Dermatophytes- skin, hair, nail infections

      1. Treatment: topical antifungals (Lamisil/Griseofulvin), Gentle removal of skin/ UV light treatment (possible benefits)

   2. Ringworm locations-

      1. Scalp (tinea capitis)

      2. Beard (tinea barbae)

      3. Body (Tinea Corporis)

      4. Groin (tinea cruris)

      5. Nails (tinea unguium)

      6. Foot & hand (tinea pedis & manuum)

   3. Oral thrush (Candida albicans)

   4. Candidiasis- opportunistic pathogen

      1. Ranges from short lived, skin irritations à fatal systemic diseases

      2. Budding cells of varying sizes; elongated pseudo hyphae & true hyphae

      3. Off white, pasty; colony smells yeasty

      4. Treatment: Superficial- topical antifungals; Systemic- amphotericin B & fluconazole

   5. Opportunistic disease from fungi-

      1. Geotrichum candidum- geotrichosis mold in soil & dairy products; secondary lung infections

      2. Fusarium spp- soil; infect eyes, toenails, burned skin

Viruses

1. Know about the general/unique characteristics of viruses

   1. General characteristics-

      1. Acellular

      2. Ultramicroscopic (electron microscope)

      3. Contains parts needed to invade & control host cell

      4. Crystalline nature: regular, repeating molecules → crystalline appearance; purified – form large aggregate/crystals

      5. Hard to kill cuz they “hide” in body’s cells; they integrate into host cells

      6. Can’t reproduce w/o host cells; assembly only

      7. DNA/RNA never both

      8. Capsid: protein coat

2. Know about the general structure of viruses > nucleic acid, capsid, envelope and their functions

   1. General structures

      1. Nucleic acid— viral genome; DNA/RNA, never both; usually double-stranded but can be single stranded

         1. Function: carries genes necessary to invade & redirect cell’s activity to make new viruses  

      2. Capsid—protein coat encloses & protects nucleic acid

         1. Function: to protect genetic material until release

         2. Types of capsids:

            1. Helical- spiral tube of protein coils around genetic material

            2. Icosahedral- spherical shape of capsomeres shell (proteins) protecting the genetic material; may have outer envelope

            3. Envelope—an external covering to protect outside host cell; can sometimes have spike proteins to attach to host cell

3. Know about simple and complex viral structures

   1. Simple- either helical/icosahedral capsid

   2. Complex- have both helical & icosahedral capsid

4. Know about virus multiplication (from adsorption top release)

   1. Adsorption- virus binds to specific molecules on host cell

   2. Penetration- genome enters host cell

   3. Uncoating- nucleic acid released from capsid

   4. Synthesis- viral components produced

   5. Assembly- new viral particles constructed

   6. Release- assembled virus released by budding (exocytosis)/ cell lysis

5. Know about bacteriophage multiplication (lytic cycle vs lysogenic cycle)

   1. Adsorption- virus binds to specific molecules on host cell

   2. Penetration- genome enters cell

   3. Replication- viral components produced

   4. Assembly- viral components assembled

   5. Maturation- completion of viral formation

   6. Lysis & Release-

      1. Lytic- infect host cell → replicate → destroy host cell to release new virus cells

      2. Lysogenic- integrate genetic material into host cell’s DNA→ replicate with host cell w/out destruction of host cell

6. Know about how viruses are cultured and identified

   1. Cultured:

      1. In vitro- controlled outside living organisms; tubes & petri dishes

      2. In vivo- studies on living organisms; bird embryos & live animal inoculation

   2. Identified:

      1. Electron microscope: vizualize virus particles

      2. serological tests: detect antibodies/viral antigens

      3. PCR (polymerase chain reaction): detect viral genetic material

7. Know about prions and their diseases in human and animals

   1. Prions: misfolded protein, no nucleic acid; Resistant to sterilization techniques

   2. Diseases:

      1. Sheep & goats- scrapie

      2. Cow- bovine spongiform encephalopathies (BSE) “Mad cow”

      3. Elk- wasting disease

      4. Humans- Creutzfeldt-Jakob Syndrome (CJS); fatal brain disease, rapid cognitive decline/ dementia-like symptoms

DNA viruses

1. Know why pox virus is different from other viruses (morphological structures)

   1. Pox Virus

      1. No capsid; covered by a lipoprotein & coarse fibrils (feet)

      2. Largest & complex animal virus

      3. Ds DNA

      4. Replicate in cytoplasm in cell

2. Smallpox virus and importance of vaccine in its eradication

   1. Smallpox: 1^st to be eliminated by vax

      1. Inhalation/ skin contact exposure

      2. Variola

      3. Major- highly virulent, toxemia, shock, intravascular coagulation

      4. Minor- less virulent

      5. Vax- Edward Jenner; a mild version of cow pox

3. HSV1 vs HSV2

   1. HSV1- oropharynx, cold sores, fever blisters; early childhood

   2. HSV2- lesions → genitalia, possibly oral; spread w/o visible lesions, 14-29 yrs

4. Know about the Hepatitis b virus and its difference from Hep A and Hep C

   1. Hep B- Multi. Exclusively in liver, continuously seeds blood w. virus; inflammatory, swelling of liver & necrosis of liver cells, jaundice; Only DNA

   2. Hep A- contaminated food; less virulent; RNA

   3. Hap C- blood; transfusion hepatitis; RNA

5. Epidemiology of Hep B infection (mode of transmission, pathogenesis, disease symptoms and prevention)

   1. Mode of Transmission- blood products, sexually transmitted (homosexuals & drug addicts)

   2. Pathogenesis- skin breakage/ mucous membrane/ injection to bloodstream

   3. Symptoms- Jaundice, inflammation of liver & necrosis of liver cell (chronic liver disease; cirrhosis), fever, rash, arthritis

   4. Prevention- passive immunization w. Hep B Ig (newborns being born from positive mothers)

RNA Viruses

1. Influenza viruses:

   1. Mutation: shifts & drift mutations

   2. H and N glycoproteins:

      1. H glycoprotein (Hemagglutinin): 18 subtypes; binds to hosts cells

      2. N glycoprotein (Neuraminidase): 11 subtypes; hydrolyzes mucous & assists viral budding & release

   3. Antigenic shifts and drifts:

      1. Shifts: one gene/RNA strand substituted w. a gene/strand from another influenza virus from different animal host

      2. Drifts: constant mutation; gradually change amino acid comp

2. Mumps and measles

   1. Mumps (Epidemic parotitis): painful swelling of salivary glands; short term

      1. Symptoms: fever, muscle pain, malaise (swelling of one/both cheeks), Males → epididymis & testes become infected, sterility = rare

         1. Vax- live attenuated MMR

   2. Measles (Morbillivirus): Red measles/rubeola, not German measles; contagious, respiratory aerosols, humans only reservoir

      1. Symptoms: sore throat, dry cough, headache, conjunctivitis, lymphadenitis, fever, Koplik’s spots (oral lesions; small & white), Exanthem (red rash)

3. Rabies: clinical phases of rabies

   1. Phases:

      1. Prodromal: fever, nausea & vomiting, headache, fatigue; some pain, burning tingling at site of wound

      2. Furious: agitation, disorientation, seizures, twitching, hydrophobia

      3. Paralytic: paralysis, disorientation, groggy

      4. Coma → Death

4. Corona viruses: SARS and CoVID19, mechanism of disease manifestation and treatment/preventions

   1. SARs (severe acute respiratory syndrome)

      1. Mechanisms of disease manifestation: flu-like symptoms, chills, headache, body ache, diarrhea, sore throat

      2. Treatment: supportive; provide O2, fluids, managing symptoms

      3. Prevention: mouth & nose covering

   2. CoVID19 (SARS-CoV-2)

      1. Mechanisms of disease manifestation: flu-like symptoms (like SARS) w. loss of taste & smell

      2. Treatment: vax

      3. Prevention: mouth & nose covering

5. Arboviruses: examples and vectors involved

   1. Examples: West Nile (mosquitoes), Zika virus (mosquitoes), Colorado tick fever (ticks)

   2. Vectors: mosquitoes, ticks, flies, gnats

6. HIV-AIDS: Reverse transcriptase, epidemiology, virulence factors, stages of AIDS

   1. Reverse transcriptase: HIV enzyme converts RNA —> DNA —> enters host cell nucleus —> Host replicates HIV protein —> more HIV cells that are noninfectious (becomes dormant)

   2. Epidemiology: sexual intercourse & blood transfusion/ products; babies contract before/during birth & from breastfeeding

   3. Virulence factors: virus attach to CD4 & coreceptor, HIV fuses w. cell membrane

7. Stages (determines on 2 factors)

   1. Level of virus

   2. Level of T-cells in blood

   3. Acute retro-viral syndrome (acute HIV infection) → Clinical latency (goes dormant) → AIDS
      

Immunology

1. Human normal flora: resident, transient and pathogenic microbes

   1. Resident: microbes that stay; new “neighbors”

   2. Transient: transition/transport; don’t stay long

   3. Pathogenic-

      1. True- cause disease in healthy people

      2. Opportunistic- immune system must already compromised

2. Microbial flora of specific regions

   1. Skin: Staphylococci sp.

   2. Mouth:Streptococcus; S. sanguinis, S. salivarius, S. mitis

   3. Respiratory: Staphylococcus aureus (nasal & pharynx regions), Neisseria sp. (mucous membranes of nasopharynx), Streptococci & Haemophilus (tonsils & lower pharynx)

   4. Lg intestine: Bacteroides, Bifidobacterium, Fusobacterium,Clostridium

   5. Genitourinary tract; sterile

3. Factors in development of infections

   1. True- cause disease in healthy people

   2. Opportunistic- immune system must already compromised

   3. Virulence factors- characteristics/structure that cause disease

4. Process of human diseases: patterns, signs and symptoms

   1. Patterns:

      1. Localized infection: microbes enter body & remain on specific tissue

      2. Systemic infection: spread to several sites & tissue fluids in blood stream

      3. Focal infection: breaks loose from Lg intestine & carried to other tissues

      4. Mixed infection: several microbes grow at the same time at infection site (polymicrobial)

      5. Primary infection: initial infection

      6. Secondary infection: following infection by a different microbe

      7. Acute: comes rapidly, severe but short-lived effects

      8. Chronic: progress & persists for a long period of time

      9. Direct contact: physical contact/fine aerosol droplets

      10. Indirect contact: passes from infected → intermediate conveyor → new host

   2. Signs: objective evidence noted by observer

   3. Symptoms: subjective evidence sensed by the patient

5. Nosocomial infections: hospital acquired infections

6. Host defense mechanisms: First line defenses- physical & chemical barriers

   1. Skin

   2. Mucous membranes

   3. Tears

   4. Stomach acid

   5. Flushing effect; vomiting, defecation, urination

7. Human blood cells: types (names)

   1. Leukocytes (WBC)

      1. Granulocytes- lobed nucleus

      2. Neutrophils: lobed nuclei; phagocytes

      3. Eosinophils: bilobed nuclei, destroy eukaryotic pathogens

      4. Basophils: bilobed nuclei, release potent chemical mediators

   2. Agranulocytes- unlobed & rounded nucleus

      1. Lymphocytes

      2. B cells: antibodies

      3. T cells: modulate immune functions & kill foreign cells

      4. Monocytes: Largest cells, phagocytic (eat other cells)

      5. Macrophages: monocytes after leaving circulation system

      6. Dendritic cells: trap pathogens & participate in immune reactions

   3. Erythrocytes (RBC)

   4. Platelets

8. Second line of defenses: inflammation, phagocytosis (cells involved), mechanisms of phagocytosis

   1. Inflammation: earliest symptom of disease, result of activation of body’s defenses; fever, swelling, pain

      1. Edema: fluid accumulation

      2. Granulomas & abscesses:

      3. Lymphadenitis: swollen lymph nodes

      4. Redness (Rubor): increased circulation & vasodilation

      5. Warmth (Calor): heat given off by increased blood flow

      6. Swelling (Tumor): edema & pus

      7. Pain (Dolor): stimulation of nerve endings

   2. Phagocytosis: survey, ingest, extract immunogenic info

      1. Neutrophils: general; react first to bacteria, foreign materials, & to dmg tissues

      2. Eosinophils: parasites & allergens

      3. Macrophages: scavenge & process foreign substances to prep for reactions w. B & T cells

      4. Mechanisms:

         1. Chemotaxis: phagocytes à inflamed site à gradient of stimulant product

         2. Phagolysosome formation: think stomach inside a cells that eats foreign “trash” (ranges from germs & bacteria to dead/dmg cells and dust/tiny particles); Macrophages= trash collectors, phagolysosome= trash compactors  

         3. Destruction & elimination: respiratory burst (O2 rush used to make powerful chemicals), lysosomes, lactic acid, & nitric oxide released, debris not digested—exocytosis

9. 3^rd line of defenses: adaptive and acquired immunity

   1. Adaptive/acquired: specific & acquired (antibodies)

   2. Innate- first line of defense of the body (physical & chemical) & always active

10. Specificity and memory: cooperation between B-cells and T-cells

    1. Specificity: antibodies produced, function against antigen that they were produce for

    2. Memory: Lymphocytes (B & T cells) programmed to recall the first encounter w. an antigen & respond rapidly to new encounters

11. T cells: Types and functions: recognition of self and foreign cells

    1. Types & Functions

       1. T Helper (CD4); Regulate immune reaction to antigens including other T & B cells, activates macrophages & increase phagocytosis

       2. Cytotoxic T cells (T_c & CD8); Destroy foreign/abnormal cells secreting perforins & granzymes

          1. Perforins: make tiny wholes in cells surface

          2. Granzymes: enzyme that tells the cell to self-destruct

       3. Natural Killer cells (NK); identify & destroy infected/cancerous cells

12. B cells: types and function: antibody production and memory

    1. Types & Functions

       1. Plasma cells: secrete Lg production of antibodies to destroy foreign microbes

       2. Memory B cells: remembers specific pathogens

13. Antigens, superantigens, haptens, auto antigens

    1. Antigen: any foreign substance that causes the immune system to respond (viruses, bacteria, toxins)

    2. Superantigens: potent T-cell stimulators

    3. Haptens: tiny foreign molecules that cannot trigger an immune response

    4. Auto antigens: cell markers found in some people but not in others

14. Antigen processing and presentation: T-cell dependent antigens must be processed by phagocytes called antigen-presenting cells before T-cells can recognize them

    1. Processing: T-cells need antigen-presenting cells (phagocytes) to process antigens before they can recognize them.

    2. Presentation: antigen is displayed → T-cells recognize & respond

15. T cell and B cell activation mechanisms (in brief)

    1. T-cell activation:

       1. T-cell receptor (TCR) binds to antigen presented on an MHC molecule by another cell

       2. requires co-stimulatory signal (CD28-B7)

       3. Leads to:

          1. Helper T cells (CD4*) —> help other immune cells

          2. Cytotoxic T-cells (CD8*) —> kill infected cells

          3. Memory T-cells —> long term immunity

    2. B-cell activation:

       1. B-cell receptor binds directly to a free-floating antigen.

          1. Can happen:

             1. With T-cell help (T-dependant) —> strong response, memory cells, class switching

             2. Without T-cell help (T-independant) —> weaker, mostly IgM antibodies

          2. Leads to:

             1. Plasma cells —> produce antibodies

             2. Memory B cells

16. Antibody-antigen interactions

    1. Opsonization: coating microorganisms/other particles w. specific antibodies to be readily recognized by phagocytes

    2. Neutralization: fill the surface receptors on a virus/active site of microbial enzyme to prevent from attaching

    3. Agglutination: antibody aggregation; cross-linking cells/ particles into Lg clumps

    4. Complement fixation: activation of pathways results in rupturing cells & some viruses

    5. Precipitation: solid/tiny particle substances (antigens) clump together to trigger immune response

17. Classes of Immunoglobulins and functions

    1. Ig G: monomer, long term immunity; memory antibodies, neutralizes toxins & viruses

    2. Ig A: monomer circulates blood, dimer in mucous & tears

    3. Ig M: pentamer; first response to antigen, can be served as a B-cell receptor

    4. Ig D: monomer; Receptor on B-cells for antigen recognition

    5. Ig E: antibody for allergy & worm infections

18. Vaccines and acquired immunity

    1. Vax:

       1. Killed whole cell/inactivated viruses

       2. Live, attenuated cells/viruses

       3. Antigens from bacteria/viruses

       4. Genetically engineered microbes/microbial agents

    2. Aquired immunity:

       1. Active- person challenged with antigen that stimulates production of antibodies; creates memory, takes time to develop & lasts (Getting infection)

       2. Passive- preformed antibodies donated to an individual; no memory, acts immediately & short term (Mother to child)

       3. Natural- part of normal life (immunotherapy)

       4. Artificial- through medical procedure (vax)

19. Types of allergies

    1. Type 1: Immediate allergies

       1. Anaphylaxis

       2. Hay fever, asthma

    2. Type 2: Antibody-mediated incompatibilities

       1. Blood group incompatibility

       2. Pernicious anemia

    3. Type 3: Immune complex

       1. Lupus

       2. Rheumatoid arthritis

       3. Serum sickness

       4. Rheumatic fever

    4. Type 4: T-cell mediated hypersensitivities

       1. Infection reactions

       2. Contact dermatitis

       3. Graft rejection

       4. Autoimmunity disorders

20. Stages of allergy development (sensitization and provocation)

    1. Primary contact/sensitization: first contact w. allergen

    2. Provocation: following exposure w. same allergen replicate first allergy symptoms

21. Chemical mediators of allergy

    1. Histamine: profuse & fast acting

    2. Serotonin: helps increase blood flow, influence pain, modulate immune response

    3. Leukotrienes: slow reaction of anaphylaxis

    4. Prostaglandins: regulate smooth muscle contraction

    5. Bradykinin: prolonged contraction of bronchioles, dilation of peripheral arterioles

22. Human blood grouping and ABO antigens

    1. A, B, AB, O blood types

    2. Type A: antibodies against B antigens

    3. Type B: antibodies against A antigens

    4. Type AB: no antibodies against A/B antigens

    5. Type O: antibodies against A/B antigens

23. Delayed hypersensitivity and graft rejections

    1. Delayed hypersensitivity

       1. Grafts:

          1. Host rejects graft: host immune system attacks graft; organ transplants (MHC- Major histocompatibility Complex)

          2. Graft rejects host: donor immune cells attack host; bone marrow (GVHD- Graft vs Host disease)

          3. Autograft: recipient also serves as donor

          4. Isograft: tissue from identical twin

          5. Allograft: genetically different individuals but same species

          6. Xenograft: individuals of different species

24. Autoimmune diseases

    1. Systemic lupus erythematosus (SLE; Lupus): produce autoantibodies against organs & tissues; affects- kidneys, bone marrow, nervous system, joints, muscles, HRT, GI tract

    2. Rheumatoid Arthritis: dmg to joints (chronic inflammation): affects- lungs, eyes, skin, nervous system

    3. Grave’s disease: autoantibodies stick to thyroid cells, making them release too much thyroxine (hyperthyroidism)

    4. Hashimoto’s thyroiditis: autoantibodies stick to thyroid cells & T-cells react to thyroid gland & reduce lvls of thyroxin (hypothyroidism)

    5. Type 1 diabetes mellitus: autoantibodies & T-cells harm the pancreas cells (beta cells) that make insulin.

    6. Myasthenia gravis: autoantibodies bind to receptors (acetylcholine) & block transmission of nerve signals to muscles

    7. Multiple sclerosis: T-cells & autoantibodies dmg myeline sheaths of nerve cells 

Environmental microbiology

1. Microbial ecosystem: food chain vs food web

   1. Food chain- basic image of feeding pathway

   2. Food web- multilevel food chain

2. Terms involved in microbial interactions: mutualism, commensalism etc

   1. Mutualism- mutual relationship; both parties benefit

   2. Commensalism-one party benefit, other not effected

   3. Syntrophism- metabolic byproducts of one are useful nutrients to another

   4. Synergism-two parties cooperate to break down nutrients; can’t break down individually

   5. Parasitism- one party benefits, other is harmed

   6. Competition- one party gives antagonistic substances to inhibit/kill others

   7. Predator-consumer seeks out & ingest live prey

   8. Scavengers- feeds on various food sources

3. Nitrogen cycle and roles of microbes in it.

   1. 4 steps

      1. Nitrogen fixation- nitrogen converted —> ammonia salts

      2. Ammonification- bacteria decompose nitrogen-containing compounds —> ammonia

      3. Nitrification- convert ammonia —> nitrate & nitrite

      4. Denitrification- microbes convert nitrite à nitrogen

      5. Root nodules and N2 fixation by Rhizobia

4. Root nodules- symbiosis of Rhizobia & legumes —> nitrogen fixation (natural fertilizer factories

5. Eutrophication algal bloom and red tides

   1. Eutrophication- addition of excess nutrients; natural/from sewage, agricultural, industry à Eutrophication algal bloom & sometimes cause red tides (red algae; harmful algal bloom)

6. Drinking water quality tests

   1. Membrane filter method- filtration à filter on selective & differential media à incubated à colonies identified & counted

   2. Most probable number (MPN)- confirmed & completed tests; no level of fecal coliforms, enterococci, viruses, pathogenic protozoans in drinking water

       

Applied microbiology

1. Wastewater/sewage treatment

   1. Water purification: water is treated before supplied to consumers; lg reservoirs where stored & sedimentation (settling tanks) & treated to prevent cyanobacteria; pumped into holding tanks, further settling, aeration & filtration; treated w. chlorine, ozone, or peroxide disinfectant

2. Sewage treatment-

   1. Primary phase - remove floating, bulky physical objects

   2. Secondary phase- remove organic matter by biodegradation

   3. Tertiary phase- filtration, disinfection, removal of chemical pollutants

   4. After completion, water gradually released

3. Fermentation and food microbiology

   1. Bread, wine, beer, vegetable products, vinegar, milk & dairy products

   2. Rye bread- Lactobacillus plantarum

   3. Sourdough- Lactobacillus sanfrancisco

Industrial microbiology

1. primary and secondary metabolites (metabolism)

   1. Primary metabolites- produce major metabolic pathways, essential to microbe function; must need to survive

      1. Amino & organic acids; organic acids synthesized during exponential phase

   2. Secondary metabolites- extra chemicals/byproducts for special purposes, may not be critical to microbe function

      1. Vitamins, antibiotics, steroids