Micro Master

PRION VIRUS BACTERIA

SIZE = SIZE = .3-2 u

Prokaryote
DNA & RNA
Organelles not membrane bound
Binary Fission Replication
OXYGEN REQUIREMENTS

1: Obligate aerobes need oxygen because they cannot ferment or respire

anaerobically. They gather at the top of the tube where the oxygen
concentration is highest.
Tuberculosis Mycobacterium
Pseudomonas

2: Obligate anaerobes (ABCs) are poisoned by oxygen, so they gather at

the bottom of the tube where the oxygen concentration is lowest.
A ntinomyces
B acteroides
C lostridium

3: Facultative anaerobes can grow with or without oxygen because they

can metabolise energy aerobically or anaerobically. They gather mostly at
the top because aerobic respiration generates more ATP than either
fermentation or anaerobic respiration.
Enterobacteriaceae

4: Microaerophiles need oxygen because they cannot ferment or respire

anaerobically. However, they are poisoned by high concentrations of
oxygen. They gather in the upper part of the test tube but not the very
top.
Helicobacter
Campylobacter

5: Aerotolerant organisms do not require oxygen as they metabolise

energy anaerobically. Unlike obligate anaerobes however, they are not
poisoned by oxygen. They can be found evenly spread throughout the
test tube.

Anaerobic bacteria can be identified by growing them in test tubes of

thioglycollate broth:

TERMINOLOGY

OXIDASE +
CATALASE +

Normal Flora
Subtopic 1

BLOOD NONE

SKIN Staph Epidermidis

NOSE Staph Epidermidis, but colonized by Staph Aureus

OROPHARYNX Viridans Steptococci

DENTAL PLAQUE Strep Mutans

Infants: Bifidobacterium
COLON
Adults: Bacteroides Fragilis > E. Coli

VAGINA Lactobacillus, but colonized by E.Coli & B Group Strep

Staining/Culturing/Media

Staining/Culturing/Media

Gram Staining Culturing Media

MacConkey = Gram Negative

Blood Agar = a,b,g Hemolysis = Strep
CRYSTAL VIOLET
-Primary stain BCYE = Legionella
EMB = E.Coli
-Stains Gram ( + ) & ( - )
GRAMS IODINE Chocolate Agar = Nisseria, Homophaelus
TCBS
-Mordant
-Forms Crystal violet iodine complexes Cholesterol, Purine & Pyrimidine = Mycoplasm
Cysteine = Francisella, Brucella, Legionella, Pasteurella
DECOLORIZER
-Acetone + Methanol X(heme) & V(NAD) = Haemophilus
-Removes Crystal violet iodine complex from thin peptidoglycan layers
-Dissolves outer layer of Gram negative org
GRAM SAFRANINE
-Counter stain
-Red colored
-Stains thin walled GRAM NEG
-Pus cells cytoplasm & lobes of nuclie also stain red

A patient Treatment with antimicrobial agents may cause gram-positive

bacteria to appear gram-negative.

Weakly Gram Staining

spirochetes,
rickettsias,
chlamydiae,
mycoplasmas,
mycobacteria
Coxiella and
Legionella.
Most are too thin in diameter for the light microscope

GRAM STAINING
Col

reagent GRAM ( - ) GRAM ( + )

CRYSTAL VIOLET PURPLE PURPLE

GRAMS IODINE PURPLE PURPLE

DECOLORIZER COLORLESS PURPLE

*PINK *PURPLE
SAFRANINE

GRAM POSITIVE VS GRAM NEGATIVE

GRAM POSITIVE VS GRAM NEGATIVE

GRAM POSITIVE GRAM NEGATIVE EXOTOXIN VS ENDOTOXIN
CELL WALL
*Lipopolysaccharide (endotoxin / LPS) – LIPID A EXOTOXINS are toxic proteins produced by bacteria and released outside.
Most are motile by peritrichous flagella --H antigens. Gram (+ / - )
Capsule – K antigen ( Vi for Salmonella). B component Binds N-acetylglucosamine and N-acetylmuramic acid are |
Cell envelope (wall) A component is Active (toxic) polymerized to form the peptidoglycan backbone of the cell wall.
various outer membrane proteins. Enterotoxins
Pili - various antigen types, some encoded by plasmids Neurotoxins GRAM POSITIVE
Cytotoxins THICK Peptidoglycan cell wall
Cytolysins Teichoic Acid

ENDOTOXINS are bacterial toxins consisting of lipids that are part of the GRAM NEGATIVE
cell wall; released when Bacteria is lysed; THIN Peptidoglycan Cell Wall
Gram ( - ) = LIPID A of Lipopolysaccharide Lipopolysaccharide Toxin
+ Listeria Monocytogenes (gram (+) ) -Lipid A
--> Fever -O Antigen
--> Septic Shock -Core
Periplasmic Space - B-Lactamase
Porin

GRAM (+)
Staphylococcus
GRAM (+)
CATALASE (+) (H2O2)
FACULTATIVE ANAEROBE

Staphylococcus
GRAM (+)
CATALASE (+)
FACULTATIVE ANAEROBE
-Grapelike Clusters
-Non-Motile
Staph Genus
-Oxidase (-)
-Fermentation (+/-)
-Slime Capsule Coagulase (+) Coagulase (-)
-0.5-1.5µm in diameter
-Non spore-forming

Family: Staphylococcaceae
Staph Aureus Staph Epidermis Staph Saprophyticus
Genus: Micrococcus and Staphylococcus

-Small YELLOW colonies in media - Novobiocin Sensitive - Novobiocin Resistant

IMPORTANT:
-B Hemolytic like Streptococcus
*S. Aureus
-Fermentation (+) CLINCAL MANIFESTATION
S. Epidermis - Part of skin Flora
- Colonizes mucosa (25% of adults are carriers). CLINICAL MANIFESTATION
S. Saprophyticus INFLAMMATORY DISEASE
- Transmitted by direct contact and fomites
S. pseudointermedius Produces a polysaccharide slime
- Food Poisoning common for Custard, potato salad, pastries, canned meats CLINCAL MANIFESTATION
M. Luteus -Abscesses and mastitis (also known as glycocalyx or
- Contains Superantigen (aureus & pyogenes) SKIN INFECTIONS
-Surgical Wound Infections extracellular matrix) made by - 2nd most common cause of UTI
UTI
Staph. epidermidis which serves - in newly sexually active females
PREDISPOSING FACTORS INFECTIVE Infective endocarditis (acute)
*Surgical Wounds as a ‘glue,’’ creating biofilms that
ENDOCARDITIS --> Fever, malaise, Leukocytosis, Heart Murmur Saprophyticus gives ya
Foreign Bodies (tampons) are difficult to clear without
'honeymoon cystitis'
-Acute removal of the device.

VIRULENCE FACTORS -Productive

PNEUMONIA TREATMENT
-Relatively heat resistant -Empyema
-Resistant to high concentrations of salt -Nosocomial Pneumonia Vancomycin
-Can survive long periods on dry inanimate objects
-Metaphysis most common area of Staph invasion due to hair-pin loop;
OSTEOMYELITIS
*PROTEIN A - Prevents complement fixation of IgG --> Inhibits Phagocytosis -Most common overall cause of osteomyelitis CLINCAL MANIFESTATION
SLIME LAYER - Prevents immediate immune response;
TOXIC DISEASE
LIPOTEICHOIC ACIDS - When cell is lysed play a role in Septic Shock
CATALASE ( + ) - prevents phagocytic killing by neutralizing peroxides; Food poisoning WOUND opportunist requiring entry
MRSA contains ALTERED PENICILLIN BINDING PROTEINS - changing interaction with binding *(Caused by PRE-FORMED ENTEROTOXINS A-E in food) INFECTIONS (surgery, medical devices)
proteins; RAPID ONSET ACUTE - 2-6 Hours
FOOD POISONING Survives in salty foods; SUBACUTE BACTERIAL
in artificial valve 2 months after surgery
TOXINS *Vomiting --> Area Postrema ENDOCARDITIS
ENTEROTOXINS A-E - pre-formed in food which causes Food Poisoning; Diahrrea --> Loss of brush border cells
surgical oppurtunist
Heat and salt stable
-Rare but life-threatening; medical devices

EXFOLIATIVE TOXINS A & B (ETA,ETB) = SSSS -Sharp drop in blood pressure that can lead to organ hypoxia;
--> Cadherin Desmoglein 1 in Stratum Granulosum -Malaise, confusion, Diahrrea, Fever, Seizures,
-Widespread sunburn like rash particulary on the palms and soles;
TSST-1 'SUPERANTIGEN' = Toxic Shock Syndrome -mc in women caused by Staph Auresu infected TAMPONS
TOXIC SHOCK SYNDROME
- Prevents dettachment of T-Cell TCR to MHCII Complex -Can occur in men and women due to open wound exposure to Staph;
--> increase cytokine release -Mostly <19yrs age;
-Can happen post childbirth;
Cytolytic Toxins
Alpha = β hemolysis Enterotoxin Type B or TSST-1
Beta = sphingomyelinase
-Staphylococcal Scalded Skin Syndrome (in newborns & infants) -
Delta = attacks RBCs, macrophages, lympphocytes, neutrophils, platelets
Gamma = hemolytic Spectrum of Superficial Epidermal blisterstering due to Exfoliative Toxins
(exfolatins ETA & ETB);
Leukocidin = RBC hemolysis
Leukotoxin = WBC destruction Spares Mucus membranes
STAPHYLOCOCCAL *Not to be confused with Toxic Epidermal Necrosis (TEN) which does NOT
Coagulase = Converts Fibrinogen to Fibrin --> creates a Fibrin clot for reproductive SCALDED SKIN spare mucous membrane, is more deadly, Idiosyncratic, all ages;
SYNDROME
environment --> Heart Tissue;
Hyaluronidase = “spreading factor” of S. aureus -Folliculitis - inflamed puss fillled hair follicles
-Boils (furuncles)
Nuclease = cleaves DNA and RNA in S. aureus
Staphylokinase - fibrinolysin -Carbuncles - sever abscess
-Impetigo - sores around mouth --> coagulase
DNase
FAME (fatty acid modifying enzyme)
Toxic Epidermal Necrosis (TEN):
-Idiosyncratic (mc cuase is SA of drugs)
-Does NOT spare mucous membrane,
TEATMENT
-More deadly,
S. Aureus
-All ages;
Methicillin (B-Lactam)
- >30% of body affected
MRSA - impt in nosocomial
Vancomycin (expensive & toxic)
SJS (Steven-Johnson Syndrome)
VRSA
-same as above except <10% affected
Dalfopristine and quinupristin- Block 50S ribosomes
-Rash --> Bullae
Linezolid - Blocks Initiation of protein synthesis
-Productive Cough w/ Purulent Sputum;
Ceftobiprole (5th Gen Cephalosporin) - Cell wall inhibitor (B-Lactam)
-Arthralgia;
Trimethoprim/sulfamethoxazole -
-target appearance
Blocks de novo folate synthesis --> Inhibits DNA synthesis;
ID: Mannitol agar -Fever
-Malaise
OTHER -Excessive Crying
-Poor Suckling
-Septic Shock upton bacterial destruction (Septic / Endotoxic Shock)

Streptococcus
GRAM (+)
CATALASE (-)
FACULTATIVE ANAEROBE

Streptococcus
GRAM (+)
CATALASE (-)
FACULTATIVE ANAEROBE
-CHAINS (sometimes pairs) IDENTIFICATION
-Oxidase (-)
Hemolytic Pattern + 1 Additional ID
Habitat primarily in the Respiratory Tract and secondarily
the GI and Urogenital tracts;
HEMOLYTIC PA TTERN Lancef ield Groups
TREATMENT
Penicillin Group
'Sheep Blood A gar' -Cell Wall Carbohydrate A ntigen
-B-Lactam 'P.V.A .P.E'
-Cell Wall inhibitor
Groupable Non-Groupable
a-HEMOLYTIC B-HEMOLYTIC y-HEMOLYTIC
A B D -S. Pneumoniae
- Partial Hemolysis -Complete Hemolysis -NO Hemolysis -Viridans Streptococci
- Green Color Tx = Trimethoprim Sulf amethazole (SXT) S. Pyogenes S. Agalactiae Enterococci (S.Mutans)
S. Bovis - gut, colon cancer
Enterococcis Bovis in the Blood, Cancer in the Colon

Strep Pneumoniae Viridans S. Agalacitae S. Pyogenes

- grows in 6.5% Saline &
Bile
- NOT Bile soluble - Bacitracin Resistant -Bacitracin Sensitive
- Bile Soluble (test)
- Optochin Resistant
- Optochin Sensitive
- NO Capsule - Normal colonic Flora
- Colonizes Vagina - Colonizes skin and upper respiratory tract mucosa.
- PENICILLIN G RESISTANT*
top 3 most common cause of Bacterial Meningitis - mc common - Faculatative anerobe - Survives on hard surfaces; - Vancomycin Resistant Enterococci --> nosocomial
- Dental procedures cause Viridans to enter the blood - Mainly affects babies (partum transmission) - spread by fomites, respiratory droplets, and direct contact.
- No virulence without capsule. - Colon malignancies increase RISK os Streptococcus Bovis
- Opportunist --> adhere to fibrin-platelet aggregates; in the absence of specific antibody, - Requires colonization & skin trauma ' Bovis in the Blood, Cancer in the Colon '
opsonization, recruitment, & phagocytosis do not proceed; - Contains Superantigen (aureus & pyogenes)
- “rusty” sputum
- Oropharyngeal mucosal colonist/opportunist. - Risk Factors: *acquired by Cystoscopy
Prematurity VIRULENCE FACTORS
- Transmission by respiratory droplets
- Lancet-Shaped Diplococci
Strep Mutans Strep Sanguins Membrane rupture STRUCTURAL ID: Negative Nitrite urine test on dipstick
Maternal S. Agalacitae carriage M PROTEIN - Antiphagocytic adhesin; Responsible for Post Strep Acute
- sepsis in sickle cell disease and splenectomy. (compared to Gram - Enterobacter species producing positive)
F PROTEIN - adherence
Normal Oropharynx flora involved in: in damaged heart valves, can cause: ID: HYALURONIC ACID - inhibits phagocytic uptake;
**Most common cause of: TREATMENT
DENTAL CARIES SUBACUTE BACTERIAL ENDOCARDITIS - screen pregnant women at 35-37 weeks LIPOTEICHOIC ACID - Cytotoxic
MENINGITIS (in adults) Vancomycin
if culture is +, treat with: FIMBRAE: attachment and adherence
PNEUMONIA (in adults)
OTITIS MEDIA (in children) INTRAPARTUM AMPICILLIN / PENICILLIN
Sanguinis = blood. Think, “there is lots of
CLINICAL MANIFESTATION PATHOGENIC
SINUSITIS blood in the heart” (endocarditis). S. sanguinis CLINICAL MANIFESTATION
*STREPTOLYSIN O - Hemolytic & Cytolytic, beta-hemolysin.
makes dextrans, which bind to fibrin-platelet
CLINICAL MANIFESTATIONS STREPTOLYSIN S - beta-hemolysin
VIRULENCE FACTORS aggregates on damaged heart valves.
*POLYSACHARIDE CAPSULE - reduces effectiveness of complement & antibodies; TRANSIENT *PYROGENIC ERYTHROGENIC TOXINS A & B -
Viridans group strep live in the mouth because UTI
BACTEREMIA -promotes pro-inflammatory cytokines IL-1, IL-2, IFN-γ, and TNF-α
--> decreases phagocytic uptake they are resistant of-the-chin (op-to-chin
IgA PROTEASE - degrade IgA, allowing mucosal colonization; --> SHOCK
resistant). PNEUMONIA in babies BILIARY TRACT
DNASES & HYALURONIDASE - 'spreading factor' of Necrotizing Fasciculitis
INFECTIONS
MENINGITIS in babies STREPTOKINASE A and B - lyse clots
plasminogen --> plasmin SUBACUTE
ID: Capsules are typed by the quellung reaction (apparent capsular swelling when
GBS SEPSIS in babies
mixed with the specific matching antibody). ENDOCARDITIS
| SEQUELAE
GROUP b FOR bABIES Glomerular Nephritis & Rheumatic Heart Disease
TREATMENT: ' 40% BILE '
Class I M proteins extend through the cell wall;
Penicillin is first line
--> Rheumatic heart disease
Erythromycin or Vancomycin in penicillin allergy or resistance
Class II M proteins are not exposed on the surface.
--> glomerulonephritis.
PREVENTION
A. 7-valent polysaccharide-protein conjugate vaccine (T-cell dependent) for infants.
ID Pharyngitis: rapid antigen detection RADT test with culture;
B. A 23-valent polysaccharide vaccine for patients 65 years or older, asplenics,
All other infections: culture.
diabetics, Human immunodeficiency virus (HIV) positive, COPD, and so forth.
*ASO (Antibody to Streptolysin O) is a marker of recent mucosal infections and
or rheumatic heart disease which is culture negative.
Encapsulated Virulent Organisms
CLINICAL MANIFESTATION
TREATMENT
*Some - Strep Pneumoniae Penicillin for Pharyngitis
Killers - Klebsiella Pneumoniae
most common cause of: Have - Homophillus Influenzae
Pretty - Pseudomonas Originosa CLINICAL MANIFESTATION
in immunocompromised
Nice - Nisseria Meningitis
MENINGITIS &
Capsules - Cryptococcus Neoformins
adults
PYOGENIC
in immunocompromised
PNEUMONIA ' quelling test '
' rusty sputum ' Sorethroat, Headache, Malaise;
PHARYNGITIS Purulent
OTITIS *mc cause of bacterial pharyngitis
in children
MEDIA (in children)
IMPETIGO & Subcutaneous Nodules
SINUSITIS CELLULITIS - highly communicable in infants

TOXIGENIC

Fever
Rash
SHOCK Shock
Necrotizing Fascilitis = Skin & subcutaneous tissue death
> 50% mortality

FLESH EATING
Necrotizing Fascilitis = Skin & subcutaneous tissue death
PROTERIES

Complication of when strain is Lysogenized

SCARLET FEVER
--> rash on chest which spreads to extremeties;

IMMUNOLOGIC SEQUELAE

Erythrogenic Toxins;
arthritis, carditis, chorea, redness

Type II Hypersensitivty reaction

RHEUMATIC HEART DISEASE --> our anti bodies attack heart valves due to
structural homology of antigenic determinants
and the Heart Tissue;

*causes Heart Murmur

Streptolysins S & O
POSTSTREPTOCOCCAL
GLOMERULONEPHRITIS Type III Hypersensitivity
(M-Protein IgM complex is causing the damage);

*Syndenham Chorea
OTHER
*Joint Pain

SEPTICEMIA

'licks the joints and bites the heart'

Bacilli / Rods
GRAM (+)

Bacilli / Rods
GRAM (+)
IDENTIFICATION

ENDOSPORE FORMERS NON-ENDOSPORE FORMING IRREGULAR SHAPES

BACILLUS CLOSTRIDIUM Listeria Monocytogenes Erysipelothrix Cornyebacterium Mycobacterium fillamentous BRANCHING RODS
Aerobe Anaerobe Diphteria - acid fast
- No Capsule - Aerobic
- **TUMBLING MOTILITY
-20% death rate
- Animals and rotting organic material;
- Traumatic implantation.
aerobe *V* - obligate aerobe Nocardia AntiNOmyces
-Facultative Anaerobe -Anaerobic
-Catalase (-)
-Motile Rods
-Catalase (-)
-Chain Forming
- Animal Feces, Rotting Vegetation, and occasionally in
Soft Cheeses, deli meats, and cabbage CUTANEOUS ERYSIPELOID primarily in fishmongers, butchers, and
-ACID FAST -NO ACID FAST
- Children NO CAPSULE
-Mostly saprobic (Scavenger which feeds on dead tissue)
-Source of antibiotics Ovoid subterminal spores (OST) used for ???
--> Transmitted by contaminated food
- Oppurtunist, requiring compromised immune system
veterinarians. - Club-shaped, Chinese character-like clusters. - No flagella -aerobic -anaerobic
- Non-Motile - Grow Slowly
-SOIL - As soon as Clostridium infection is suspected, Antitoxins must be Elderly & Newborns --> Diphtheroids - Poor Gram-staining
-Can survive for decades in dry environment; administered; -FACULTATIVE INTRACELLULAR pathogen; they move from cell to cell by
- Respiratory Droplet spread - Ubiquitous - Branching, NonMotile
actin polymerization, which propels the bacterium directly into an - Part of normal GI Flora VIRULENCE FACTORS - SOIL & WATER - Normal Oral Flora
adjoining cell without exposure to extracellular milieu.
WAXY CELL SURFACE - prevents destruction by lysosomes and - Tropical and subtropical regions - most misdiagnosed disease since it looks so close to fungus;
Bacillus Anthracis Bacillus Cereus Lactobacillus Clostridium Perfringens Clostridium Dificil Clostridium Tetani****** Clostridium Botulinum -Avoids humoral immune system VIRULENCE FACTORS
DIPHTHEROTOXIN - EXOTOXIN
macrophages
(1) Porin proteins allow aqueous transport;
Mexico, Central and South America,Africa and India
-Oppurtunist requiring immunocompromised
- Found following trauma and invade necrotic tissue?

VIRULENCE FACTORS 2 part toxin – (2) Resists drying 3 clinical presentations

-*Only Gram (+) Bacteria that produces ENDOTOXIN*
VIRULENCE FACTORS – FOOD POISONING 1-6 HOURS AFTER INGESTION Norma Vaginal bacteria which -Spores introduced by severe trauma; - Major cause of nosocomial Diarrhea TETANUS via Tetanospasm -SOIL & DUST part B binds and induces endocytosis; (3) Allows the survival of nontuberculous mycobacteria in soil. NOCARDIA ASTEROIDES 1.chronicity, progress across tissue boundaries, mass like
-*Resistant to cold, heat, salt, pH extremes and bile; part A inactivates Elongation factor E2 'Tuberculosis-Like' but not contagious 2. develop sinus tract, resolve and recur
Survives well in Heat --> NAUSEA & VOMITTING produce Acid and neutralize 1-7 Day incubation - 3-5 cays after clindamycin treatment; -Heat resistant
-Ability to replicate in the cytoplasm of cells after inducing phagocytosis;
POLY-D GLUTAMIC ACID CAPSULE - protects from phagocytosis by host or Fungi; -Only affects damaged/traumatized tissue; -Normal GI Flora --> *ARRESTS PROTEIN SYNTHESIS; Due to their Aerobic needs, Granuloma is formed trapping the bacteria and 3. refractory/relapsing after a short course therapy
neutrophils --> WATERY DIAHRREA -->Sporulation VIRULENCE FACTORS - tranmission throughn skin VIRULENCE FACTORS ID: eliminating oxygen supply; NOCARDIA BRASILIENSIS

*Only Bacteria with D-GLUTAMATE capsule;
ANTHRAX TOXIN
3 protein components:
Protective antigen (PA),
*Edema factor (EF) Increases cAMP
Lethal factor (LF) cleaves MAP
PA plus LF produces lethal toxin -> Tissue Death
PA plus EF produces edema toxin -> Edema
-Large, Block-shaped rods;
TOXIN A, enterotoxin, binds to the brush border of the gut. Tetanus Toxin acts on Synaptosomes Pre-Formed Heat Labile Botulinum Toxin (absorbed from GI) Loffler's Medium Subcutaneous Skin lesions ID: Fluorescent Microscopy
ID: Rapid diagnostic tests using ELISA available Pseudomembrane and swelling of Pharynx ID: Ziehl Neelsen Stain
-Found in nature, notably in rice. VIRULENCE FACTORS TOXIN B, cytotoxin, causes cytoskeletal disruption via actin --> Blocks release of inhibitory neurotransmitters, GABA & glycine from -->inhibits Acetylcholine release at NMJ;
It germinates and produces Pre-Formed toxin in LECITHINASE / ALFA TOXIN depolymerization Renshaw cells in spinal cord. Conditions, history ID: TB Media
TREATMENT
poorly refrigerated cooked rice (especially fried). -- > breaks down Phospholipids --> pseudomembranous colitis Spores (babies)
Ampicillin and trimethoprimsulfamethoxazole
Serological assay
A. Israelii
--> Myonecrosis --> diarrhea. Causes
Spastic Paralysis TREATMENT
Prevention – pasteurization and cooking TREATMENT
Mycobacterium Tuberculosis Mycobacterium Leprae Mycobacterium Kansasii TREATMENT
Sulfonamides
Kinase 'that rice gave me some CEREUS DIAHRREA ID in blood or egg-yolk agar - Often 2° to antibiotic use, especially clindamycin or ampicillin. Trismus (lockjaw), Trivalent equine ANTITOXIN Antitoxin
- Does not respect borders,, grows contiguously in tissue;
Risus sardonicus (raised eyebrows and open grin) Penicillin or erythromycin
CLINCAL MANIFESTATIONS - Estimated 1/3rd of world population is carrying; - Transmission by contaminated water; These opportunists cause respiratory diseases in PELVIC DISEASE assd with IUCD (copper T)
TREATMENT TREATMENT Prevented by toxoid vaccine series and boosters
- Only 5% infected people develop clinical disease; Hansen’s bacillus/Hansen’s Disease patients with low CD4+ counts such as acquired immunodeficiency
Removal of dead tissue (*Priority) metronidazole or oral vancomycin. - tetanus vaccine. CLINICAL MANIFESTATIONS - Untreated, the disease progresses slowly; LUMPY JAW =
Strict pathogen – has not been grown on artificial media or tissue culture syndrome (AIDS) patients or patients on chemotherapy. They are
Penicillin For recurrent cases, consider repeating priornregimen, fidaxomicin, or - Majority of TB cases contained in LUNG APEX *Slowest growing of all species not contagious from person to person and are acquired from showers or - Very slow-growing draining abscess containing Puss
CLINICAL MANIFESTATIONS fecal microbiota transplant. Treatment In children, neonates, & immune compromised
MENINGITIS - Slow growing, gradually symptoms get worse Multiplies within host cells in large packets called globi dust. - mc Angle of Jaw
antitoxin +/− vaccine booster, - CSF Pleocytosis
Botulinism from 'Honey' - Untreated, 60% mortality rate Causes leprosy, a chronic disease that begins in the skin and mucous - Absent of puss --> Neoplasm
- ID by one or both toxins in stool by PCR. Diazepam (for muscle spasms) - transmitted by airborne respiratory droplets;
FLOPPY BABY SYNDROME --> ingested SPORES germinate in the GI & produce Botulinum GASTROENTERITIS membranes and progresses into nerves
Inhalation of spores (6mo-2yr) --> Toxic infection -Extremely rare CLINICAL MANIFESTATIONS PNEUMONIA-LIKE SYMPTOMS
--> Flu-like symptoms Good Prognosis SEPTECEMIA IN VIRULENCE FACTORS
Rapid progression to CLINICAL MANIFESTATIONS PREGNANT WOMEN CORD FACTOR - Mycolic acids in the cell wall, CAUSE OF DISEASE TREATMENT
PULMONARY Fever, Ingestion of Pre-Formed Tpxins thick, ropelike 'serpentine' growth of Tuberculosis
'Dairy Products' RESIRATORY
ANTHRAX Pulmonary Hemorrhage FOOD POISONING Respiratory paralysis Mycobacterium without cord factor will NOT cause disease Subtopic 1 'Sulfur Granules' buzzword
'entire family gets deathy ill' CLINICAL MANIFESTAITON DISEASE
in ADULTS Cranial nerve Palsies 'Rocket Tails'
Hemorrhagic Lymphadenitis Normal GI Flora activated by Antibiotic
PSEUDOMEMBRANOUS Death 'Tumbling'
--> RD & Cyanosis -->Secretes an enterotoxin & Cytotoxin SULFATIDES - Inhibits Phagolysosome fusion; 'Chronic Pulmonary Disease oppurtunist'
COLITIS Auntie Lump-Jaw was sulffuring with her IUD
Widening of mediastinum -->Major cause of nosocomial Diarrhea PERIPHERAL
CLINICAL MANIFESTATIONS NEURITIS
CUTANEOUS Painless papule surrounded by vesicles GASTROENTERITIS Clinical tuberculosis divided into:
' Sulfur granules '
ANTHRAX with black eschar;
Primary TB = LUNG
*more common in animals, in
2 stages of disease: - Min Infectious dose is 10 cells;
questions look for exposure to farm - Phagocytosed by alveolar macrophages and multiply intracellularly;
1. Local Infection –
animals
CLINICAL MANIFESTATIONS - Upper respiratory tract Infection - After 3-4 weeks immune system attacks, forming tubercles containing Caseating Granuloma;
- sore throat,
- nausea, vomiting, Secondary TB = REACTIVATION
- swollen lymph nodes; - If patient doesn’t recover from primary tuberculosis, reactivation of bacilli can occur.
CELLULITIS
DIPHTHERIA - Pseudomembrane Formation (can cause asphyxiation)
FASCIITIS beta toxin-producing C.Perfringens Type C
Dessimated TB = Ubiqutuous
MYONECROSIS -fermentation of muscle glycogen --> GAS
2. Diptherotoxin production and toxemia target organs, primarily heart and - During secondary TB, bacilli disseminate to regional lymph nodes, kidneys, long bones, genital tract,
GAS GANGRENE
nerves; brain, and meninges.

alfa toxin-producing C.Perfringens Type A These complications are grave.

Tox+ C. diphtheriae;
- Acute Pain
FOOD POISONING Most cases occur in non-immunized children living in Inadequate nutrition, Debilitation of the Immune System, Poor access to medical care, Lung Damage,
- Diarrhea
crowded, unsanitary conditions. and Genetics are all predisposing factors;
- quick recovery
Bacillus very resistant;
Corynebacterium jejenum causes infections via
crepitus = crackling noises of skin INFECTIONS
catheters and foreign bodies in immunocompromised hosts.
ID:
stormy fermentation 3 Consecutive oral samples of sputum
' children, pharyngitis, gray pseudomembrane '
Lowenstein Jensen Medium
' arrests protein synthesis EF2 ' X rays
Direct identification of acid-fast bacilli in specimen
Cultural isolation and biochemical testing

TREATMENT
6-24 months of at least 2 drugs from a list of 11
One pill regimen called Rifater (*isoniazid, *rifampin, pyrazinamide)
Vaccine based on attenuated bacilli Calmet-Guerin strain of M. bovis used in other countries
Side effect of Isoniazid is neuropathy;
In Multi Drug Resistant TB, must be resistance to atlease isonazide or Rifampin;

CLINICAL MANIFESTATIONS

- Violent coughing
- Greenish or bloody sputum,
- Fever,
- Night Sweats
TUBERCLES
- Anorexia
GRANULOMA
- Fatigue
-->CASEOUS NECROSIS

granulomas consisting of a central core containing bacilli surrounded by

WBCs;
--> Form Caseous lesion healed by calcification;

GRAM (-)
GRAM NEGATIVE

- Most are motile by peritrichous flagella --H antigens;

- Capsule – K antigen (Vi for Salmonella).
- Thin peptidoglycan layer
- Pili - various antigen types, some encoded by plasmids

ENDOTOXIN (LIPID A OF LPS) – O antigen;

- LPS is composed of lipid A, core polysaccharide, and O-specific polysaccharide.
- Lipid A = Responsible for Endotoxins
-->Activation of complement, cytokine release, fever, impaired organ perfusion
& acidosis, hypotension, SHOCK, death;

Reference laboratory antigens

O (lipOpOlysacharide)
H (FLAGELLAH)
K (KAPSULE)

Comma Shaped
oxidase ( + )

Comma Shaped
oxidase ( + )
-Enterics-

Camylobacter Jejuni Helicobacter Pylori Vibrio Cholerae

42* C urease ( + ) A lkaline

Medium
*most common cause of INFLAMMATORY DIARRHEA in developed countries; - Microaerophilic
*most common cause of Food Borne Illness in the United States; - Curved / Spiral
- Facultative Anaerobe
- Microaerophilic & *Thermophilic - Polar Flagella
- Polar Flagella
(grows in 42* C) rapid corkscrew movement
- Asian countrties
- Helical 'Seagull-Winged' - Orally transmitted
- Transmission is fecal-oral
- Motile w/ Flagella - 30% of population affected
- High Mortality
'rapid darting' uncommon in children
- Found in water
- Ingestion of contaminated *Poultry, Unpasteuried Milk, unsanitary water; - The immune system appears not to routinely eliminate H. pylori.
- Highly sensitive to acid --> (*high infectious dose necessary)
- <1 yrs old & 15-24yrs
--> Proton pump inhibitors will increase chances of acquiring pathogen;
- 2-21 day duration Colonizes gastric mucosa in duodenum or esophagus;
- H. Pylori's Mucus layer coat causes Chronic Inflammation;
VIRULENCE FACTORS
VIRULENCE FACTORS - Non – invasive but recruits and activates inflammatory cells*
CHOLERA TOXIN - B Frag. Binds to epithelial cells of small intestine brush border microvilli;
CYTOLETHAL DISTENDING TOXIN (CDT) = nuclease damages DNA & arrests division; Releases Urease which produces ammonia
A Fragment: Increases cAMP by turning on Stimulatory G Protein;
ADHESINS --> Neutralizes stomach acidity, favoring bacterial multiplication.
--> disrupts electrolyte & fluid balance
GBS --> Ammonia may also cause injury and potentiates the effects of a cytotoxin
--> Hypersecretion of Bicarbonate & Chloride;
produced by H. pylori.
CAMYLOBACTER JEJUNI - 80% --> Acute Infection
VIBRIO CHOLERAE
CAMYLOBACTER COLI
Explosive diarrhea
CAMYLOBACTER FETUS VIRULENCE FACTORS
--> 15-20 L/ day fluid loss
UREASE production - neutralizes HCL
--> Metabolic Acidosis & Hypovolemic shock
MUCINASE - protects H. Pylori in Mucosal cells
TREATMENT VACUOLATING CYTOTOXIN - Epithelial Cell Damage
VIBRIO PARAHAEMOLYTICUS
> 95% of infections clear up on their own. CATALASE ( + ) - prevents phagocytic killing by neutralizing peroxides
Sharts (mild diarrhea)
Fluids
Antidiarrheal medications; ID: (ELISA)
ID: TCBS (Thiosulfate Citrate Bile Salts Sucrose...Alkaline medium)
If severe, - deteciton of antigen in stool
Macrolides (Erythromycin & Azithromycin) Urease test, Histology, Urea breath test (radioactive carbon-labeled urea swallowed &
TREATMENT
Urease activity detected)
Prompt replacement of fluids and electrolytes;
3. Lab ID: Diagnosed by the finding of numerous darting microorganisms in the stool along with blood - Detection of H Pylori antigen in stool
and excess neutrophils (indicating invasion with inflammation). Proper therapy reduces the fatality rate from 60% to 1%.
Tetracycline should be given to prevent the patient from infecting others;
TREATMENT if antibiotics not given, patient will recover but will shed organisms for as long as 1 year.

CLINICAL MANIFESTATION Combination of a proton pump inhibitor (omeprazole) +

Amoxicillin or Clarithromycin;
CLINICAL MANIFESTATION

**most common cause in Developed Countries

- Watery Diarrhea that can contain Pus and Blood CLINICAL MANIFESTATION
Abrubt onset of:
- Fever
Intense vomitting
- Abdominal pain
INFLAMMATORY CHOLERA Voluminous 'rice water' Diarrhea
- Myalgia 70% of gastric ulcers are colonized by H. Pylori
DIARRHEA Death in 2-3 days (if no treatment)
Vibrio Cholerae
-Ulceration & Inflammatory lesions to the Jejenum, Ileum & Colon GASTRITIS, Epigastric pain (sometimes with nausea & vomiting)
- invasion of M-Cell (Peyers patches) DUODENAL & Anorexia
'Traveler's Diarrhea' PEPTIC ULCERS Belching GASTROENTERITIS
Vibrio Parahaemolyticus
Peptic ulcers are characterized by burning epigastric pain lessened by
Asymptomatic carriers primarily people who are exposed to Camylobacter eating;
ASYMPTOMATIC ' rice water diarrhea'
chronically;
Most gastric adenocarcinomas and lymphomas are concurrent ' sushi '
post viral sequelae GASTRIC
with or preceded by an infection with H. pylori
ADENOCARCINOMA
'Acute, rapid Symettrical ascending flacid paralysis (demyelinating)'
GUILLAIN-BARRE
-Post viral infection MALT LYMPHOMA
SYNDROME (30%)
--> ICU!* (eventual respiratory muscle paralysis)
low incidence
- due to Immune response to O ANTIGEN cross-reacting with peripheral
potential sequela
nerve Gangliosides;

SEPTICEMIA

' contact with farm animals '

' CAMPylobacter --> HOT CAMPFIRE '

GRAM (-)
RODS

RODS
- Enterics-

Lactose Fermenters NON Lactose Fermenters

'Pink on MacConkey' 'Clear on MacConkey'

Oxidase ( - ) Oxidase ( + )
FAST SLOW

Shigella Salmonella Yersinia Proteus PSEUDOMANAS AERUGENOSA

Klebsiella Escheria Coli Enterobacter Citrobacter Serratia
oxidase ( - ) ENTEROBACTERICIAE Family ENTEROBACTERICIAE Family ENTEROBACTERICIAE Family ENTEROBACTERICIAE Family
- AERobic
ENTEROBACTERICIAE Family
ENTEROBACTERICIAE Family ENTEROBACTERICIAE Family ENTEROBACTERICIAE Family ENTEROBACTERICIAE Family
- Oxidase ( + ) - Oxidase ( + ) - NOT normal Flora --> CONTAMINATION - NOT normal Flora --> CONTAMINATION - NOT normal Flora --> CONTAMINATION - Facultative Anaerobes - Non-Motile
- Facultative Anaerobes - Motile ENTEROBACTERICIAE Family - Facultative Anaerobes - Facultative Anaerobes - Food, Finger, Feces transmission - Food, Finger, Feces transmission - Food, Finger, Feces transmission - Grape-like odor
- Immotile; found in the colon and in water - Majority of Normal GI Flora Proteus - Green blue sputum
- Majority of Normal GI Flora - Oppurtunist pathogen - Facultative Anaerobes - Facultative Anaerobes - Facultative Anaerobes - Facultative Anaerobes Most common isolates: P. mirabilis. - Frequently in found in water (hot tubs)
- Opportunists; cause ventilator-associated pneumonias. - Fecal-Oral Transmission CLINICAL MANIFESTATION - Non-Motile (no flagella) --> No H antigen - Survive in Macrophages - Transmission by pet feces, contaminated milk or pork Cause urinary tract infections and bacteremia. - Oppurtunist
Risk factors for pneumonia: - Facultative anaerobes BRS - Does not produce GAS like salmonella - Motile Produce urease, making the urine of the patients of UT infection with Cystic Fibrosis
alcoholism; - Humans are the only reservoir - TRANSMISSION: VIRULENCE FACTORS Proteus alkaline, promoting stone formation by precipitating Mg and Ca. Diabetics
compromised pulmonary function. VIRULENCE FACTORS a. General characteristics - Fecal-Oral route (ATM) Fecal-Oral route (ATM) in Typhi Burn Victims
-PILLI (1) Gram-negative rods that ferment glucose. --> ' feces food, fingers, flies ' Chicken, meat, eggs, Exotic animal pet in Enteritiditis
VIRULENCE FACTORS -IRON CAPTURING ABILITY (enterochelin) - 3-5 week duration - Very difficult to treat
*CAPSULE - causes the 'jelly' sputum . - Invade M cells of the large intestine / illeum and then move cell to cell - 30% to 50% Mortality rate, depends on preexisitng debilitation;
via host cell actin; creates 'shallow ulceration' usually without CLINICAL MANIFESTATION VIRULENCE FACTORS
Produce copious amounts of their polysaccharide capsule. **ENTEROTOXIGENIC E. COLI --> Profuse Diarrhea (3) Have antigens that may be used in identification: O antigen (cell CLINICAL MANIFESTATION
- 'Traveler's diarrhea' envelope), H antigen bloodstream invasion; VIRULENCE FACTORS EXOTOXIN A - Inactivates EF-2
K. pneumoniae and HEAT LABILE (LT-1) ENTEROTOXINS (flagella), K antigen (capsule), Vi antigen (Salmonella typhi capsule), and Cell --> Cell Encapsulated - avoids Phagocytosis --> Inhibits Protein Synthesis
increases cAMP P antigen Adhesions – both fimbrial and non-fimbrial CAPSULE POLYSACHARIDE SLIME
ACUTE DIARRHEA
K. oxytoca causing intense prolonged hyper secretion of chloride ions. (pili). VIRULENCE FACTORS Enterotoxin - may be involved in gastroenteritis
HEAT STABLE (STa) ENTEROTOXIN - Type III secretion System aka 'injectisome' --> direct delivery of Outer membrane proteins - involved in the ability of Salmonella to survive Right lower abdominal pain due to mesenteric adenitis and/or terminal TREATMENT
PSEUDOAPPENDICITIS
ID: 'currant jelly sputum' Increases cGMP; TREATMENT toxins to eukaryotic host cell. inside macrophages ileitis; Quinolones
Chest X-Ray (similar to TB) short onset; stimulates fluid secretion; poorly immunogenic; Cephalosporin - Highly Acid resistant --> only need few organisms to cause disease; Flagella – help bacteria to move through intestinal mucous Aminoglycosides
inhibits the reabsorption of sodium and chloride SHIGA TOXIN - Inactivates 60S Ribosomes (Shigellos Dysentry only) *after recovery, 3% remain carriers (Gallbladder)
TREATMENT COLONIZATION FACTORS (CFAs) facilitate the attachment of E. coli --> Cell Death --> Bloody Diarrhea
3rd gen Cephalosporin strains to intestinal epithelium. Usually are pili in nature. SALMONELLA ENTERITIDIS CLINICAL MANIFESTATION
MILD infection - diarrhea
**ENTEROHEMORRHAGIC E. COLI --> Dysentry & HUS Classified into four O antigenic groups: SEVERE infection - bloody darrhea
CLINICAL MANIFESTATON - most common strain producing disease in developed countries; - Poultry, eggs, pets, and turtles are common sources
CORNEAL INFECTTION contact lenses
- distinguish from the rest by 'does not ferment sorbitol' SHIGELLA SONNEI causes mild disease; the most common cause of - Only treat if symptoms are sever
SHIGA 'LIKE' TOXIN - Bind & disrupt 28S ribosomes shigellosis in the United States. Chronic Pneumonia in Cystic Fibrosis patients
PNEUMONIA
SALMONELLA TYPHIRIUM *V Diabetes
NOSOCOMIAL in diabetics and alcoholics when aspirated;
ENTEROPATHOGENIC E. COLI --> Diarrhea, Pediatrics SHIGELLA FLEXNERI causes more severe disease; common in the United V1 ANTIGEN = Virulence Antigen
LOBAR PNEUMONIA - Dark red “currant jelly” sputum (blood/mucus). OTITIS EXTERNA in swimmers
- pili are involved in attachment to the intestinal mucosa. States. Causes typhoid fever
- Destruction of surface microvilli - bacteria leave the intestine, multiply within cells of the reticulo-
NOSOCMIAL UTI UTI
-Stimulation of intracellular calcium SHIGELLA BOYDII causes more severe disease; rarely found in the United endothelial system then re-enter the intestine, causing GI symptoms.;
' Pneumonia in Alcoholics ' States. - 10-14 day incubation
in IV drug users
'Currant jelly sputum' ENTEROINVASIVE E. COLI --> Dysentry - may last for several weeks. OSTEOMYELITIS
Diabetics
- invades intestinal mucosa via PILI; SHIGELLA DYSENTRIAE causes the most severe disease; rarely found in - Contaminated Water
4 A’s of KlebsiellA: - Outer membrane proteins are involved in direct penetration, invasion of the United States, unless imported Rapidly progressing necrotic tissue lesion caused by Pseudomonas
*Shiga Toxin (Heat-Labile Protein)--> Dysentry TREATMENT ECYTHYMA
Aspiration pneumonia the intestinal cells, and destruction of the intestinal mucosa. bacteremia;
GANGENOSUM
Abscess in lungs and liver - There is lateral movement of the organism from one cell to adjacent Tx = Antibiotic *most are self-limiting 2-5 days (in immunocompromised patients)
Alcoholics cells. Ceftriaxone
di-A-betics Fluoroquinolone SEPSIS BURN WOUND INFECTION
ENTEROAGGREGATIVE E. COLI TREATMENT
Encapsulated Virulent Organisms
- mucosal damage adherence - Fluid & Electrolyte ID: isolated in MacConkey then differentiated on Hextoan --> BLACK;
EAST (Enteroaggregative Heat Stable Toxin) - Floroquinolones, Chloramphenicol, Tetracycline
*Some - Strep Pneumoniae
secretion of large amounts of mucus, and diarrhea.
Killers - Klebsiella Pneumoniae
CLINICAL MANIFESTATION
Have - Homophillus Influenzae
ID: Diptsick Nitrite test ID: isolated in MacConkey then differentiated on Hextoan --> BLACK;
PSEUDDO Pretty - Pseudomonas Originosa
Rapid diagnosis can be made using PCR and DNA probes.
Pneumonia Nice - Nisseria Meningitis
TREATMENT 'SALMONELLESIS' Sepsis Capsules - Cryptococcus Neoformins
-Fluid replacemnt for intestinal
otitis Externa
- Cephalosporin, Floroquinolone for Extraintestinal CLINICAL MANIFESTATION Loose Diarrhea ' grape like order'
UTI
Nausea ' swimmers ear'
Diabetes
Vomitting
Osteomyelitis
CLINICAL MANIFESTATIONS 2-5 days ' green-blue' sputum'
'SHIGELLOS'
most Shigella Peritonitis
- Oppurtunist
*GASTROENTERITIS
Cystic Fibrosis
Diarrhea - majority of cases need no therapy
ENTERIC *DEHYDRATION
Fever (eg. simple watery diarrhea)
Diabetics
& Burn Victims
Headache some cases produce DYSENTRY
WATERY DIARRHEA ELECTROLYTE IMBALANCE
Difficulty Concentrating Salmonella Enteriditis
- nausea,
Salmonella Typhimurium
- abdominal cramps less common & caused
- low-grade fever for 1-5 days by Shigella Dysentrae: Rose Spots on Abdomen
DIARRHEA
- more mild than cholera Constipation followed by Diarrhea
*Enterotoxigenic E. Coli HUS = ENTERIC 'TYPHOID' Abdominal Pain
HEMOLYTIC
Enteroaggregative E. Coli 1. Hemolytic Anemia FEVER Gradual Fever that progresses as the day goes on
UREMIC
Enteropathogenic E.Coli 2. Acute Kidney Failure (Uremia) *Bradycardia
SYNDROME (HUS)
3. Low Platelet count (Thrombocytopenia) Salmonella Typhimurium
BLOODY, MUCUSY, PUSSY DIARRHEA
DYSENTRY Enteroinvasive E. Coli Sudden onset of abdominal pain & cramps - High remittent Fever
Enterohemorrhagic E. Coli Diarrhea & fever B Blood 1st week
DYSENTRY - Little to No GI involvement
after 1 to 4 days: A Agglutination 2nd week
SEPTICEMIA - 5-10% of Salmonellesis
HUS = Stools contain mucus, pus, and occasionally blood S Stool 3rd week
Salmonella Choleraesuis mc
HEMOLYTIC 1. Hemolytic Anemia U Urine 4th week
any Salmonella
UREMIC 2. Acute Kidney Failure (Uremia) ' SHIGELLA SHRIVELS you up'
SYNDROME (HUS) 3. Low Platelet count (Thrombocytopenia)
'food, fingers, flies, feces' ASMPTOMATIC
Enterohemorrhagic E. Coli
OSTEOMYELTIS
EXTRA-ENTERIC only in Sickle Cell Disease*
rest is Staph Aureus*
* most common cause of UTI
*UTI - fimbrae
- Urinary frequency, Dysuria, Hematuria, Pyuria;

NEONATAL MENINGITIS capsule

NOSOCMIAL INFECTIONS capsule

SEPTICEMIA Lipid A

ENTEROTOXIGENIC E. COLI
LABILE in the Air (labile toxin inhibits cAMP)
STABLE on the Ground (stable toxin inhibits cGMP)

GRAM (-)
Coccoid Rods
Coccoid Rods
-Respiratory-
Coccoid =

Haemophilus *V* Bordetella Pertussis *V* Legionella Pneumophila

top 3 most common cause of Bacterial Meningitis - Obligate Aerobe - Facultative Intracellular
- Young children (6mo - 6yr) mc affected - Respiratory droplet transmission; Highly Infectious - *Poorly Gram staining
- Facultative Anaerobe - Strictly human pathogen, primarily infants & children - Respiratory Droplet transmission only, grows best in WARM & WET;
- Non-Motile, Pleomorhic, Short Rods - 7-10 day incubabation *Air-Conditioners
- Transmitted via Respiratory Droplets & diret contact w/ secretions - Mainly affects children & infants WhirlPool Spas
- ASPLENIC PATIENTS & immune compromised most at risk - Non-Invasive, only Inflammatory Sauna / Mister
- Encapsulated - Opportunist requiring underlying illness / weak immune system;
:) NONCAPSULATED = H. PARAinfluenzae (Normal Respiratory Flora) :) Nosocomial Infections
:( CAPSULATED = H. Influenzae (95%) Cause problems :( VIRULENCE FACTORS Elderly
FILAMENTOUS HAEMAGLUTIN (FHA) - Adherence to respiratory mucosa Smokers & COPD
VIRULENCE FACTORS Progressive destruction of Ciliated cells - 15-75% Mortality for Legionnaire's Disease
*POLYSACCHARIDE CAPSULE (SEROTYPE B) - Antiphagocytic *PERTUSSIS TOXIN - Exotoxin causes local tissue damage; - 2-10 day incubation
*IgA PROTEASE - neutralizes mucosal IgA & attachament *Increases cAMP by disabling Gi (ADP-ribosylates Gi Protein)
LIPID A (reminder) - Shock --> impares phagocytosis; VIRUENCE FACTORS
FIMBRAE - attachment SECRETION SYSTEM
PSEUDOPOD - Phagocytosis INTO Macrophage for intracellular replication;
HAEMOPHILUS INFLUENZIAE TYPE B ID: Symptoms, then
- CAPSULE* *Bordet-Gengou agar of Naso-Pharyngeal swabs ID: Buffered Charcoal Yeast Agar BCYE
HAEMOPHILUS DUCREYI - Cysteine & Iron for growth
- sexually transmitted TREATMENT Silver Stain
Macrolide (50s) Antibiotics: Azithromycin * L. Pneumophilia Antigen in Urine*
TREATMENT (the only Pneumonic bacteria with urine antigen test)
Ceftriaxone (for meningitis) VACCINE
amoxicillin-clavulanate DTP Vaccine - killed bacterial cell suspension (conjugated); TREATMENT
Rifampin (for close contacts) 2-15 month Macrolides (Erythromycin)
Floroquinolones
VACCINE DTaP (diphtheria, tetanus, and acellular pertussis) has three pertussis
Capsular polysaccharide-protein Conjugated Vaccine components:
*only protects against H. Influenzae Type B 2, 4, and 6 months and then again between 4 and 6 years. CLINICAL MANIFESTATION
Boosters are given every 10 years.
ID: Chocolate AgaR (Factor V & X)

Atypical Pneumonia w/ Non-Productive Cough

CLINICAL MANIFESTATION LEGIONAIRES DISEASE Major Confusion
CLINICAL MANIFESTATIONS (Severe Presentation) Diarrhea
nosocomial
Acute tracheobronchtis ATYPICAL PNEUMONIA 15-75% Mortality
- Rapidly progressive begins mild, then develops into sever coughing over 1-4 weeks; 4,000 deaths per year in US
- Permanent CNS deficits (hydrocephalus, mental retardation, and speech
BACTERIAL and hearing problems) in a third of the cases. Catarrhal Stage - Mild, Upper respiratory, low fever PONTIAC FEVER
WHOOPING Fever.... WITHOUT pneumonia
MENINGITIS Paroxysmal Stage - Severe, Lower respiratory, Hacking, (5-20/20sec) (Mild Presentation)
COUGH
in unvaccinated *prevented by vaccination Convalescent Stage - Less severe, may persist for months
WATERY DIARRHEA
Capsulated Form
H. Influenzae Type B 'cough on expiration, whoop on inspiration' HYPONATREMIA
“100-day cough”
EPIGLOTTITIS *prevented by vaccine Legion:
in unvaccinated H. Influenzae Type B ASYMTOMATIC / Stumbling Drunks
mainly in young adults & adults
MILD Contaminated Water & Air
PNEUMONIA H. Influenzae Type B
Diarrhea in the toilets;
SINUSITIS H. Influenzae Type B
Lung Loving Legionella
Pain
Redness
OTITIS MEDIA *NOT prevented by vaccine
H. Influenzae Type B
H. Parainfluenzae

PINK EYE / Subtopic 3

CONJUCTIVITIS

Genital Ulcer formed by H. Ducreyi;

CHANCROID only Black Micro culture
PAINFUL (unlike Syphylis) you cry with Ducreyi, but not with syphylis
STD
Haemophilus Ducreyi

Influenze is the invader

Some Killers Have Pretty

GRAM (-)
Diplocci
Neisseria
- Aerobic, Capnophilic
- Non-Motile 'Kidney Shaped' Diplocci
- Colonizes Upper Respiratory tract & Genitourinary tract;

VIRUENCE FACTORS
IgA PROTEASE
CELL MEMBRANE PROTEINS

ID: Thayer-Martin Medium (Chocolate Agar + Vancomycin (inhibits Gram

+, Colistin (inhibits Gram -), Nystatin (inhibits Fungi) & Trimethoprim;

GLUCOSE MA LTOSE & GLUCOSE

FERMENTER FERMENTER

Neisseria MeninGococci
top 3 most common cause of Bacterial Meningitis (all ages)
- Colonizes Nasopharynx
- Respiratory droplet & Oral transmission
- About 10% of healthy people are carriers who have sufficient immunity to
block disease but still have mucosal colonization.
- Opportunist Pathogen
young children & trauma victims
- 25% Mortality

PATHOGENESIS
NM binds to nonciliated mucosal cells with pili and then passes through the
mucosa into the submucosa and eventually into the bloodstream;
--> Dissemination
In immunocompromised, organisms disseminate to most tissues (especially the
skin, meninges, joints, eyes, and lungs)
--> Causes permanent CNS deficits, skin necrosis, seizures, deafness;
Neisseria Gonococci
VIRULENCE FACTORS
POLYSACCHARIDE CAPSULE - Antiphagocytic (allows survival in the blood)
- Sexually or Perinatally Transmitted PILI
- Oxidase ( + ) CELL MEMBRANE PROTEINS - Inflammation
- Diplococcus with a ‘‘paired kidney bean’’ morphology
- Sometimes Intracellular after phagocytosis ID:
Kernig sign
VIRULENCE FACTORS Burzinski Sign
PILI - cause adherence to mucus membranes:
Cervix (cervicitis) or vagina in the female PREVENTION
Urethra (urethritis) or penis in the male Vaccine
*Pili also show antigenic variation, causing recurring episodes
TREATMENT
ANTIBIOTIC RESISITANCE: Cetriaxone
1. Plasmid-encoded beta-lactamase production High-Dose IV penicillin (passes through the inflamed blood–brain barrier)
2. Chromosomally-mediated changes in cellular permeability inhibit entry of +
penicillins, tetracycline, erythromycin, aminoglycosides; Rifampin to eradicate oropharyngeal colonization & use in immunocompromised
close contacts;
TREATMENT
- Immediate systemic ceftriaxone and lavage is needed to prevent loss of
eyesight. CLINICAL MANIFESTATIONS
- Prophylaxis with erythromycin or silver nitrate prevents neonatal transmission;
- Azithromycin if newborn is coinfected with Chlamydia
- Slapping the penis ('the clap').... No longer the treatment;
begins as mild pharyngitis + occasional fever

Adrenal INsufficiency
CLINICAL MANIFESTATIONS WATERHOUSE-FRIEDRICHSEN SYNDROME =
Hemorrhage
Menningococcemia = disseminated disease
Circulatory Shock

Purulent Meningitis
Urethritis
Fever
Cervicitis
MENINGITIS Pneumonia
Salpingitis
Stiff Neck
Pelvic Inflammatory Disease
*FATAL IN 1-5 DAYS
Proctitis
Creamy Purulent Discharge

* Chronic exposure can cause sterility in both sexes

* OFTEN ASYMPTOMATIC IN WOMEN

GONORRHOEAE / HEMMORHAGIC PURPURIC

UROGENITAL
CUTANEOUS SKIN RASH due to overproduction of capsule (containing LPS)
INFLAMMATORY DISEASE

Meningitis + Skin Rash Kidney shaped diplococci

VIRULENT ENCAPSULATED BACTERIA

Some - Strep Pneumoniae
Killers - Klebsiella Pneumoniae
Acquired during birth Have - Homophillus Influenzae
- Symptoms start 2 to 5 days after birth Pretty - Pseudomonas Originosa
- Eyes are purulent (hyperpurulent) with pus reaccumulating within *Nice - Nisseria Meningitis
minutes of lavage. Capsules - Cryptococcus Neoformins
- Eyesight is rapidly destroyed from apparent pressure necrosis of the
corneal surfaces due to the rapid accumulation of pus under the eyelid.

*Neonates may be coinfected with Chlamydia, which is more common.

NEONATAL
CONJUCTIVIS

REACTIVE / REITERS
Disseminated disease
ARTHRITIS
+
Type III Hypersensitivity Reaction
NECROTIC SKIN LESIONS

FITZ-HUGH-CURTIS SYNDROME infection of the liver capsule and “violin string” adhesions of peritoneum to liver

Kidney shaped diplococci

GRAM (-)
ZOONOTIC

ZOONOTIC

Bartonella Brucella Francisella Pasteurella

Subtopic 1 Subtopic 1 Subtopic 1 Subtopic 1

CLINICAL MANIFESTATION CLINICAL MANIFESTATION CLINICAL MANIFESTATION CLINICAL MANIFESTATION

CAT SCRATCH
DISEASE

GRAM (-)
ATYPICAL
BACTERIA
doxycycline

ATYPICAL
BACTERIA

RICKETTSIACEAE FAMILY
- OBLIGATE Intracellular replication
- Zoonotic Infection
- Thin Cell wall STAINLY WEAKLY and
has only small amounts of LPS

*NO TOXINS OR IMMUNOPATHOLOGY;

Abrupt fever, chills & unremitting headache

ID: Giemsa Stain

*will not show up on Gram Stain

TREATMENT
Doxycycline

RICKETTSIA
(common)
Die quickly outside of host
- Transmission by Vector (fleas, ticks, mites, lice)
- Requires ATP and active process to enter host cell

CLINICAL MANIFESTATION

Headache
Fever
Flu-Like Symptoms
Rash that starts at wrists and anlkes
*ROCKY MOUNTAIN and spreads to trunk, palms and soles;
SPOTTED FEVER <19, transmitted by Tick Bite

Ricketsii Rickettsia Ricketsii

Rash starts centrally and spreads out,

except face, palms, soles;
Sever

TYPHUS

Typhi