ReKAP: Gram + Utilize teichoic acid or Lipoteichoic acid for attachment.

Gm - contains the endotoxin

lipopolysaccharide (LPS).

ReKAP:Endospores helps with transmission. E.g. Bacillus and Clostridium

ReKAP: Pathogenicity Colonization (Pili/Fimbriae, Teichoic acids, Adhesins, IgA Proteases, biofilms).

ReKAP:Avoiding iMmune Destruction:Capsules and slime layers, Antiphagocytic surface components, IgA
Proteases

ReKap:Capsules helps with protection from phagocytosis and adherence.Some Killers HavePretty NiceCapsules
= Strep pneu, klebsiells, haemophilus, pseudomonas, neisseria, cryptococcus neoformans

ReKap:Endotoxin (LPS) from Gram neg rodsExample: Lipid A toxic will cause cell dealthLPS will activates
macrophages, release of cytokines, shock, DIC

Exotoxin are secreted proteins:Toxoid A-B. B binds to receptor. A active is toxic. Thre are enterotoxins,
neurotoxins, cytotoxins.Cytolysins will lyse cells by damaging membrane.

ReKAP:LPS will cause monocyte to create a cytokin storm:IL-1beta, IL6, IL10, TNF, PAF, etc.

ReKAP:Inhibit Protein Synthesis:EHEC and Shigella. Nick 28S subunit of 60S ribsome.Pseudomonas and C.
Diphtheriae will Ribosylates EF2

ReKAP:Increase Intracellular cAMPCholera, ETEC will ribosylates Gs proteinPertussis will Ribosylates Gi

ProteinAnthrax acts as adenylate cyclise

ReKAP:Microaerophilic require low but not full oxygen tension. Example: Campylobacter, helicobacter

ReKAP:Staph aureus is coag +S. Saprophyticus and S. Epidermidis is negative coagulase.

Catalase test can be used to differentiate Staph (+) from Strep! * Catalase is an enzyme produced by bacteria
when exposed to O2

ReKAP: HemolysisAlpha - Viridans Strep, S. pneumoniaeBeta - S. pyogenes, S. agalactiaeGamma – Enterococci

Coagulase Test:Alpha -> Greenish discoloration - partial decomposition of HbBeta -> Complete breakdown of
HbGamma -> lack of hemolysis

Staph Aureus:- Only Staph that is Coagulase positive!- Ferments Mannitol* Aureus = Gold (yellow)

HIGH YIELD Staph Aureus: Has enterotoxins (heat stable) -> Heat kills the bact but NOT the toxin (food
poisoning!) -> Incubation period is SHORT: 2-4hours!

Chronic Granulatous disease: NADPH oxidase def (leads to defective Oxidative Burst)-> Susceptibility to
Catalase + organism

ReKap: Staph aureuaPathogenesis -Protein A binds Fc component of IgG (inhibits phagocytosis)Enterotoxins:

fast acting and heat stableToxic Shock Syndrom toxin-1

Staph Aureus:- Protein A -> interferes with Opsonization (binds to Fc component of IgG)

ReKAP:Superantigens (SAgs) are a class of antigens that result in excessive activation of the immune system.

Superantigen will bind OUTSIDE of antigen binding site (MHC II and TCR) -> Excessive production of Cytokines
-> Stimulation of TNA-alpha and SHOCK!

Exfoliative toxins (proteases that hydrolyze Desmosomes)-> ETA associated with Bullous Impetigo-> ETB
associated with Scalded-Skin Syndrome

Osteomyelitis: Staph is More common staphSickle cell anemia patients -> Salmonella!
UTI + Gram positive + Catalase positive + resistant growth to Novobiocin--> S. saprophyticus

"B"eta hemolysis is the "B"est at eating RBC--> Complete hemolysisAlpha Hemolysis--> "A"lmost -->
GreenGamma Hemolysis--> "G" ross (enterococci)--> No hemolysis--> White

COBEDS--> phage-mediated pathogenic factors--> C (Cholera) O (O antigen from Salmonella) B ( Botulinum

Toxin) E (Exotoxins A–C/ Pyogenes) D ( diphteria toxin) S (Shiga toxin)

Step Pyogenes--> Rheumatic Fever--> Ab cross react (Type II hypersensitivy) with heart Ag--> 2 weeks after
pharyngitis

Question--> 6 y/0 male + sore throat + fever + headache + inflammaed throat + peritonsilllar exudate + Gram
Positve + B hemolytic on blood agar--> Dx: Strep Pyogenes--> M protein--> Antiphagocytic--> Rheumatic Fever,
Post Strep Glomerulonephritis

Strep Agalactie--> Group B--> Weakly hemolytic, CAMP positive (Listeria is potive too)--> Neonatal Meningitis--
> Bulging fontanelle

Sorry for the confusion: Agalatie is weakly B hemolytic.

Viridans--> Dextran biofilm--> adherence to enamel or heart valve that is already damaged--> Subacute
endocarditis

Question--> 14 y/o female + dysuria + catalase positive and "Gamma hemolytic" on blood agar--> Dx: UTI-->
Staph Saprophyticus. MCC of UTI is E. Coli (B hemolytic + catalase positve)

Bacillus Anthracis--> Poly-d-glutamate capsule

Bacillus Anthracis--> Toxin--> 3 Proteins--> 1. Protective antigen (B component)--> Mediates entry. 2. Lethal
Factor--> Kills cells. 3 Edema Factor--> Adenylate cyclase.

Bacillus Cereus--> Toxins--> Emetic: 1-6hrs + vomiting + diarrhea + fried rice. Diarrheal: 18 hrs + watery
diarrhea due to high cAMP

Clostridium--> Spore is at the end of the rod--> "lollipop"," drumstick"

C. Tetani--> Spore forming in tissue of low O2--> Tetanus toxin--> Motor neuron--> binds to Ach receptor-->
Retrograde axonal transport--> CNS--> Blocks release of GABA and Glycine--> Excitatory neurons are
unopposed--> Spastic Paralysis

REKAP: Bolutism - Infant have underdeveloped stomach/GI system, with low acidity, giving Abx to infants with
botulism poisoning you will kill the bug but all the toxin will be released.

REKAP: C perfringens - G+ rod, get into wound, Nagler reaction - egg yolk agar plate (hydrolyze lipids),
virulence factor phospholipase C that disolve lipid membranes,

REKAP: Corynebacterium diphtheria - tellurite agar; Silver stain - helobacter, bartonella, legionella, PCP
Pneumonia, chlamydia; String test - Giardia (not used anymore, mainly use O and P); Xenodiagnosis with tics -
Q fever, RMSF,

REKAP: C Septicum: septic shock in colon cancer patients,

ReKap: C difficile: toxin A is the most important, causing diarrhea; Abx overuse (Abx kill all bacteria in colon,
thus C diff spores grow and flourish), when there is too much bacteria it causes diarrhea by turning on Toxin A;
Toxin B forms pseudomembranous colitis; Vancomycin is the ONLY treatment (MDZ was old), Fecal transplant

Rekap: Inactivation of Elongation factor-2 think diphtheria and pseudomonas;

Rekap: enteroinvasive e coli, listeria and shigella have actin jet pulsion, all three escape phagolysosome and
replicate in the cytoplasm, Actin jet trails on histopathological slide
Rekap: bacterial toxins acquired from lysogenycholera toxin, O antigen from Salmonella, botulinum exotoxin,
erythrogenic exotoxins of Strep pyogenes, diphtheria toxin, Shiga toxin

REKAP: Listeria also seen in transplant patients due to lack of T cells and secondary to immune deficiency

Rekap: in order to be a disease causing diphtheria, you must have a prophage (which is a virus in a bacterial
DNA),

Rekap: NUMBER 2 CAUSE OF MYOCARDITIS IN THE USA IS C DIPHTHERIA, cardiac dysfunction, (only if toxin
gets in blood stream)

Rekap: ELEK test: not done anymore; ELISA done more commonly.

Rekap: Diphtheria toxin kills myocardial cells; Giardia or malaria - you do not see eosinophils;

Actinomyces israelii:-Branching rods in oral infection with characteristic sulfur granules.-Gram + branching,
anaerobic filament, non-acid fast.-Causes oral/facial abscesses that drain through sinus tracts.-often associated
with dental caries/ extraction and other maxillofacial trauma; forms yellow “sulfur granules”.-Can also cause
PID with IUDs -Treat with Penicillin.

Nocardia:-gram positive that forms long, branching filaments and appear like fungi. -an aerobe.-Weakly Acid
Fast.-Found in soil, opportunistic organism.-Associated with pulmonary infections in immunocompromised.-
Can also be associated with cutaneous infections after trauma in immunocompetent.-Can spread to the CNS.-
Treated with Sulfonamides, such as TMP-SMX.-Ziehl-Neelsen stain (carbol fuchsin), stain identification. -Urease
+ Catalase positive.

Mycobacterium Tuberculosis:-Facultative intracellular organism.-Sulfatides: inhibit phagosome-lysosome

fusion, allowing intracellular survival.-Cord factor: causes serpentine growth in vitro; inhibits leukocyte
migration; disrupts mitochondrial respiration and oxidative phosphorylation.

Mycobacterium Tuberculosis:-Facultative intracellular organism.-Sulfatides: inhibit phagosome-lysosome

fusion, allowing intracellular survival.-Cord factor: causes serpentine growth in vitro; inhibits leukocyte
migration; disrupts mitochondrial respiration and oxidative phosphorylation.

Primary pulmonary TB – Symptoms can include fever, dry cough -Organisms replicate in naive alveolar
macrophages, killing the macrophages until Cell Mediated Immunity is set up (Ghon focus).-Macrophages
transport the bacilli to the regional lymph node (Ghon complex) and most people heal without disease -
Organisms that are walled off within the Ghon complex remain viable unless treated .

2. Reactivational TB: -Symptoms can include fever, hemoptysis, night sweats, weight loss. -Erosion of
granulomas into airways (high oxygen) later in life under conditions of reduced T-cell immunity can lead to
mycobacterial replication and disease symptoms. -Complex disease with the potential of infecting any
organ system.-May disseminate (miliary TB): kidneys, GI tract, brain, spine (Pott disease).

Mycobacterium leprae:• Acid fast rods (seen in punch biopsy).• Obligate intracellular parasite (cannot be
cultured in vitro). • Optimal growth at less than body temperature.•Reservoir: human mucosa, skin, and
nerves are only significant reservoirs; some infected armadillos in Texas and Louisiana.•Transmission:
nasal discharge from untreated lepromatous leprosy patients Pathogenesis: obligate intracellular parasite;
cooler parts of body, e.g., skin, mucous membranes, and peripheral nerves.Disease(s): leprosy: a
continuum of disease, which usually starts out with an indeterminate stage called “borderline”.

Tuberculoid Leprosy:-Characterized by a strong Cell mediated immune response (Th1).-A lepromin skin
test is usually positive.-low number of organisms found in tissue biopsy.-Clinical features arises from
damage secondary to cell mediated immunological responses, granuloma formation results in nerve
enlargement and eventually nerve damage. Nerve damage results in loss of sensation increasing the risk of
burns and trauma.
Neisseria Meningitidis:-Contains a capsule (most important virulence factor-Ki capsule-meningitis in
neonates).-Vaccine available for young adults.-Postal of entry: respiratory.

Neissesia Gonorrhea:-NO Capsule.-No Vaccine.-Port of entry: Genital.-Ferments: Glucose.-DOES NOT

Ferment Maltose.-Tx: Ceftriaxone, usually with Azitromycin for Chlamydia co-infection.

Neonatal Conjuctivitis:•<1 week Neisseria Gonorrhea.•>1 week Chlamydia trachoma’s.

Neisseia Gonorrheoeae: UTI associated symptoms- burning, pain, frequency. •Neisseira G

Discharges:Greenish Yellow-mucopurulent (PUS-dead neutrophils with dead after eliminating organisms).

DISCHARGE DIFFERENTIALS:1. Trichomonas Vaginalis: yellow-green, foul-smelling, discharge. Tx:

Metronidazole. 2. Bacterial Vaginosis: thin, white-discharge with a fishy order. Tx: Metronidazole.3.
Candida Vulvovaginitis: Thick, white, “Cottage cheese” discharge. Antibiotic usage, diabetes mellitus, itchy.
4. Neisseira G Discharges: Greenish Yellow-mucopurulent (PUS-dead neutrophils with dead after
eliminating organisms).

Complement Deficiency: •1. Early Complements deficiency (C1-C4): Associated with increased risk for
severe, recurrent pyogenic sinus and respiratory tract infection and SLE. •2. Terminal Complement
Deficiency (C5-C9): associated with a increased susceptibility to recurrent Neisseria bacteremia.

Pseudomonas:-gram negative ROD.-"Non-ferming organism causing infection".-Grows on Eosin-Methylene

Blue or MacConkey- Only gram negative RODS.-Endotoxin-shock.-Exotoxin A: ADP ribosylates EF-2,
inhibiting protein synthesis (Psuedomonas mainly targets the LIVER). -HY: Hot tub folliculitis, contact
lenses keratitis, burn patients, cystic fibrosis patients. •PneumoniaSepsisEcthyma gangrenosum,

Legionella Pneumophila:-Gram negative Rod.-Silver stain.-Grows on Charcoal Yeast extract. Needs Iron
and Cysteine for growth.-Dx: Urine antigen.-HY: Hyponatremia on CBC. -Transmitted through aerosols,
water sources (Air-conditioners, hot water tubs).-Tx: Macrolides or Quinolone. -Smokers and patients with
Chronic Lung Disease are at higher risk.-Legionnaires Disease: is characterized by severe pneumonia
(Lobar & Unilateral), fever, GI (diarrhea or constipation), and CNS manifestations.

Bordetella Pertussis: -Produced the Pertussis Toxin, which results in the over-activation of adenylate
cyclase (cAMP). The toxin bings to the Gi protein, inhibiting the inhibitor, resulting in over-activation. This
hyper-activation further results in the impairment of phagocytosis, creating a happy place of quarantine
for the the Bacteria (Talk about quarantine).-Whooping Cough: characterized by a child cough that is worst
on expiration and “whoops” on inspiration.

B Melitensis--> Sheeps and goatsB. Abortis-> CowsRisk population: Farmers, veterinarians, butchers

H. Influezae--> Type B most invasive. Grows on chocolage agar ( with Factor X and V), not blood agar.
Grows near S. aureus on blood agar--> MCC of meningitis, pneumonia, sinus infections, epiglotitis (in
unvaccinated) (Staph Aureus is most common in vaccinated people)

Hyaluronic acid = Grp A strepPolysachharide= Strep pneumo and neisseriaGlutamate = B.

AnthracesAlginate = Pseudomona Ribytol = Haemophilus

H. Influenzae vaccination--> Against Type B ( most invasive)--> Conjugated vaccine--> Polyribitol capsule
conjugated to protein--> Diphtheria toxoid or N. meningitidis outer membrane proteins--> T-cell
dependent vaccine

Haemophilus ducreyi--> You do cry--> Painful chancre

P. Multocida--> Cat/Dog bite--> Endotoxin/capsule--> spreads through the skin--> cellulitis with
lymphadenitis

Bartonella Hensealae--> 2 pathologies--> Cat Srcatch disease--> flu like symptoms fro 3-6 months--. Dx:
Silver Stain. 2. Bacillary Angiomatosis--> Vascular involvement--> bright red raised spots and nodules-->
Common in AIDS patients ( rarely in mucosa). DIfferentiate from Kaposi Sarcoma ( same presentation
includijng mucosa)

Bloody diarrhea--> E coli, Salmonella, Shigella, and Campylobacter sp. Aeromonas

C. Jejuni--> Gram-negative curved rods with polar flagella--> Invades the mucosa--> Inflammatory
reaction--> Inflammatory diarrhea= RBCs + WBCs (different from EHAC)

GBS--> Asoc with C. Jejuni (most common)and Influenza--> Ascending paralysis motor and sensory
affected.

H. Pylori--> Motil, Curved rod, oxidase +, urease +--> goes to stomach --> urease breaks urea into amonia
and CO2-> increases the pH--> evades destruction

H. Pylori--> Dx: Urea breath test--> Radio labeled Urea--> detect the radio labelled CO2 In the breath-->
Identifies Urease--> Indicative of H. Pylori

Vibrio--> Curved rod, motile, growth on alkaline media--> Cholerae--> Shellfish carriers--> Enterotoxin
(Choleragen)--> upregulates cAMP by activating Gs protein by phosphorylation--> irreversible--> the
increased cAMP--> opens Cl- and Ca channels--. CL leaves, CA enters--> Loss of negative charge, gain of
positve charge--> K, NA, bicarbonate leave to mantain charge--> Water leaves as well

Enterobacteriaecae--> Gram negative rods, facultative anaerobes, "ferment glucose", "oxidase negative",
catalase positive

Enterobacteriacea--> Pathogenesis--> Antigens O(cell envelope), H ( flagellar/motility), K (capsular

polysaccharide ), Vi (virulence/Salmonella capsular antigen)

E. COli--> Pyelonephritis--> Due to PAP or P-pilli--> Adheres to the uroepithelium

E. COli--> Neonatal Septicemia and Meningitis--> Due to Capsule (K1). Agalatie and Listeria also cause
neonatal meningintis.

-------Meningitits-------Strep P--> AdultsHib--> unvaccinatedImmnunocompromised and elderly-->

ListeriaAIDS--> CyrptococusNenates--> Agalactie, listeria

-------Meningitits-------Strep P--> AdultsHib--> unvaccinatedImmnunocompromised and elderly-->

ListeriaAIDS--> CyrptococusNeonates--> Agalactie, listeriaAdolescents--> N. Meningitidis

E"T"EC--> Travelers, "T"wo en"T"erotoxins (LT: (Gs--> cAMP), ST: guanylate cyclase--> cGMP))

EPEC = Entero"p"athogenic -- > "P"lasmid-containing virulence genes --> Adherence factor (EAF)-->
adheres to M cells, causing rearrangement of actin and effacement of the brush border microvilli--> 2nd
mcc of infant diarrhea

E"I"EC = Entero"invasive"--> Invades large bowel--> actin “jet trails”--> Watery diarrhea + PMNs + fever +
abdominal pain

E"H"EC = Entero"hemorrhagic"--> Verotoxin--> O157:H7--> Hemorrhagic colitis , hemolytic uremic

syndrome --> No fever

E"H"EC = Enterohemorrhagic --> Plasmid-associated verotoxins = Shiga-like toxin--> Both toxins inhibit
protein synthesis by nicking 60S ribosome

Question--> low fever + New valvular regurgitation + Gram-positive, catalase-negative cocci--> Subacute
endocarditis due to low grade fever ( acute= high fever= Stap A.) due to Strep Gallolyticus (Bovis)-->
Undiagnosed Colon Cancer

Kleibsiella P.--> Endogenous--> Large and thick capsule--> UTI and Aspiration pneumonia in alcoholics.
KPC--> Kleibsiella pneumonia carbapenemase--> resistant to carbapenenes

K. Granulomatis--> bainless Beefy red ulcers--> Donovanoiss

K. Granulomatosis--> intracelullar--> Likes plasma cells and macrophages

Shigella--> Gram -, non lactose fermenter, no flagella.

Yersinia Pestis--> facultative intracelllular--> Flea bite--> go to lymph nodes --> Bubonic plague-->
progresses to gangrene-->Black Plague

Y. Enterocolitica--> Enterocolitis--> Pseudoappendicitis in Older kids/young adults (also by Yersinia

pseudotuberculosis).

Proteus Mirabilis--> Endogenous-> Motile--> Stones due to Urease

Salmonella--> Produce H2S (hydrogen sulfide/HE hektoen enteric ), motile.

S. Typhi--> Human reservoir--> Ingest from someone else--> uses M cells to go in--> Monocyte--> Blood-->
Septic: fever + consitpation + rose spots on torso--> When bug goes to GI (week 4)--> diarrhea (pea
green)--> lethal

S. Enterica (non typhi)--> humans, chickens and turtles are reservoirs--> trasnmitted by raw chicken,
turtles, snakes

Non Typhi Salmonella--> Endotoxin--> invades GI--> Immnube response--> Inflammation--> Increase Pgs-->
increases cAMP--> Loose diarrhea. Can also lead to : enterocolitis, septicemia, and osteomyelitis (sickle
cell disease).