1. Microbes and diseases: what to study-1
1. Causative microbe: name, morphology (shape, size, Gram stain, etc.), physiology (aerobe, anaerobe, etc) and some info on classification (what's it related to?)
2. Pathogenesis and clinical disease:  what disease does it cause (signs and symptoms) and how does it do it (capsule, toxins..)?
3. Transmission and epidemiology: how do you get the disease?

2. Microbes and diseases: what to study-2
4. Diagnosis: How does the lab usually identify the causative agent?
5. Treatment: antibiotics prescribed (or not- no cell wall, no penicillin) or other treatment (oral rehydration therapy for cholera).
6. Prevention and control (stop the spread; condoms, kill urban rats..)

3. Staphylococcus: G+ coccus
S. aureus and S. epidermidis.
S. aureus much worse, S. epi an opportunist.
Sturdy, salt tolerant, fac anaerobes; clusters
S. epidermidis common on skin, S. aureus less.
Diseases of S. aureus
Food poisoning, skin diseases (impetigo, folliculitis, furuncles & carbuncles, scalded skin syndrome), systemic diseases (TSS, bacteremia, heart, lung, and bone infections)
Diseases spread by fomites and direct contact.

4. Characteristics of S. aureus infections
tray.dermatology.uiowa.edu/ DIB/SSSS-002.htm rorelse/popup/01d1x.htm

5. S. aureus virulence factors & Rx
Coagulase, triggers blood clotting.
Capsules, beta-lactamases (destroy penicillins)
Toxins: various, including TSS toxin, exfoliatin, and enterotoxins (heat stable)
95% resistant to penicillin, but now many resistant to methicillin, oxacillin. Treatment usually clindamycin (oral) or vancomycin (IV).

6. Streptococci: G+ cocci
Genera: Streptococcus and Enterococcus
Aerotolerant anaerobes, catalase negative
Grow in chains, pairs
Strep: Lancefield groups, viridans, S. pneumoniae
Group A strep: S. pyogenes
Pharyngitis, scarlet fever, pyoderma, erysipelas, TSS, necrotizing fasciitis
Sequelae: rheumatic fever and glomerulonephritis

7. Characteristics of Streptococcal infections

8. Virulence factors, etc. S. pyogenes (“pus-producing”)
M protein and capsule: avoids phagocytosis
Streptokinase, streptolysins for escape & attack
Pyrogenic erythrotoxins (SPEs)
at least 3 different types
Cause scarlet fever: fever, rash; toxic shock
Beta hemolytic on blood agar
Viridans group: greenish alpha hemolysis
Common in throat, mouth, but can be opportunists
S. mutans associated w/ dental caries

9. Clostridium: G+ rods Strict anaerobes! Endospore formers. Toxigenic
Common in soil, sewage animal GI tracts
Produce neurotoxins, enterotoxins, histolytic toxins
Four important species: C. perfringens, C. botulinum, C. tetani, and C. difficile.
C. perfringens
Food poisoning: cramps and diarrhea
From injury: myonecrosis to gas gangrene
Fermentation in tissues, killing of tissues and spread of cells into anaerobic areas.
Oxygen treatment, debridement, amputation

10. More clostridia C. difficile: normal GI microbiota
Cause of pseudomembranous colitis, resulting from overgrowth following broad spectrum antibiotics
Damage to GI wall can lead to serious illness
Nosocomial infection, easily transmitted
C.botulinum: cause of botulism
Usually acquired by ingestion: intoxication
Food borne, infant (no honey), wound
Produces neurotoxin, inhibits acetylcholine release
Flaccid paralysis; Botox: deadly poison / beauty
Mouse bioassay; administer antitoxin

11. Opposing muscle groups
When biceps contracts, triceps relaxes.
When triceps contracts, biceps relaxes.
Excitatory neurons send signal to contract, inhibitory neurons send signal to NOT contract.

12. Function of nerves

13. More clostridia-2 C. tetani: cause of tetanus
Growth in anaerobic wounds, makes tetanus toxin
Toxin prevents action of inhibitory neurons
Opposing muscle pairs both contract
Spastic paralysis, leading to death.
Recommendation is booster shot every 10 years
DPT, Toxoid vaccine
Booster: DT (with diphtheria toxoid)
No natural immunity: you would die first.

14. Mycobacterium: G+ rods
Many non-pathogenic species, most disease: M. tuberculosis and M. leprae
Mycolic acids as part of complex cell wall
Protects against desiccation
Protects against destruction by phagocytes
Requires acid-fast staining
Generally grow very slowly (chronic illnesses)
Can grow intracellularly

15. Acid Fast stain of Mycobacteria

16. M. tuberculosis Causes disease tuberculosis, mostly lung dis.
Disease: cells enter lungs, infect macrophages
Macrophages not activated, can’t kill invader
Cell mediated immunity fights back, walls off infection; forms tubercle (caseous necrosis occurs)
Disease remains controlled, cured, or returns
Disseminated TB: spreads thru body
Worldwide problem; lowered immunity=risk
Skin test, chest x-ray, drug treatment, vaccine?

17. M. leprae Cause of Hansen’s disease, aka leprosy
Slow growing, likes it cool; armadillos as model
Grows in peripheral nerve and skin cells
Numbness is characteristic of disease
Tuberculoid vs. lepromatous leprosy
Mild, severe, respectively, depending on cell mediated immune response.
Numbness vs tissue destruction
Spread mostly by direct contact
Treatable with antibiotics, but long term

18. Gram negative rods and cocci
Endotoxin: Lipid A, the superantigen
Part of LPS of the Gram negative outer membrane
Causes an over-stimulation of macrophages with production of various cytokines
Fever, vasodilation, inflammation, shock, and disseminated intravascular coagulation
While Gram negative pathogens can have other virulence factors (capsules, fimbriae, exotoxins), all have endotoxin and are thus dangerous.

19. Enterobacteriaceae: Gram negative rods
Gram negative, small rods, facultatively anaerobic, oxidase negative; found in soil, water, and GI tracts
some strictly pathogens, others opportunists
Coliforms (ferment lactose) and non-coliforms
Virulence factors
Endotoxin, capsules, fimbriae, exotoxins, others.
Enteric bacteria identified by biochemical tests
Selective/differential media, IMViC tests, etc.
Strains identified by serological techniques

20. Serology and enteric bacteria
Because enteric bacteria are very closely related to each other, differentiation requires serology
Use of antibodies to identify particular antigenic molecules on cell surfaces
O antigen: repeating sugar group on LPS
H antigen: flagellar protein
K antigen: capsule antigen around cell.
Example: E. coli O157:H7 describes particular serotype which happens to also produce a dangerous exotoxin.

21. http://www. ratsteachmicro

22. E. coli: friend or foe?
E. coli: cause of 90% of urinary tract infections
Most strains common to GI tract, not harmful there.
Strains have fimbriae needed for attachment
Proanthocyanidins in cranberry juice interfere
E. coli: common cause of diarrhea
Many strains possess genes (some on plasmids) that code for additional virulence factors like exotoxins which cause disease
E. coli O157:H7: possesses shiga toxin; strain causes hemolytic uremia syndrome, damages kidneys.
E coli strains classified as EHEC, EIEC, EPEC, etc.
Enterohemorrhagic, enteroinvasive, etc.

23. Truly pathogenic enterics
Salmonella: species so closely related that they are really all S. enterica. But medically, species epithets still used: S. typhi and others. Divided serologically.
Present in eggs, poultry, on animals such as reptiles
Large dose results in food poisoning; diarrhea, fever, etc.
Cells phagocytized by intestinal lining cells, kill cells causing symptoms, may pass through into blood.
S. typhi: typhoid fever. Spread through body
Gall bladder as reservoir; Typhoid Mary
Importance of clean water and sewage treatment.

24. Truly pathogenic enterics-2
Shigella: especially S. sonnei (most common) and S. dysenteriae (most serious); cause shigellosis.
Food, flies, fingers, feces, fomites: very small infectious dose, personal hygiene important in prevention.
Infection of intestinal lining damaged, cells pass directly from cell to cell; cramps, diarrhea, bloody stools.
S. dysenteriae produces shiga toxin which inhibits protein synthesis, increases damage.
Most serious problem with diarrheal diseases in general is dehydration.

25. Truly pathogenic enterics-3
Yersinia: Y pestis is cause of plague, other species cause food-borne infections
Plague: 3 cycles: sylvan, urban, and human
endemic in sylvan cycle; mixing of woodland and urban rodents brings urban cycle, fleas jump from dying rats to humans.
Infection leads to large swollen lymph nodes: buboes
Bubonic plague, with high fever.
Septicemic plague: with DIC, bruising (black death)
Raises mortality from75% to near 100%
Pneumonic: coughed out and spread human to human
100% mortality

26. The S.F. earthquake and plague

27. Other Gram - rods Francisella: F. tularensis, cause of tularemia
Also called rabbit fever, tick fever, deerfly fever, etc.
Most cases in US in Arkansas/Missouri Ozarks
Survives phagocytosis, lives intracellularly
Present in many animals, transferred to humans by vector, ingestion, direct contact, inhalation
Chills, fever, malaise, swollen nodes

28. Other Gram – rods-2 Legionella: L. pneumophila and several others
Fastidious in culture, requires special media
Very common in aquatic environments: ponds, cooling towers, hotwater heaters, showers.
Grows normally in amoebae, so also grows in phagocytes
Most dangerous as opportunistic pneumonia, inhalation
Mild form of disease: ‘pontiac fever’
bicentennial.html

29. Chlamydia Very small, obligate intracellular parasites
Cell and outer membrane, but no peptidoglycan
Spread directly rather than by vectors
Two stage life cycle
Elementary body: tiny ( µm) and inert
Spore-like: dormant and resistant
Infectious: form that moves between cells
Reticulate body: µm, metabolically active, reproduce inside host cells

30. Chlamydial diseases
C. trachomatis: infects cells of mucous membranes, conjunctiva. Mostly eye & STD
Infection kills cells, stimulates inflammation which also causes cell destruction
Trachoma- leading cause of non-traumatic blindness. Caused by certain strains.
Infection of conjunctiva causes scarring, turning in on eyelashes which scratch cornea.
Scarred cornea, with ingrown blood vessels, obscure vision.
STD strains can also infect eyes, self-inoculation.

31. Sexually transmitted Chlamydial disease
Non-gonococcal urethritis, about 50% of cases
Chlamydia infections are the most common STD, but even more are infected and asymptomatic
85% of women asymptomatic; others can develop PID; scarring of uterine tubes can lead to sterility, ectopic pregnancy.
Eye infections of newborns prevented with antibiotic drops.
Also protects against N. gonorrhoeae

32. Gram negative curved rods
Vibrio: comma shaped
Like enteric but oxidase positive; polar flagella
Halotolerant to halophilic, grow in estuarine and marine environments
V. cholerae: cause of cholera
Toxin-mediated severe diarrhea
Salt, fluid leave intestinal cells, patient dies of dehydration.
Oral rehydration therapy (ORT): water, salts, and glucose, now saving lives.
Causes pandemics that spread around the world
Lack of adequate sewage treatment

33. Campylobacter
Campylobacter jejuni: number one cause of bacterial gastroenteritis; zoonotic
More common than Salmonella and Shigella combined for food borne disease.
Most retail chickens are contaminated; improperly cooked chicken and contaminated milk typical vehicles.
Low infectious dose
Gram neg. curved rod

34. Helicobacter pylori Cause of ulcers and gastritis
2005 Nobel Prize for Medicine or physiology to Barry Marshall and J Robin Warren
Unusual because it can live in stomach
Produces urease enzyme
Released ammonia neutralizes stomach acid, irritates stomach lining.
Basis for radioactive urease test.
Correlated with stomach cancer.