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Endospore formation:
ensures survival of
“bacteria” in harsh
conditions. Spore
germination requires O2
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Characteristics Transmission Defenses & Prevention
Immunity
Bacillus Cereus Large Large MOTILE Vegetative cells Two Enterotoxins: CHINESE Unknown Fluid &
Gram (+) granular & spores - Necrotic toxin: heat-labile RESTAURANT electrolyte
rods in pairs colonies on AEROBIC normally found toxin (LT) that stimulates cell’s syndrome replacement if
or chains nutrient agar in soil, dust, adenylate cyclase. Causes necessary. No
Biotyping not decaying diarrhea Emetic Food Poisoning: other
MOTILE Mesophilic & used organic matter – upper GI disturbance w/ medication.
nutritionally also in rice, - Heat-stable enterotoxin (ST) vomiting toxin forms in
Aerobic require meat products acts by diff. mechanism than rice ==> consume Vancomycin
amino acid “LT”, leads to vomiting but reheated rice w/ toxin for eye
Endospores supplements Non-invase inf. not to diarrhea ==> food poisoning infections.
centrally Occurs when symptoms arise in about Multiple drug
located bacteria and/or Endospore formation: 6 hrs after eating toxin- resistance
(metacentric) spores ingested. surivival in harsh conditions. laden food.
Germination requires oxygen
Spores survive Diarrheal Food
cooking & Lecithinase (phospholipase C) Poisoning: lower GI
germinate ==> enzymes – active on cell disturbance w/ diarrhea.
produce toxin & membranes (associated w/ Toxin forms in meat /
ingest pre- ocular infection) vegetables ==> consume
formed toxin reheated foods laden w/
(food bacteria (& toxin)
Cereolysin (potent hemolysin)
intoxication) symptoms arise w/in
& Necrotic toxin (associated
w/ ocular infection) 24hrs, food inf. May last
for 2 days
Post-traumatic
endophthalmitis (eye
infection) leads to
edema. Drug abusers are
á risk, may cause
blindness
Food poisoning
unpasteurized milk,
turkey
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Characteristics Transmission Defenses & Prevention
Immunity
Clostridium Large Not usually Organism not Spores normally Botulinum toxin: MOST Botulunum food Immunity to Anti-toxin
botulinum Gram(+) rod cultured usually grown found in soil, TOXIC COMPOUNDS poisoning reinfection is needs to be
b/c dangerous. dust and in known. Eight (INTOXICATION) type specific & given early
Pairs or decaying immunologically diff. toxins permanent enough to
chains Most labs can not organic matter. produced Early symptoms: neutralize
4 groups detect toxin vomiting, nausea but no toxin monitor
type 1 Endospores Vacuum-packed Types A, B, & E are most fever. Diplopia (double hyper-
and 2 formed (sub- Spore stain useful canned goods, commonly causing human vision), dysphagia sensitivity rxn
terminal the spores may disease. (difficult swallowing), &
location) germinate & dysphonia (thickness Respiratory
under poor produce toxin. Toxins are pre-formed in speech) support
growth Food food. Labile at 121 C at 15
conditions intoxication min or boiling food for 20 Late symptoms: flaccid Surgical
min (heat sensitive) paralysis, respiratory debridement
Found in soil, * Inadequate distress ==> can be fatal of wounds &
not in canning, pH < 7, Toxins are “secreted”, released metronidazole
patients smoked fish, by cell autolysis. Infant botulism for infection
canned tuna (INFECTION): infects
Spores Botulinum toxin acts as a infant’s GI tract & Less than Guanidine HCl
resistant to Infant botulism neurotoxin. It blocks the produce toxin. Toxin1isyr old treatment
associated w/ release of acetylocholine most common source1-6 of months stimulates
boiling for
several hr honey loaded neurotransmitter from spores. Symptoms: acetylcholine
w/ spores & poisoned neurons at weakness, feeble cry, release
Obligate wound infection myoneural junctures. W/in paralysis, respiratory
anaerobic ==> subsequent 36hrs flaccid paralysis (Botox distress. Maybe fatal,
toxin poisoning for cosmetic purposes) Blocks could be cause of SIDS.
Non-motile AcH w/ infants! FLOPPY BABY Gastric
SYNDROME (limp baby lavage to
Endospores formation: syndrome) Honey may neutralize
survivial in harsh conditions contain spores! the toxin
Wound Botulism: Penicillin and
entrance of endospores trivalen
into wounds ==> vaccine
Snare protein will
undergo germinate ==> toxin
Light proteolysis
chain of 1-2
snap25,
microgram/
syntaxsin
kg)
botulium Injection of
toxim wil heroin, skin
cause popping
lysis od 18-36 hrs
snare after
protein ingestion
Inhalation
botulism,
purify con and
aerosolized-
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Characteristics Transmission Defenses & Prevention
Immunity
Clostridium Large Not usually Toxins A & B are C. difficile is Exotoxins A and B (==> ANTIBIOTIC Commensal, no Discontinue
difficile Gram(+) rod cultured detected by lethal part of normal hemorrhagic necrosis) ASSOCIATED COLITIS strong host current antibiotic
effect on cell flora of 10% (AAC), ULCERATIVE response treatment &
Obligate cultures (within humans (á in Toxin A: enterotoxin causes COLITIS Most common substitute
anaerobic 24hrs) hospitalized) diarrhea & colitis agent; occurs in GI tract Need to restore quinolone,
(hemorrhagic necrosis). normal flora sulfonamide or
Spore- Toxin detected by 75% of neonates Cause infl. Damage to host “pseudomembranous aminoglycosides
Antibiotic formers a) Latex colonized & tissues colitis, arises few days TMP-SMZ.
associated agglutination serve as after antibiotic treatment
pseudome motile b) ELISA kit – reservoirs to (clindamycin, ampicillin Vancomycin
mbranous detect toxins A&B others in Toxin B: cytotxin lethal to & cephalosporins) best!
enterocolitis Anaerobic hospital & at cultured cells.
home Depolymerizes host actin * Explosive, bloody Metronidazole –
NEONATES are altering host cell cytoskeleton diarrhea, fever & less effective
asymptomatic ==> cell loses shape ==> pseudomembrane in
necrosis colon (detected by
Nosocomial endoscopy)
spread in adults Endospore formation
is activation in
carrier via
changed
bacterial
balance Cause disease in
associated w/
Ampicillin
US and Europe clindamycin,
antibiotic use highly virulent lincomycin,
flouroquinolo
nes
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Characterist Transmission Defenses & Prevention
ics Immunity
Clostridium Large Double beta Obligate Spores normally 5 different serotypes based on Gas gangrene 80% Antibodies & Respiratory
perfringens Gram(+) rod hemolysis on anaerobic found in soil, dust exotoxins produced. All serotype A. Infection is other host support
blood agar & in feces serotypes ==> alpha toxin result of trauma or defenses
Anaerobic Double beta (lecithinase) surgery. Rapid spread, ineffective. Surgical
Thioglycolate hemolysis (1 Wound tissue necrosis & debridement
Sub-terminal medium ring beta / 1 contamination Exotoxins systemic intoxication Antitoxin to of wounds &
spores ring partial) with dirt leads to - Alpha toxin ==> lecithinase (via blood) alpha toxin is metronidazole
(spores in infection. = phospholipase C (converts ineffective & for infection
soil, not in Lecithinase (+) lecithin in cell membrane to Myonecrosis by alpha leads to
patients) form ppt rings C. perfringens diglyceride & toxin, gas production hypersensitivity. Refrigerate
of insoluble similar to c. novyi, phosphorylcholine) ==> RBC due to fermentation of meats after
Non-motile diglycerides c. septicum, c. lysis, destroys membranes & muscle carbohydrates No immunity to cooking
histolyticum, c. mitochondria (saccharolytic activity) reinforcement
Need to bifermentans - beta, epsilon & iota toxins Maintain
Large confirm A & C leads to necrosis & lethality Anaerobic cellulites sterility of
gram (+) serotypes Gas Large amount of (beta toxin ==> w/ pig bel) similar to gas green surgical
bacilli gangrene have C02 produced w/ limited to fascia (no instruments
different causes necrosis. Spores á Spreading factors: muscle invasion)
growth. Restricted - kappa toxin = collagenase Hyperbaric O2
blood flow ==> gas (collagen digestion & Myositos (muscle environment
gangrene / liquefication, destroy bone, infection)
myonecrosis cartilage, & skin, found in Penicillin &
extracellular matrix) Food poisoning other broad
Organism can also - mu toxin = hyaluronidase spectrum
colonize GI tract & - nu toxin = DNase Enteritis Necroticans antibiotics
female genital tract - delta toxin = hemolysin (Pig-bel) associated w/
(leads to septicemia - lambda toxin = proteinase serotype C producing Penicillin G –
& organ abscess) in (degrades gelatin & alpha & beta toxin antibiotics (pg
immuno- hemoglobin) 128)
compromised by - Enterotoxin (heat liable) Septicemia & organ
drug &/or other inhibit fluid absportion from abscesses:
disease gut associated w/ serotype A
food infection. Trypsin
Food poisioning - Neuraminidase
(beta toxin) - fibrinolysin
- theta toxin: heat & O2 labile Necrotizing
(sensitive) hemolysin; enterocolitis or pig
membranolytic bell, due to beta
toxin producing type
C
Mot: ingestion of
meat ptoducts ,
short incubation
period ( 8-24 hrs)
Cell Colony Lab Source & Virulence Factors Associated Host Treatment /
Features Features Characteristics Transmission Diseases Defenses & Prevention
Immunity
Clostridia Large Forms Culture C. tetani Spores are Exotoxins: Deep wound Ab against Vaccination with
Tetani Gram(+) rod transparent from wound site normally found a) tetanus toxin infection ==> toxin develop tetanus toxoid (@
In pairs or colonies on (anaerobic) but also in soil, dust & (tetanospasmin): coded for TETANUS. Spores in host but too 1st, formalin-
chains serum agar culture aerobically may be on plasmid, produced after enter deep wound late to stop inactivated toxin
cultured to check 2ndary introduced into germination of spores, tetanus & as part of DPT
Tennis ANAEROBICAL bacterial invaders host via released (during cell Spastic paralysis due death. with boosters give
racket or LY Staph, Strep puncture autolysis) as pretoxin & to unremitting Recovery does long lasting
drumstick (O2 sensitive) wounds, activated by bacterial muscle contraction. not confer protection)
appearance gunshots, & 3 doses
protease. immunity to 2, 34, 6
burns Diagnosis: organism reinfection DPT involves
Endospores injections
months)
- Toxin blocks the may cultured
located exocytosis of inhib. anaerobically beginning of 3
terminally Transmitters, Glycine, and months. Once
GABA. Results in spastic Difficult swallowing immunity, booster
Obligate (rigid) paralysis of voluntary due to LOCK JAW every 5-10 years.
Anaerobic muscles due to un-opposed
excitation (tetani) of motor Opisthotonos: arched Tetanus antitoxin-
Motile neurons back & neck human derived ab
to the toxin;
“LOCK JAW” (TRISMUS) Risus sardonicus respiratoryATS
for disease ==> fascial grimace support; passive
hyperbaric oxygen
Tetanolysin: is a hemolysin Respiratory distress:
Strict serologically related to Surgical
due to tetanus of
anaerobe Streptolysin O (& debridement of
non diaphragm. Resp.
listeriolysin & wounds &
encapsul arrest
pneumolysin). Also these metronidazole
ated Tetanus
are found S. Pyogenes, S. (kills bacteria)
neonatorum
Neonatal tetanus
Pneumoniiae, Listeria Lyses ==> infection of Vaccinate
RBC, PMN, macrophages, all mother Antibiotics: inhibit
umbilical stump.
bacterial growth â
platelets & fibroblasts. Infant weak on the 7
month of toxin production
Endospore formation: Localized tetanus pregnancy
C. tetani is
survives harsh conditions
sensitive to
Cephalic tetanus
Poor prognosis pencillin. Pen.
Inhibits normal
GABA.
Cell Colony Lab Source & Virulence Factors Associated Host Treatment /
Features Features Characteristics Transmission Diseases Defenses & Prevention
Immunity
Gram (+) rod Cultured Propionic acid part of normal Lipases (Lipophilic)* split Acne vulgaris PMN attracted Benzyoyl peroxide
Propionibact sometimes anaerobically production flora of skin, off fatty acids from skin (common acne) to bacterial topical
erium acnes branching mouth & eyes lipids. Inhibit other bacteria substances bacteriostatic
Indole (+) but can contribute to tissue Chronic effect by oxidation
Anaerobic grows in acne inflammation inflammatory Complement of area
(anaerobic Contaiminates lesions infection of hair activiation
diphtheroid) blood cultures, b/c Able to enhance host’s follicles. Papules, occurs Trimethoprim for
it’s on skin metabolize skin- immune system to produce comedones systemic treatment
Non-motile dervived lipids, a strong acute inflammatory (blackheads),
blocks sebaceous response pustules or cysts on Retinoids (Vit A)
Not spore! glands cuase face for cystic acne
acne & other
pustular rxn. Bacteremia: ==>
May enter via endocarditis
wounds. (opportunistic!)
Swallowed ==>
abdominal disease.
Infection ==> appendix,
trauma, or performated
ulcer
Pelvic Actinomycosis:
serious infection, caused
by chronic IUD
----------------------------------- (intravenous used drug)
Disease ===> section use / inflammation
----------------------------------- associated w/ STD
A = Actino
A.mycosis A.mycetoma A. bovis: “lumpy jaw”
Obligate Aerobic Actino: dental plaques
Anaerobe intracellular
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Characteristics Transmission Defenses & Prevention
Immunity
Nocardia Gram (+) Cultured Acid fast stain of Abundant in soil & Catalase & Superoxide Nocardiosis (not Host generates Caught early:
asteroides aerobically sputum or pus for cause of Dismutase enzymes: high contagious, but lethal, & acute Sulfonamide
Short rods on blood branching, opportunistic levels resist PMN’s may relapse after inflammatory
Nocardia agar filamentous infections in intracellular oxidative burst. treatment) (pyogenic) Or else:
brasiliensis Long chains bacteria. immuno- response due to 80% fatality
Smells compromised Formation of long filaments Pulmonary abscesses: PMN
Branch & musty Use modified patients w/ AIDS, á ability resist phagocytosis cavitating lesions in lungs phagocytosis. TMP-SMZ for
filamentous acid-stain corticosteroids. ==> TB, Crhonic lobar Ab needed for propylaxis
Grows slow (sulfuric acid) . Mycolic acid pneumonia phagocytosis
Aerobic Considered Most common: (require
Rough “paritial/weak - Infection initiates Sepsis: spreads from lungs cytokine
Non-motile surface (may acid fast” via respiratory route via blood to other organs production).
have aerial (inhale) often to CNS ==> brain Activated CD8+
Stained w/ filaments) Catalase (+) abscess, skin ==> kidney T cells are toxic
modified - Enters by skin lesion to N. asteroides
(non- Superoxide trauma w/ foot the
alochol) dismutase (+)
usual site of Actinomycetoma (aerobic
acid-fast infection actinomycosis): chronic
b/c of granulomatous infection of
mycolic acid subcutaneous tissues. Sinus
6% tracts are formed draining
pus to skin surface. Can
In vivo: lead to damaged bone.
INTRA-
CELLULAR! Foot is the usual site of
infection after injury:
Non-Runyon’s mycobacteria
- M. tuberculosis
- M. bovis
- M leprae
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Characteristics Transmission Defenses & Prevention
Immunity
MOTTS g(+) Runyon Acid-fast stain MOTT species are 1. Mott are low virulence Group I T cell mediated Group I
Groups I-III ubiquitous in 2. produce no catalase - M. kansasii, pulmon. Inf. DTHR - Kansaii: multi-
slender rods are cultured Produce no niacin nature 3. protein antigens (killself) - M. marinum, swim pool drug + INH
long chains, aerobically 4. survives in macrophages granuloma AB ineffective - Marinum:
branching & grow very Cause disease by 5. survives in acid/basic, dry b/c bacteria are rifampin &
slowly opportunistic 6. MOTT are multi-drug Group II intracellular ethambutol
waxy infections resistant - M. scrofulaceum, cause
surface – “scrofula” Granulomas Group II
mycolic acid No person to person may form w/ - Scrofulaceum:
transmission Group III MOTT rifampin
non-motile - M. Avium Intracellulare infection
(MAC) Group III
aerobic - MAC:
Group IV ethambutol,
visualize w/ - less mycolic acid streptomycin,
acid-fast - M. smegmatis (foreskin) rifampin
Group IV
- Smegmatis,
amikacin
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Characteristics Transmission Defenses & Prevention
Immunity
Myco- Gram (+) Grows very Acid fast staining Mammals are only Cord factor: ( Trehalose Causes pulmonary T Cell Mediated Decontaminate
bacterium slowly Of sputum reservoir b/c under dimycolate) gathers M. Bovis infection, similar to TB delayed w/ concentrated
Bovis Slender rods zoonotic. Into chains. hypersensitivity NaOH
in long Colonies Chest X-ray Infections: (TDTH)
chains- develop in 4- Infection occurs by Catalase (-) ==> INH (-), - GI tract Prevent
branching 8 weeks PPD skin test (+) ingestion of Raw resistant - scrofuloderm (skin inf) AB are development of
Milk obtained from - osteoarticular TB (joints) ineffective b/c drug-resistance,
Waxy Grown on Colonies, colorless infected animals. Proteins antigens of outer intracellular in use combo of
surface Mueller- surface stimulates self- Use of immuno- macrophage drugs.
(mycolic Hinton agar, NO NIACIN Human to human destructive host suppressive drugs
acid) Jensen- transmission can hypersentivity (steroids) re-activate Macrophage
Lowenstein Catalase (-), occur via respiratory primary M. Bovis. fuse to form
Obligate agar or resistant to droplets from Other factors enable Langhans giant
aerobe Middlebrook isoniazid, INH individuals with organism to survive in PPD + indicate exposure to cells.
7H10 serum (differs from TB) secondary TB macrophages M. Tuberculosis or M. Bovis Granulomas
Non-motile agar (INTRACELLUULAR) form w/
Detected by epitheliod
Acid-fast Cord factor Bactec within 10 Waxy layer (mycolic acid w/ surrounding
(trehalsoe days cultivation trehalose) contributes to central necrosis
Catalase (-) dimycolate) bacteria’s ability to survive
produce under acidic/basic, dry
pathogenic conditions & to resist
strains leads exposure to many
“serpentine disinfectants.
cords”&
surface Multiple Drug Resistant
pellicle in (MDR) b/c of the waxy layer
liquid or porin size.
culture.
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Characteristics Transmission Defenses & Prevention
Immunity
Myco- Gram (+) Grows very Acid fast stain of MAC species are 1) MAC are organisms low MAC pulmonary inf. T cell mediated Multi-drug
bacterium slowly sputum ubigquitous in virulence common in AIDS patients (DTHR). Anti- therapy b/c
avium- Slender, nature (soil, dust, & 2) Do not produce catalase, body ineffective most are multi-
intracellulare rods, in long Grown on Catalase (-) throats) of normal there INH becomes resistant MAC pulmonary inf. b/c bacteria are drug resistant
chains Mueller- humans & animals 3)Protein antigens of outer similar to TB intracellular (MDR)
MAC Hinton agar Colonies are coat stimulate self-
complex Aerobic colorless & do MAC can cause destructive host hypersensit. PPD(+) may appear (-) b/c 1st line drugs:
Middlebrook not produce disease by 4) Bacterial factors enable suppressed T cell, T_s - ethambutol
Runyon Waxy surf= 7H10 serum niacin OPPORTUNISTIC organism to survive in - streptomycin
Group III mycolic acid agar (w/o infections of birds macrophages. Therefore, * Main route of inf. into - rifampin
& MOTT pigment Nitrate Red. (-) & immuno- INTRACELLULAR AIDS patients is the GI
Non-motile production) compromised 5) Bacteria survives in tract.
Chest X-ray humans, AIDS acid/basic
Acid-fast patients w/ â CD4 6)MAC are naturally mult- MAC residing in macro-
Bactec test: test for T cell. drug resistant phages INTRA-
Catalase (-) C02 production CELLULAR disseminate
from lymph nodes to
PPD skin test spleen & lungs forming
sometimes (+) lesions. May spread to all
organ systems
PPD(-) when
immuno- Tubercle (granuloma)
compromised formation in MAC inf. of
patients w/ AIDS AIDS patients is NOT
observed. Tubercle seen
in M. Tuberculosis.
Facultative intracellular
pathogen: enter phagocytic
vesicles & avoids death. Similar
to N. Gonorrhea in non-ciliated
mucosal cells
Nitrate reduction
to nitrite only
Yellow pigment
production
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Characteristics Transmission Defenses & Prevention
Immunity
Acinetobacter G(-) Grows on Oxidase (-) Widely distributed in 1. LPS (endotoxin) Acinetobacter species are NA TMP-SMA
Baumannii blood agar nature (free living 2. drug resistance(s) hospital acquired in warm (Bactrim) similar
Coccobacilli Does not ferment saprophyte) seasons S. Saprophyticus
Produce sugars but
Obligate colonies that glucose oxidized Often associated w/ Post-surgical infections of Alternative:
aerobe are non- hospitals soft tissue with abscesses is - Kanamycin,
hemolytic often seen. - Colistin,
Non-motile Organism is able to - Tetracycline
survive on moist Organism may be also
Oxidase (-) surfaces & skin involved w/ respiratory tract
infections and urinary tract ----------------------
Non- Acinetobacter is only infections. Resistant to
hemolytic 2nd to the non- Penicillin b/c of
fermenting beta-lactamase
Glucosa Pseudomonas
oxidized aeruginosa in causing
nosocomial infections
– maybe associated w/
hospital outbreak
Ex. Acinetobacter,
Xanthomonas,
pseudomonas, can
colonize mechnical
ventilator ==>
introduce into
respiratory tract of
patient undergoing
assisted ventilation
G (-) bacilli Cell Colony Features Lab Source & Virulence Factors Associated Host Treatment /
Features Characteristic Transmission Diseases Defenses Prevention
Immunity
Bordetella G(-) Phase I – most Nasopharyngeal Humans, the 1. Capsule: A good marker for 3 stages of Ab made Erythromycin
pertussis virulent grows on swab ==> only reservoirs!!! vaccine effectiveness but ab is whooping cough or against
Coccobacilli Bordet-Gengou incubate 10 days not protective. pertussis (intense capsule. Alternative:
(WHOOPING (contains potatoe Horizontal 2. Exotoxin cough) Infection is Tetracycline
COUGH!) Singly or starch, glycerol, & Oxidase (+) transmission is 3. PERTUSSIS TOXIN (PT) is non-invasive chloramphenicol
pairs, chairs 50% blood) has a by respiratory heat-labile binary toxin. 1. Catarrhal stage: w/ bacteria
pili & O-antigen are Direct droplets among Deactivates inhibitory GTP Most infectious, remaining in Paroxymal stage:
Obligate expressed fluorescent Ab children binding* proteins (Gi) by ADP- most bacteria. respiratory oxygen therapy
aerobe test (DFA) ribosylating them Most contagious. tract. may be effective
Produce small HIGHLY Active B (adhesion factor) RRHEA & steroids â
NO carbo- “pearl-like” or ELISA CONTAGIOUS composed 5 unique polypeptides 2. Paroxymal stage: severity.
hydrate “metallic” colonies (90% gets & mediates w/ A subunit, violent cough,
fermentation infected) results in á cAMP. Toxin blocks vomit. CNS Vaccination:
& oxides Produce small zone PMN & inhibits movement by damage. Less Kills phase I
amino acids of hemolysis chemotaxis & activates contagious. bacteria, DPT
pancreatic insulin production by VIOLENT stage vaccine w/
Non-motile á CO2 help growth Islet cells. 3. Convalescent boosters 4,6, 18
Cyclolysin: dual f(x) toxin, stage: gradual months.
Requires: Cell sensitive to hemolsyin + adenylate cyclase reduction in cough,
nicotinic acid heat, dry, & chem.. 4. Adenylate Cyclase: inhibit cell may last 1-6months This vaccine has
Blood, helps f(x), especially WBC, edema been replaced by
neutralize inhibitory factor of B. anthracis. ACELLULAR
effects of fatty acid, Hemolysin: inhibit leukocyte vaccine w/
sulfides & H202 chemotaxis, phago & killing reduced side
5. tracheal cytotoxin: effects. PT,
Phase II & II less peptidoglycan frag, damages FHA, pertactin,
virulent. No blood ciliated cells. Stim IL-1 release & pili are
on phase IV. 6. Adhesion factors: pili commonly used.
(fimbriae) display phase
VIR gene variation on/off
7. Filamentous Hemagglutinin
Phase variation (FHA) attach to ciliate epithelial
(exp. on/off gene) cells
8. Pertactin: adhesion factor
9. LPS = endotoxin Lipid A & X,
X more potent!!!
** B. bronchispetica: motile, causes cough in dogs, kennel cough, unique-nitrate reduction (+), mild symptoms
Phase Description
Phase I Pili & O-antigen expressed
Phase II & III Bacteria express different antigens, less virulent
Phase IV Pili & O-antigen NOT expressed. Avirulent
G (-) bacilli Cell Colony Features Lab Source & Virulence Factors Associated Host Treatment /
Features Characteristic Transmission Diseases Defenses Prevention
Immunity
Haemophilus G(-) Grows on chocolate Catalase (+) Humans are 1. Capsule: Type b is most Nasopharyngitis: Neonate got Ceftriaxone or
influenze agar producing only reservoir commonly associated w/ H. influenzae ab from cefotaxime
Coccobacilli small colonies that Fermentation rxn for H. disease including meningitis infections (include mother &
bipolar stain are non-hemolytic are variable influenzae. (90% caused by strains) Type b non-typable or was Combination of:
contrast to (glucose only) capsule is composed of non-encapsulated protected for Cefotaxime w/
chains/filam Non- polyribitol phosphate (PRP) strains) Infection first few ampicillin
ents Beta-Hemolytic: Tryptophanase (+) encapsulated Capsules can elicit Quellung may become months of
- H. Ducreyi variants are rxn (serotyping) sinusitis, otitis life. Alternative:
facultative - H. hemolyticus Nitrates used as considered to be media or cellulites Eventually, (sensitive Pen.)
anaerobic terminal electron normal flora of 2. IgA protease: prevents also pneumonia, reproduce chloramphenicol
Capsule: Quellung acceptors the pharynx & opsonization by IgA chronic bronchitis, it’s own.
Capnophilic Rxn, destroyed by conjuctiva. epiglottitis.
CO2 autolysis by Vancomycin Carrier rate is 3. Beta lactamase: encoded on Vaccine:
endogenous enzyme sensitive ~30% plasmid, confers resistance to May lead to Composed of
Non-motile penicillin bacteremia & septic polyribitol
Requires: (hexe, navy) Requires X & V Hortizontal arthritis phosphate (PRP)
Naturally - Factor X: HEME factors and CO2 transmission 4. Pili: adhesion factor, not conjugated to
competent!!! - Factor V: NAD primarily well characterized Epiglottitis: protein. Used as
Specimens: CSF, respiratory inflamed epiglotis a booster
grows on chocolate blood & carry out droplets 5. LOS swollen, red,
agar antigenic typing of edematous tissue
capsule (Quellung Individuals had leads to airway
H. influenzae rxn) protective ab to obstruction
recovered during type b capsule by
primary isolation on age 5-6 Meningitis: H.
standard blood influenzae (type b)
agar. Also grows in Carriage is #1 cause of
close proximity to S. mostly by non- meningitis in
Aureus (beta encapsulated young children - 6
hemolytic) strains, maybe
non-typable Purulent
Satellite encapsulated conjunctivitis
phenomenon: test strains. Lead to (pink eye): caused
for nutritional req. localized by H. aegypticus
infections, w/o (Koch’s Weeks
dissemination bacillus)
G (-) bacilli Cell Colony Features Lab Source & Virulence Associated Diseases Host Treatment /
Features Characteristic Transmission Factors Defenses Prevention
Immunity
Haemophilus G(-) Grows on blood Catalase (+) Humans are the 1. LPS H. ducreyi causes SOFT chancre na Erythromycin
ducreyi agar produce small only reservoir – (endotoxin) (chancroid), painful, gential
Coccobacilli colonies that are Glucose is in genital tracts lesions & lymphadenopathy Alternative:
bipolar stain hemolytic fermented (enlarged lymph nodes). Enters Sulfa drugs
Hortizontal via break in skin. Can carry to (sulfonamide) or
facultative Requires only heme Requires Factor X transmission inguinal lymph nodes & streptomycin
anaerobic (Factor X) no need (heme) occurs via sexual multiply. May result in massive
NAD b/c can contact swelling. Highly contagious.
Non-motile synthesize Vancomycin
resistant
G (-) bacilli Cell Colony Features Lab Source & Virulence Associated Diseases Host Treatment /
Features Characteristic Transmission Factors Defenses Prevention
Immunity
Klebsiella G(-) Grows on blood Oxidase (-) Widely distributed Capsule: resist 1. Lobar pneumonia & Ab made Cefotaxime &
pneumoniae agar produce slimy in nature (soil, phagocytosis, bronchopneumonia: associated against gentamycin
Large & long – mucoid colonies Slow fermentation vegetables) attracts w/ hospital acquisition by capsule
(Friedlander’s bacilli b/c of capsule, non- of glucose, lactose macrophages alcoholics, diabetics, & patients Sensitive Pen:
bacillus) hemolytic. & sucrose (pink Often associated to area w/ chronic pulmonary disease. TMP-SMZ
facultative “Spreading” colonies on w/ nosocomial Symptoms include: fever, (Bactrim)
anaerobic MacConkey infections: Urease: productive cough, empyema,
lactose agar) develop UTI hemoptysis (spit blood) & thick
Non-motile K. pneumoniae is “currant jelly” sputum.
Bile salt selectin normal flora of R plasmid:
human colon. codes for Pen. 2. Urinary Tract Infection:
Indole (-) & common in hospital settings, b/c
Nosocomial aminoglycosid compromised by surgery,
Methyl red (-) infections: e resistance catheters, bladder retention etc…
organism is
Voges-Proskauer transmitted by LPS, endotoxin 3. Bacteremia caused by
(+) dwelling catheters Klebsiella & E. Coli in hospital
& endotracheal ST & LT settings.
Citrate (+) tubes enterotoxin
4. Tropical sprue
Urease (+) Mostly in immuno-
compromised,
H2S (-) hospital patients
3. Endocarditis (inflame.
Of heart muscles)
4. Guillain-Barre Syndr.
(asc paralysis more
commonly associated w/
Campylobacter infection)
G (-) bacilli Cell Colony Features Lab Source & Virulence Associated Host Treatment /
Features Characteristic Transmission Factors Diseases Defenses Prevention
Immunity
Helicobacter G(-) Organism grows on Oxidase (+) Human GI tract is 1. LPS 1. Chronic Immuno- Combination of
pylori selective agar Catalase (+) reservoir. Oral 2. Motility – burrow through Gastritis: competent drugs:
Pleomorphic TSI (-) fecal route is mucin layer stomach lining Causative agent!!! patients have
(s-shaped, Chocolate agar or Urease (+) involved in Acute infection of chronic Pepto-bismol
bacilli, modified Thayer- Nalidixic acid horiztonal 3. Resistance to stomach stomach inflammator (Bismuth salts),
curved rods, Martin incubate for resist. transmission acidity enhanced by epithelium. y response amoxicillin, &
spirochete) a > 1 week under Nitrate reduct. (-) (human to human) movement of Helicobacter Organism causes w/ metronidazole.
microaerophilic Hippurate into & within the protective superficial mucosal moncytes,
Produce: conditions hydrolysis (-) mucous layer of the stomach inflammation & is macrophages Pen. Sensitive:
corkscrew (chocolatization Cephalothin sensit. (not epithelia). non-invasive. & Sub. Amox w/
motility detoxifies agar) Microaerophilic nature Symptoms: nausea, lymphocytes Tetracycline
Endoscopy: detect organism helps survival abdominal in stomach
Micro- by biopsy. discomfort. mucosa. Also include
aerophilic 4. Enzymes: proton pump
(grow in 6% 14C-urea in food & a) Mucinase causes 2. Duodenal peptic Antibody inhibitor ex.
O2, 10% look for 14CO2 in breakthrough of mucous ulcer: (#1 causative formation omeprazole
CO2) patient’s breath & layer in stomach (resist acid) agent) follows not
somewhat serology b) Urease: stomach lining chronic gastritis. protective
tolerant to produce small amounts of Symptoms: therefore
stomach urea .. leads to ulceration burning abdominal patients after
acidity pain 1-3hr after treatment
5. Adhesion factors: attach meals that may be may relapse
to stomach (resist peristalsis) relieved by eating
& antacids.
6. Hemolysin (128kD) found Complications
w/ cytotoxin protein include: bleeding,
& perforation of GI
7. Vacuolating toxin: 50% tract
isolates á virulence of strain
(pathogenicity island* á 3. Gastric
virulence, carcinoma: chronic
gastritis
8.Cag protein: stimulates
host prod. of IL-8 & other
signal transduction events
9. Catalase / superoxide
dismutase: protects from
intracellular killing phago.
10. Produce acid inhibitory
protein (induce
hypochlorhydrin)
G (-) bacilli Cell Colony Lab Source & Virulence Associated Host Treatment /
Features Features Characteristic Transmission Factors Diseases Defenses Prevention
Immunity
Vibrio g(-) Grows blood Oxidase (+) Human GI tract is Cholera toxin (CT) A subunit Explosive Diarrhea! Large Immediate &
cholerae agar Lactose (+) reservoir for this (ADP-ribosylates) cytoplasmic G Cholera, remains in inoculum continuous IV
comma Sucrose (+) organism protein (G_s) regulates host SI (duodenum) & needed to or fluid
shaped Enrich in Indole (+) adenylate cyclase. á cAMP non-invasive. infect replacement
bacilli highly Methyl Red (+) Transmitted by oral- levels, induce intestinal cells to along w/
(curved alkaline Urease (-) fecal route (by release Cl- ions into lumen. “rice water” diarrhea electroylates
rods) medium drinking water & Toxin inhibits Na+ absorp, á (large vol. – 1
(loves higher Chk rice-water intaking raw & ions, water release (diarrhea!) liter/hr) “rice”: is Replenish w/
motile pH) stool for motile undercooked seafood, mucus from NaCl / KCl –
(flagella) bacteria, culture on unpeeled fruits) LPS: endotoxin, 6 serotypes intestinal wall. add glucose to
Thiosulfate- TCBS media & see improve
Citrate-Bile- if yellow b/c V. Hortizontal 01: NON-INVASIVE cause No fever involved uptake of salts
Sucrose cholerae ferment transmission amongst epidemics, no age preference but by intestinal
(TCBS) agar sucrose humans usually in children, preg. Untreated patients cells. (try
Women, long-term immunity. may die in hrs due to Gatorade!)
Can grow Large inoculum hypotension,
w/o salt (10^7 – 10^11 cells) Non-01: sporadic infections dehydration, & Tetracycline is
b/c are killed by shock. used for severe
HALOPHIC stomach acidity 0139: INVASIVE infection in cases
indiv. > 40 yrs, no immunity Complications:
Exist in salt water for gained, possible reinfection. - electrolyte
long periods of time / imbalance
found associated w/ Flagelluem (H antigen): an - metabolic acidosis
plankton, shellfish, adherence factor. Motility - hypoglycemia: kid
bacteria to enter into mucous - abortions
layer, non-motile is avirulent.
Dehydrationleads to:
Adhesion factors: mediate - sunken eyes
bacterial adherence to SI - loss of skin turgor
epithelium. AF + CT to cause - patient, comatose
full-blown disease - death
Non-invasive Invasive
Lactose Ferm. sugar Organisms
- ETEC - EHEC Occurs E.Coli, Klebsiella, Enterobacter
- Vibrio cholerae - Shigella Not occur Shigella, Salmonella, Proteus, Pseudomonas (Acinetobacter)
- EPEC - Salmonella Occurs slowly Serratia, Vibrio
I M V C
E.Coli + + - -
Enterobacter - - + +
aerogenes
Cell Colony Lab Source & Virulence Factors Associated Host Treatment /
Features Features Characteristic Transmission Diseases Defenses Prevention
Immunity
Salmonella g(-) Grows on Oxidase (-) Animal & human GI LPS = exotoxin: mediates Non-typical Strong Most often is
Typhimurium almost any Lactose (-) tracts are reservoirs endotoxic shock, involves Salmonellosis inflammatio self-limiting
rod in pairs agar medium Indole (-) (poultry, reptiles such inflammatory response of (Enterco-colitis): n response
AKA or chains large Methyl red (+) as turtles & iguana). intestinal mucosa. S. Resistant Initial invasion of w/ PMN & Treatment
VogesProskauer (-) Oral-fecal route by mucosal cells of T-Cells. enterocolitis:
(S. enteritidis anaerobic Indole (-) consume Invasion factor(s): bacteria ileum & large CMI is - fluid &
or S. enterica) Citrate (+) contaminated water invades host’s mucosal cells of intestines may be important electrolyte
motile TSI (+) H2S or food involved in the ileum & LI. Organism is able followed by systemic b/c of replacement
Urease (-) hort. Transmission. to survive in macrophages, not invasion. intracellular
PMN. location. Antibiotics
Serology: Use antacids Symptoms: FEVER, don’t eliminate
Kaufman – White predispose for Flagellum (H ag): strong nausea, water Salmonella
Scheme infection. motility enable bacteria to enter diarrhea, headache, from GI but â
REMEMBER: KOH into mucus layer. enteric inflammation, duration.
K = capsule, fibriae Chronic carrier status & pus in stools.
O = LPS somatic Inhibition of phagosome- Ciproflaxin,
H = H ag, flagella Cutting lysosome fusion: salmonella Entercocolitis may TMP-SMZ
boards/knives (need multiply in macrophage, then mimic appendicitis (bactrim) used
Culture stools on to clean w/ bleach) lyse macrophage & spread to for systemic
selective medium nearby cells. Bacteremia: intestines infections
Raw eggs to blood stream.
Capsule (K ag): help bacteria Leads to endocarditis, Avoid raw
Survives freezing survive stomach acidity bile duct infection, eggs & use of
water, food or water septic arthritis, antacids
for several weeks Multi-drug resistant factors pneumonia. AIDS
patient may have Wash hands
Enterotoxin: epidermal growth recurrent bacteremia before eating
factor (EGFR) on host cell to
bind to, leads to á Ca in cell. á Osteomyelitis:
leukotriene synthesis opens up salmonella bone
Ca channels lead to rearrange infections arising
actin. Results: leukotrienes á from bacteremia seen
inflammation. in sickle cell anemia
patients
VIR genes turned on inside host
cell ==> antigenic variation Post-inf. Reiters
Syndrom: arthritis,
Pathogenicity island (SP-1, SP-2) HLA-B27
Bacteremia: intest. to
blood stream, subacute
endocarditis, bile duct
inf.
Reiters Syndrome:
arthritis (see S. enterica)
Abortion: enteric fever
* Most invasive! Enterics are resistant to bile
Cell Colony Lab Source & Virulence Factors Associated Host Treatment
Features Features Characteristic Transmission Diseases Defenses Prevent
Immunity
Shigella g(-) Grows on Oxidase (-) Human GI tract & GI Enterotoxin: Shiga toxin has 1. Bacillary Strong acute Infection is
species almost any Lactose (-) tracts of higher same activity. RNase activity Dysentery inflammatory self-limited.
rods in agar forming Indole (-) primates cleaves euks 28S ribosomal RNA. (shigellosis): invades response to
pairs or large gray Methyl red (+) Stops protein synthesis, results in mucosa of LI but not infection by Fluid &
chains colonies. On Urease (-) Can survive for bloody diarrhea. Verotoxin: underlying muscle PMN. electrolyte
EMB, TSI (-) for H2S months, but it is ONLY S. dysenteriae (see chart replacement.
non-motile organism is Citrate (-) delicate. below) Symptoms include: Secretory IgA
colorless or VogesProskauer (-) Watery diarrhea against Antibiotics
Lactose (-) white Five F’s: LPS (endotoxin): epithelial progresses to bloody bacterial shortens
NON-MOTILE!!! - food necrosis end of ileum & colon. diarrhea, fever, & infection duration but
NON- - fingers inflammation w/ pus not lessen
MOTILE SERENY TEST: - feces Polysach. somatic O antigen to in stools. Toxin kill CMI important intensity
(inoculate guinea - flies avoid phagocytosis, serum mucosal cells of b/c of
anaerobe pig or rabbit eyes) - fomites resistant intestine. Often intracellular Bactrim
found in children & location (TMP-SMZ)
Get specimen from Common among Invasion factors: similar to EIEC. elderly. used for
rectal swab, homosexual men Plasmid encoded & mediates serious
sigmoidoscopy invasion & destruction of 2. Hemolytic-Uremic cases, stop
epithelium of colon. Syndrome: Shigella transmission
infection may result .
Commandeering of Actin in actue renal failure, Nalidixic
filaments in host cell for hemolytic anemia, & acid or
mobility in host cell ==> helps thrombocytopenia. newer
-------------------- spread to nearby cells quinolones
Innately 3. Post-Shigellosis
non-motile but Shigella are able to survive Reiters Syndrome: Prevent
once inside the acidity of stomach: infection arthritis associated from
host becomes requires very small inoculum w/ HLA B27 consuming
motile b/c of 50-300 cells uncontaimin
actin filaments ted food &
Multi-drug resistance plasmids water
Test question: Which pair organisms are associated wit h hemolytic-uremic disease? Shigella dysenteriae & EHEC
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Characteristic Transmission Defenses Prevention
Immunity
Bacteroides g(-) Grows Anaerobic growth, Human GI tract is 1. Polysaccharide capsule 1. Intraabdominal Both Debridgement
fragilis anaerobically penicillin resistant resvoir for (K antigen): major VF w/ Disease (abscesses): humoral & & surgical
slender on complex Bacteroides anti-phagocytic activities. opportunistic, associated CMI drainage
rods, pleo- agar Superoxide Attach to peritoneal w/ post-op. peritonitis, involved in before
morphic medium, dismutase (+) MOST numerous mesothelium inf. abdomen w/ combating antibiotic
brain heart bacterial species in intestinal contents Bacteroides treatment
obligate infusion – Catalase (+) human body 2. catalase & superoxide gunshots, stab wounds, infections - clindamycin
anaerobe forms gray dismutase: allows organism surgery, cancer, (80% by
glistening Indole (+/-) Outnumbers E. coli to remain viable for days w/ b. fragilis) UTI in women Seriously ill:
non-motile colonies due in colon. O2 (aerotolerant) lead to pelvic abscesss - chlora-
to capsular Growth in 20% bile (PID), & brain & lung mphenicol
capsule polysacch. Alcoholics, immuno- 3. Enzymes contribe to infection
Antibiotic Resistant compromised Bacteroides (act as Alternatives:
NO - colistin patients, patient w/ spreading factor): 2. Soft tissue & cellulites: - erythromycin
endotoxin - kanamycin anesthesia can lead to - heparinase for mixed infections w/ or moxalactam
activity b/c - vancoymcin pulmonary infections intravascular clotting peptostreptococcus,
it lacks (opportuntistic) - collagenase bacteroides,
Lipid A !!! - hyaluronidase fusobacterium, &
Mixed w/ - lipases actinomyces (all
an/aerobes - nucleases (DNases, anaerobes) Post-opt.,
May have synergistic RNases) cutaneous & or
interaction - Pili / fimbriae mucotaneous infections.
UTI
4. Upper/Lower infection
5. Crepitant cellulites
(especially in foot),
-------------------- usually post-op inf.
Obligate
anaerobe :: 6. DIABETIC FOOT
facultaitive & INFECTIONS
anaeroebe (FECAL FALL OUT)!!!
(10,000: 1 ratio)
Cell Colony Lab Source & Virulence Factors Associated Host Treatment /
Features Features Characteristic Transmission Diseases Defenses Prevention
Immunity
Proteus g(-) Grows on Oxidase (-) Normal flora human 1. Urease: splits urea to NH4 1. Urinary tract IgA, IgG, Ampicillin for
mirabilis blood agar Lactose (-) LI (colon), crap found ions ==> alkaline urine promotes infections: a) made cystitis
pairs or forms large Indole (-) in soil & water. urolithiasis (kidney stones). pyelonephritis against
chains rods “swarming” Methyl red (+) Destroys the urinary epithelium b)cystitis. Infections various Bactrim (TMP-
colonies” w/ Urease (+) Nosocomial or & cause infection & impair may be acute or bacterial SMZ) for
facultative blood agar TSI & SIM (+) for iatrogenic infection kidney fxn chronic. components. pyelonephritis
anaerobe only w/ H2S
putrid odor Citrate (+) UTI can happen in 2. Strong motility: movies up Symptoms: PMN
highly- VogesProskauer (-) healthy & immuno- urinary tract - pain involved in
motile b/c compromised w/ - fever acute
peritrichou Phenylalanine large inoculum ==> 3. LPS (endotoxin) - pyuria infections
s flagella deaminase (+) opportunistic - hematuria (pus is
distinguish from - á urination formed)
P. vulgaris!!! Hortizontal (synchuria)
transmission Macrophage
2. Urolithiasis: Mg- s & T cells
NH4 phosphate salts respond to
form kidney stone chronic
due to NH4 infections
3. associated w/
bacteremia,
pneumonia,
endocarditis
8. FACULTATIVE
INTRACELLULAR
9. Pathogenicity island
VF regulated by
calcium & by
temperature
Fever Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
related Features Features Characteristics Transmission Defenses & Prevention
infection
Immunity
Brucella g(-) Grows Oxidase (-/+) Animals are reservoir 1. Superoxide dismutase: 1. Brucellosis: “Enteric Ab (IgM, IgG) Treated w/
Species slowly on Cabalase (+) for Brucella species. Allows survival w/in Fever” simlar to Typhoid (a)
coccobacilli blood agar Urease (+/-) Zoonotic infection of PMN & phagocytes Fever. Systemic infection CD4 & CD8 oral doxycycline
TSI (+/-) man occurs by contact involves multiple organs, Tcells, cytokines + intramuscular
aerobic Requires No fermentation w/ infected farm 2. Survives in reticular include GI tract, liver, (RES IFN gamma, & gentamycin
blood media N03 reduction animals such as cows, endothelial cells. B. = reticular epithelial organs. IL-2.
non-motile goats, & pigs. Abortus block Organs á, macrophages Granulomas are or
LPS: associated acidification. (spleen, liver, bone marrow, formed by
antigens, A = Hygiene (handwash!) Intracelluarly releases 5’ lymph nodes, kidneys) delayed (b)
abortus antigen & & inhibits May result in enlargement, hypersensitivity doxycycline +
M = (melitensis) Ingestion of raw milk myeloperoxidase halide endocarditis & p.neumonia. rxn. rifampin
antigen, are system to generate toxic
present Erythritol levels in oxygen. Symptoms: IgG á indicates difficult to treat
placenta (breast, - malaise, chills, sweats, & relapse takes 4-6 weeks
uterus, epididymis) 3. LPS (endotoxin) fatigue, weight loss, non- & it is
productive cough & fever intracellular
4. Serum resistance (intermittent).
Pregnant
2. UNDULANT FEVER/ women should
BANG’S DISEASE / use: Bactrimn +
MALTA FEVER gentamycin
- fever is intermittent or
diurnal. Untreated, results Best to
in chronic flue conditions. pasteurization
May also see bone & joint of milk &
infections, severe vaccination of
depression, & farm animals
osteomyelitis.
Granuloma formation in
liver, spleen, bone marrow
& changes in the organs.
5. Chronic (latent)
infection: osteomyelitis,
neurological symptoms,
heptatis
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Charact. Transmission Defenses & Prevention
Immunity
Francisella g(-) Grows on It is Transmitted by direct 1. Lipid capsule: blocks 1. TULAREMIA (RABBIT IgM & IgG are Difficult b/c
Tularensis medium hazardous! method or by vector. Wild phagocytosis & blocks FEVER): ineffective intracellular
coccobacilli containing animals are reservoir. opsonizaiton against
(pleomorphic, blood, 2. Ulceroglandular infection. Antibotics:
very small) glucose, & Zoonotic infection of man 2. LPS (endotoxin) tularemia: contact w/ Granulomas are tetracycline
cysteine occurs by contact w/ infected animal, arthropod formed by DTH gentamycin
facultative (recommend infected wild animals Duch 3. Survive in bite, open ulcer at entry site rxn. T cell streptomycin
anaerobic, chocolate as beaver, rabbit, squirrel & monocytes and PMN (ex. Lower extremity or mediated chloramphenicol
but prefers agar + deer. (protect from ab & trunk), possible bacteremia immunity is penicillin (some)
O2 cysteine) complement). Resistant important to
RABBIT FEVER can be to lysosomal oxidans, 3. Oculoglandular tularemia activate Prevention:
non-motile fatal! include HCl by PMN (eye): conjuctival ulcer, phagocytosis Handling
and inhibits regional lymph nodes, opens for intracellular animals, avoid
Transmissión occurs by phagosome-lysome & drains bloodstream, liver, killing, infected animals
tick, mosquito, or fly fusion spleen, lungs. Invasiness &
vectors. Contaminated goes to the blood stream. Vaccine:
water (ex. Contaminated Live-attenuated
H20) maybe envolved in 4. Pneumonic tularemia: if vaccine used
transmission… also in reach lungs by blood or by only on people
stagnant water. respiratory route (aerosol) at risk animal
then spread by person by handlers
Transmitted via aerosols person. High mortality rate.
Especially inhaled version!
Inoculum size to be ill:
10 bugs tick bites 5. Typhoidal tularemia:
50 bugs if inhale ingest food or water (larger
10^8 ingested inoculum size) GI & fever
symptoms can cause sepsis
w/ multi-organ involvement,
even pneumonia
6. Glandar: painful
adenopathy w/ overlapping
ulcers
Cell Colony Lab Source & Virulence Factors Associated Diseases Treatment /
Features Features Charact. Transmission Prevention
Bartonella g(-) White, rough, Oxidase (-) Cats (blood) are reservoir 1. LPS (endotoxin) 1. Bartonellosis (CAT Self-limiting
henselae mixed w/ tan Catalase (-) SCRATCH FEVER): symptoms
curved rods circular Zoonotic infection of man 2. Type IV pili – adhesion, begin 2 weeks exposed. Local Can scratch
Easy to see w/ occurs by the bite or twitch motility lymphadenopathy (lymph disease treat w/
aerobic Grow slowly Ag scratching of an infected nodes), fever, & pustules at needle aspiration
on selected impregnation cat 3. Facultative intracellular scratch site. It is self-limiting but NO
motile blood agar techniques pathogen last months to years. Forms antibiotics
Man to man transmission granuloma.
twichting 15% CO2 NOT observered Bacillary
motility 2. Bacillary angiomatosis: in angiomatosis &
Facultative Can survive in saliva, immunocompromised patients sepsis treated w/
intracellular inhale lice feces, crushed (AIDS) observe chronic erythromycin
pathogen lice spreading cutaneous & visceral
lesions, Kaposi’s sarcoma-like
Causes conjuctiva infection lesions may appear, differ
histologically.
Bacteremia & sepsis may also
occur in these patients
3. Sub-acute bacterial
endocarditis
5. Conjunctiva infection
(Oculoglandular syndrome):
swelling of eye, jaw, cervical
lymph nodes
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Charact. Transmission Defenses & Prevention
Immunity
Pasteurella g(-) Grows on Oxidase (+) Animals & birds are 1. LPS (endotoxin) Acute cellulitis: symptoms T-cell mediated Penicillin or
multocida blood agar Catalase (+) reservoir, upper include erythrema, swelling, immunity is ampicillin &
coccobacilli produce Indole (+) respiratory tract & saliva 2. Large polysaccharide, & pain at bite / scratch site. important. tetracycline.
w/ bipolar yellow Methyl red (-) are involved in capsule: anti- Usually the host injuries Strong acute
staining colonies w/ Non- transmission. phagocytic occur on leg, arm, or face. inflammatory Allergic patients
“musty” hemolytic response w/ - doxcycline
facultative odor Sucrose Zoonotic infection of man 3. Pili – mediates Associated w/ severe bites! PMN is very
anaerobe utilization (+) occurs by the bite or attachment important Avoid contact
Grows best scratching by infected dog Complications include: w/ wild &
non-motile w/ 02 at or cat. 4. beta lactamase: in - tendonitis domestic
37C some strains - osteomyelitis animals & birds
intracellular Man to man transmission - abscess formation
pathogen not observed
Leads to systemic septicemia
Commensals in some or meningitis
animals
AIDS patient: complication
includes sepsis
Flea Cell Colony Lab Charact. Source & Virulence Factors Associated Diseases Host Treatment /
borne Features Features Transmission Defenses Prevention
Immunity
Yersinia g(-) Grows on Oxidase (-) Animals are the 1. LPS: fatal, septic shock BUBONIC PLAGUE: Granulomas ASAP! w/
pestis blood agar. Catalase (+) reservoir – Zoonotic 2. V and W antigens: exact f(x) w/in 2-3 days of flea-bite. are result of Streptomycin
short Lactose (-) (also Vector-borne unknown but involved in Symptoms include: fever, DTH.
coccobacilli Epicellular- Urease (-) infection) extracellular survival as well as chills, painful Chloramphenicol
w/ bipolar grows both Methyl red (+) intracellular survival & lymphadenitis (buboes). Acute Tetracylcine
staining on tissue & VP (-) Fleas from infected multiplication in macrophage; Inguinal, axillary, femoral inflammatory
on plates animals RODENTS, Resists phagocytic killing & are & cervical lymph nodes response by Hypotension use
facultative Gram satín & rats, & squirrels facultative intracellular involved, & may swell. PMNS. Both dopamine.
anaerobe Grows best Wayson’s satín involved in pathogens. Bacteremia, sepsis CMI and
at 28C w/ to look for transmission of disease 3. Coagulase: blood to clot follows. Vasculitis may sIgA and IgG Disease is
non-motile oxygen bipolar cells to humans. Fatal during flea bloodmeal, lead to gangrene (Black are important prevented by
transmission, & regurgitate into the next bite death, necrosis of against rodent control
facultative Direct immuno- survives for several capillaries, blacken body). infection. but also need to
intracellular fluorescence months in infected 4. Fibronolysin: produced, Infection is fatal. If control rat flea &
pathogen carcasses, sputum, & breaks the clot & spreads swallowed, stools maybe human flea. Use
flea feces. bloody + pus (enteric pesticides.
5. Iron acquisition: inflammation). May last
May cause enteric - takes up iron (hemin) by for weeks w/ treatment.
disease from ingest siderophore-independent
contaminatation. Produce siderophore (only one) Septic plague: NO
occurrence of buboes,
Inhalation of 6. Protein capsule-complex: found in children bites
aerosolized Y. Petsis Fraction1: not produced in rat from flea. Leads to
from infected humans flea – plasmid encoded allows intravascular coagulation
or while handling for survival inside of w/ vascular & renal
infected live animals phagocytes collapse.
carcasses. 7. Promote invasion &
proliferation within host cells Pneumonic plague:
Pneumonic Plaque and resistant to killing by host already in lungs, inhales.
(rare & deadly!) LCR plasmid products are Results in
expressed at 37C and at âCa++ bronchopneumonia.
Sylvatic plaque which directs V and W antigen Symptoms include: fever,
(transmit by fleas on synthesis. cough w/ blood & loaded
rabbits, squirrels vs. 8. Pesticin: bacteriocin, makes w/ bacteria. Deadly &
urban plaque spread by the organism more virulent rarest form. HIGHLY
rats) Flea jumps onto 9. pur protein: allows uptake of INFECTIOUS! 90-100%
human. Then spread adenine & guanine nucleotides death rate.
human to human. 10. pigment production
11. Pathogencity island Sylvatic plague: fleas on
Organism survives in 12. YopE, disrupt actin filament rabbits, wild rats to fleas
animal blood & flea gut 13. YopJ/P: initiate apoptosis on urban rats to human
14. Plasminogen activator fleas to human.
15. Type III: secretion system
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Features Features Charact. Transmission Defenses & Prevention
Immunity
Rickettsia g(-) Grown in Weil-Felix Vertebrate animals are 1. LPS (endotoxin) Highly infectious (but lowest Ab may be Oral
Typhi cell culture Rxn reservori for R. typhi in pathogenicity of the important doxycycline
small (agglutinate particular rats. Zoonotic 2. Factors inducing Rickettsia). 10 organisms to initial barriers (makes teeth
Aka coccobacilli w/ Proteus infection of man occurs by phagocytosis. Inside cause disease! against yellow in
vulgaris) ex: bite of infected flea phagocytes the infection. children)
R. Mooseri non-motile (vector). In infected flea organism survives & 1. Endemic flea-borne Previous
Ox-19 (+) (rat, cat). enters into the host TYPHUS aka Murine typhus infection Preg. Women
Vec./spec aerobic Ox-2 (-) endothelial cells. Evade Systemic inf. following a flea confers long- are treated w/
Flea-ty Ox-K (-) Maybe transmitted by host cell lysis (escape bite. Rickettsemia causes lasting chloramphenicol
end OBLIGATE transovarian method from cell). vasculitis of the capillary immunity.
INTRA- (moma fly to baby fly) beds of many organs Killing rat is
ENDEMIC CELLULAR 3. Produe particularly of the liver & Observed cross- not enough, b/c
PATHOGEN Also flea bites (w/ feces) phospholipase A skin. immunity w/ flea could jump
Radiates transmitted into bite (lecithinase) which R. prowaseckii. to humans.
outward wound. lyses phagosomes Typhus produces fever,
enabling rickettsia to chills, headache, & macular
enter into host cell rash mosly on trunk
cytoplasm. (hallmark) and may
eventually spread outward
4. Organism able to to extremities.
survive in rat blood &
flea feces This differs from Spotted Fever,
rash start on palms & soles &
5. Loosely adherent radiate inward to trunk.
slime layer.
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Louse-Borne Features Features Charact. Transmission Defenses & Prevention
Immunity
Bartonella g(-) Grows very Oxidase (-) Humans were thought to 1. LPS (endotoxin) 1. Bartonellosis – Trench Both IgM and Doxycycline or
Quintana slowly on Catalase (-) be only reservoir BUT 2. Facultative Fever (5 day fever). IgG are chloramphenicol
(Rochalimaea curved rods selective cats too. Indirect intracellular pathogen Remember it is facultative important
Quintana) agar transmission from man intracellular & has Pregnant women
motile medium to man occurs by BITE of periodicity cycle in 5 day - erythromycin
“Trench (twitching) the VECTOR, the body periods. Symptoms include
warfare” louse fever, headache, exhaustion.
aerobic áâ temp. during this
Epidemic periodicity (Quintana),
responsible OBLIGATE chills severe bone pain &
INTRA- transient rash on trunk &
CELLULAR may see splenomegaly &
PATHOGEN myalgia. Self limiting but
may relapse.
2. Reemerged in AIDS
patient & homeless
(immuno-compromised)
Epidemics is common.
3. Copmlications: CNS
dysf(x), myocarditis
Cell Colony Lab Source & Virulence Factors Associated Diseases Host Treatment /
Tick-Borne Features Features Charact. Transmission Defenses & Prevention
Immunity
Rickettsia g(-) Grown in Weil-Felix Animals (wild mammals 1. LPS (endotoxin) 1. Rocky Mountain Spotted Ab may be Oral do Oral
rickettsii cell culture Rxn & birds) & hard ticks Fever (RMSF): Systemic inf. important doxycycline
very small (agglutinate 2. Produce factors following a tick bite (tick initial barriers
coccobacilli w/ Proteus Zoonotic infection of inducing saliva). Rickettsemia against inf. Pregnant
vulgaris) ex: man occurs by bite of phagocytosis. Inside causing vasculitis of the Previous inf. women are
Mnemonic non-motile infected tick (vector). phagocytes the capillary beds of many confers long- treated w/
vect/spec/dis Ox-19 (+) organism survives & organs particularly of the lasting chloramphenicol
Ricky-ticky aerobic Ox-2 (+) Infected tick, organism enters into the host lungs & skin producing a immunity.
spot Ox-K (-) may be transmitted to endothelial cells. fulminant disease. Prompt removal
OBLIGATE tick offspring by Evade host cell lysis. of ticks also
Caus. Agent: INTRA- transovarian method. Symptoms: important as
Rocky Mount. CELLULAR 3. Produces - rapid onset, high fever, preventive
Spotted Fever PATHOGEN phospholipase A nausea, vomiting, myalgia, measure.
(RMSF) (lecithinase) which headache see macular rash
#1 rickettsia lyses phagosomes
disease & non- enabling rickettsia to Rash spreads from
vector borne enter into host cell extremities to trunk. (rash
disease in US cytoplasm (also works inward)
pop. deacidify vacuole)
Disease may lead to
Also note: Has to be attached 24-48 4. Organism is able to pulmonary failure, renal
Tick’s may hr in order to become survive in rat blood & failure, encephalitis, coma,
deliver encouraged w/ blood & flea feces & death.
Rickettsia or to transmit the organism
lyme disese to man. 5. Slime layer
Test Question: #1 non-vector borne disease in US Rocky Mountain Spotted Fever – primarily found on East coast
Test Question: #1 vector borne disease in US Lyme disease (carried by tick)
Spirochetes (cork screw) Chlamydia
- outer most layer is referred to as an outer sheath (glycosaminoglycan) - Gram (-), obligate intracellular organisms w/ unusual “life cycle”
- underneath is the outer membrane (peptidoglycan, lipids + covalently linked - NOT spirochetes!!!
proteins) - Obligate intracellular parasites !!! Can not synthesize ATP!
- encase the periplasmic space where endoflagellae are located o No cytochromes or flavoproteins. Can’t metabolize glucose to pyruvic
- directly underneath the periplasmic space is inner membrane (cytoplasm) acid using pentose phosphate pathway
- Cytoplasmic tubules (body fibrils)
- NO LPS Chlamydia Life Cycle:
- Has a layer of peptidoglycan 1. Small dense cell: ELEMENTARY BODY (infectious form but NOT replicating)
it is outside of the host. Enters the host via phagocytosis DNA:RNA, 1:1 ratio =
Test Question: Endoflagella (axial filaments) inside of outer membrane NOT exposed to infectious particle
outside but can be shed in infected individual. Lives in intestines & in mouth 2. Next 8 hr, elementary body reorganizes into large, less dense cell called
reticulate (or initial) body
3. Reticulate body: (this replicates) , grows in size & divides by binary fission
(DNA:RNA ratio is 1:4) this is NON-INFECTIOUS form
4. 24-48 hr, reticulate bodies reorganize into dense elementary bodies &
developmental cycle is complete when host cell liberates the small dense
infectious cells.
Serology
a) Non-specific blood tests: (agglutination) indicate present infection, since
individual become (+) upon infection but levels decrease during chronic disease.
Interrogans:
shape, question
marks ???
complex outer
membrane
__________ structure
* Twitch contains LPS
motility
differs from
spirochetes
Lyme Cell Colony Lab Source & Virulence Associated Diseases Host Treatment /
disease Features Features Charact. Transmission Factors Defenses Prevention
Immunity
Borrelia Thin Cultured in Darkfield Primary reservoir is the 1. Glycolipid LYME DISEASE: > 1 stage IgG and IgM Stage 1:
burgdorferi vitro microscopy mouse including white (similar to against outer Oral doxycycline
Loosely coiled food mouse, dusty footed Treponema) NO Stage 1: appears surface
long spirals Grown on Use ELISA wood rat, chipmunks, LPS - Erythema Migrans (EM) or antigens Stage 2 & 3:
#1 vector (spirochete) Barbour- and DEER. Erythema Chronicum Migrans: (Osps) IV ceftriaxone
borne Stoenner- Western blot 2. Surface protein: Lesion or rash (Bull’s eye lesion) important
disease US g (-) Kelly also PCR Vectors are the primarily produces many - Symptoms: but undergo
medium Ixodid ticks different surface headache, fever, stiffneck, malaise, antigenic Prevention Tips
Use darkfield contains antigens during & lymphadenopathy. variation. Dress properly
microscopy, bovine infection. w/o skin
fluorescent serum ANTIGENIC Stage 2: exposed, use
miscroscopy + albumin VARIATION - Lyme arthritis (uniarticular ie insect repellent
acridine (BSA) & involving 1 joint) Reversible w/
organe dye or rabbit 3. penetrate treatment.
Infection of man occurs
stained by serum at epithelial cells - Symptoms: neuroborreliosis
by tick bite & transfer of
Silver 30C (meningitis, peripheral
organism during tick-
impregnation 4. Survives in blood neuropathy, encephalitis, Bell’s
engorgement!
technique. & in tick – ability to Palsy) may last for months – years
Transmitted in vector by
transovarian route. Also resist phagocytosis
Microaerophilic Stage 3:
tick saliva or deposition
5. Hemolysin Follow a latent & asymptomatic
of feces into wound.
Rotational period. Late or Chronic Lyme
motility disease.
(endoflagellae, Symptoms: similar to stage 2 but
axial filaments) worse. Mostly arthritis.
DNA is
fragmented w/
some being
linear
Cell Colony Lab Source & Virulence Associated Diseases Host Treatment /
Features Features Charact. Transmission Factors Defenses Prevention
Immunity
Borrelia Thin Cultured in Darkfield Humans are believed to 1. Glycolipid Relapsing Fever: > 1 stage IgM & IgG Oral doxycycline
recurrentis vitro microscopy be only reservoir against outer Penicillin
Loosely coiled (epidemic form of 2. Surface protein Stage 1: surface Tetracycline
Grows disease). Chloramphenicol
long spirals (VARIABLE 1st fever symptoms (maybe fatal antigens are
“relapse (spirochete) slowly on MAJOR due to shock-hypotension). important Erythromycin
fever” complex at Vectors for the epidemic PROTEIN) which Spirochetes from lice (or tick) leads to (children &
g (-) 30C organism are lice produces many penetrate the skin & skin & spread complement- pregnant women)
Epidemic (therefore, louse-borne different surface through the blood. Treat w/ dependent
Use darkfield disease) antigens, resulting antibodies will clear most lysis.
microscopy, in several relapses circulating organisms, so host
fluorescent Endemic form of disease (ANTIGENIC experience a non-febrile latency Cytokines
miscroscopy + is found in animal & VARIATION). period 7-10 days. may be
acridine human reservoirs & involved in
organe dye or appear to be spread by 3. ability to Stage 2: disease
stained by ticks. penetrate epithelial Spirochetes go through antigenic resolution
Silver cells variation & a new variant will be
impregnation produced. Results in bacteremia &
technique. 4. Survives in blood a second fever stage (relapse).
& in lice – has the
Microaerophilic ability to resist
phagocytosis
Rotational
motility
(endoflagellae,
axial filaments)
DNA is
fragmented w/
some being
linear
NOT Cell Colony Lab Source & Virulence Associated Diseases Host Treatment /
spirochetes! Features Features Charact. Transmission Factors Defenses Prevention
Immunity
Chlamydia g (-) does not Grows in Difficult to Humans are reservoir. 1. Intracellular Male STD: most common STD in Ab not Oral doxycycline
trachomatis have typical cell culture diagnose. survival US. Urethritis involve urethral effective. Sulfonamide
cell wall of Infection of man occurs a) stimulates non- discharge. (SYPMTOMATIC) (unique)
peptidoglycan LGV test by sexual contact & by phagocytic PMN
but sensitive to dead bacteria autoinoculation to other epithelial cycle to Female STD: Cervicitis, effective in Erythromycin
Penicillin injected parts of body. engulf them endometritis, PID involve killing.
Most under skin & discharge. May cause sterility Cefoxitin &
common compact look for DTH. Mother to child b)Inhibit women are ASYPMTOMATIC doxycycline if
STD inclusion body transmission is possible phagosome- concurrent w/
w/ glycogen, Serology at birth. lysosome fusion Swimming Pool Conjunctivitis: N. gonorrhea
make folic acid 15-20 (all 3 chlamydia Spread by fingers, fomites & even infection
therefore different Maybe transmitted by have them!) chlorinated water into eye.
sensitive to serotypes direct contact with ADULT INCLUSION Antibiotics such
sulfonamide fingers, contaminated 2. Unusual life CONJUCTIVITIS: STD as erythromycin
ONLY!!! towels & clothing. cycle: elementary or tetracycline
(differs from . bodies can infect TRACHOMA: are used in form
C. psittachi) Can be transmitted host macrophages Chronic eye inflammation by of eyedrops for
sexually to other adults & epithelial cells, infecting eye. new borns.
leading to genital becomes reticulate
symptoms. Can be bodies & produce Lymphogranuloma venerum:,
spread by fingers, new elementary (LGV): develop into buboes and
towels, clothing… can bodies ==> lead to elephantiasis of genitalia &
even spread in released when host rectal structures as result of
chlorinated water cell lyses. perirectal scarring.
(swimming pool
conjunctivitis) 3. Endotoxin Neonatal infection:
Due to vaginal passage can cause
4. “toxic factor” disease by either being aspirated
into lung or by conjuctiva of
5. Type III Secretion neonate.
system a) Infant atypical pneumonia:
- long term complications & otitis
media
b)Inclusion conjunctivitis:
may have similar to trachoma
Reiter’s Syndrome:
Arthritis, periostitis on calcaneus
(heel) pain AKA Lover’s Heel
NOT Cell Colony Source & Virulence Factors Associated Diseases Host Treatment /
spirochetes! Features Features Transmission Defenses Prevention
Immunity
Chlamydia g (-) does not Grows in Contact w/ parrots & 1. Intracellular survival: Psittacosis (ornithosis) Ab not Doxycycline and
psittaci have typical cell culture other psittacine birds can a) stimulates non- PARROT FEVER: effective. azithromycin
(psittaci) cell wall of spread to other animals phagocytic epithelial cycle Can exist as asymptomatic,
peptidoglycan to engulf them Alternatives:
(cattle, swine, cats, dogs) likely to be severe, PMN very
Ofloxacin,
Parrot but sensitive to frequently fatal effective in erythromycin,
Fever Penicillin Can get into: b) inhibit phagosome- pneumonia. Can involve killing. amoxicillin
environment from feces lysosome fusion other organs: jaundice, (pregnant women)
diffuse & survive a long time ! (all 3 chlamydia have acute thyroiditis, Previous
inclusion body them!) meningitis w/ delirium. It infection Quarantine
is a latent infection. Lung provides no imported birds
no glycogen 2. Unusual life cycle: inhaled form it is atypical immunity &
Elementary bodies can pneumonia. Spread by subsequently
can’t synthesize infect host macrophages & human to human. see relapse &
folic acid, epithelial cells reinfection.
resistant to
sulfonamide! 3. Endotoxin similar to LPS
4. Toxic factor
Madurella Spores
Hortaea Wereckii = Exophiala Werneckii : - thermally monomorphic molds, dematiaceous
- Dematiaceous fungi or pigmented fungi - true fungal infection, brown-colored
o Non-invasive Disease - fungal mycetoma (Eumycetoma)
o Pigmented (b/c melanin production) - madura foot, resembles nocardiasis (actinomycetoma)
- Disease: Treatment - difficult to cure
o Produce superificial inf. of skin, Tinea Nigra (black growth on skin)
but non-invasive
o Skin infections, non-scaly, smooth, brown-black painless spots
SYSTEMIC INFECTIONS: (Inhales into lungs) OPPORTUNISTIC INFECTIONS: (Colorized, immunocompromised state of host)
- ALL thermally dimorphic
- True, frank, primary pathogens Aspergillus fumigatus:
- Via respiratory rate (inhaled spores) - thermally monomorphic mold
- inhale spores immunocompromised patients
Blastomyces dermatitidis: - Fungus ball (aspergilloma) spore germinate (Farmer’s Lung) HAY FEVER!!!
- yeast like fungus, looks like figure 8’s - A. Flavus produces aflatoxin potent liver carcinogen. INVASIVE!!!
- multi-nucleated, forms granules of skin
- no cell wall, bird droppings Candida Albicans:
- Mississippi river to East coast - Dimorphic but NOT thermally but grown on corn-meal produce pseudophyae
Dxn - multi-nucleated budding yeasts, single broad-based 888’s - Use as diagnositic: Germ tubes test (true hyphae) this is a unique feature!
Disease - NAmerica blastomycosis (mild pulmonary inf), skin lesion - Part of normal flora (FurFur & tricosporum???)
- Formation of granulomas of skin & bone - Produces ==> chlamydospores are unique to this candida
- cream-colored pasty colonies
Paracoccidiodes brasiliensis: Transmission - normal commensals of human & animal GI, resp, tracts skin &
- thermally dimorphic yeast-like fungus female genital tracts
- UNINUCLEATE!, multiple budding mother cell w/ buds having narrow bones Disease ORAL THRUSH: (AIDS immunocompromised)
- Cause systemic infection, more mucosal surface - produce white patches in mouth & tongue continue to GI tract
- Found mostly in S. America blastomycosis (granulomatous spreads to lungs to other Cutaneous candidiasis: diper rash
mucous surfaces of nose, mouth, & GI tract) INTERTRIGINAS CANDIASIS (Intertrigo):
-Looks like ship’s wheel, steering wheel, pilot wheel - appendages immersed in H20 long periods, moist parts in diabetes
- endemic ONYCHOMYCOSIS: nail inection
VAGINITIS: (Moniliasis): vaginal infection of women
Coccidioides Immitis (C.Posadasii) Chronic Mucocutaneous Infection:
- dimorphic fungus: changes form to spherule at at 37C - CMI failure (T-cell deficiencies) infection associated w/ skin, oral
Cell feature - terminal arthrospores attached directly to hyphae mucosa, respiratory mucosa, GI & GU mucosal surfaces
- spherules in tissue specimens, barrel shapped! Treatment - antibiotics
Transmission - direct inhalation (mold spores, arthrospores) from soil &
dry climates Southwest US (Central or S. America) Cryptococcus Neoformans:
- likes Nitrogen associated w/ bird droppings (feces) - capsule, visible w/ India ink
Disease - Coccidiomycosis, highly infectious disease flue-like - thermally monomorphic yeast
pulmonary infection, CNS (Meningitis)!!! - capsule is anti-phagocytic
- Leads to erythema nodosum (DTH response, red tender Cell feature - oval shapped
nodule on skin) Dxn - Mayer’s stain to see PINK capsules
- Desert rheumatism “San Joaquin Valley Fever”Cali - CSF sample prep. w/ 10% KOH & India ink
- ID test looks for DTH response Disease - result in cryptococcosis (pulmonary infection)
- to meninges & brain thrives on CSF (Meningitis)
Histoplamsa Capsulatum Var. Capsulatum: - occurs often immunocompromised
- dimorphic yeast-like fungus & small oval microconidia - can be unrecognized or asymptomtic
- spiny macroconidia attatched to hyphae, knobby (tuberculate macronidia) Transmission - Via inhalation of yeast found in soil & pigeon droppings
Transmission - direct inhalation of small molds (microconidia) from soil or bird Treatment - Ampotericin B & Latex agglutination!
droppings. They are spiny & knobby looking!
- Mississippi + endemic, Ohio River, S. America, & Africa Mucormycosis (Phycomycosis or Zygomcosis): mucor, absidia, rhizopus species
Disease - Most common respiratory mycotic inf pneumonia, granuloma - invades tissues, brain (nasally) it is a bright mold!
- reticuloendothelial system (RES) found intracellularly w/in Cell feature - aseptate or coenocytic & invasive
macrophages. Like at TB test can use DTH - member of Zygomycetes (phycomycetes)
- Chronic disease: reactivation enlarged granuloma, liver, spleen… - sporangia form at 90 degree angle from hyphae
INDI Organisms # 4
Virus
Size & Structure
• 20-300 nm size (picornavirus ==> poxvirus) appears spheres or rods
• Contain either DNA or RNA, NOT both!
• All have a protein coat, capsid (repeating capsomers)
o Capsid could is outer surface
o Others could have lipoprotein envelope composed of phospholipids bilayer
§ Enveloped: picked up from nucleus or p.membrane or created from cytoplasm ether sensitive
• Composed of nucleic acid & capsid protein is called nucleocapsid
• Shape: spherical (icosahedral) or helical symmetry
o Exception: poxvirus looks like a brick shaped (complex)
• All human viruses have helical nucleocapsid are enveloped
• No naked helical viruses infect humans.
• Icosahedral nucleocapsid can be either enveloped or naked
Virus Family DNA type Virion Envelope DNA replicates in: Major viruses
(associated polymerase)
Parvovirus ssDNA No Naked Nucleus B-19
Papovirus dsDNA No Naked Nucleus Papilloma
circular Polyoma
Adenovirus dsDNA No Naked Nucleus Adenoviruses
linear
Herpes virus dsDNA No Enveloped Nuclues; virus HSV: Varicella-
linear (nuclear) assemble in nucleus Zoster, EBV
Virus Family RNA structure Virion Envelope Shape Multiplies Major viruses
(associated polymerase)
Calicivirus ss(+) RNA No polymerase Naked icosahedral cytoplasm Norwalk agent
Linear hepatitis E
Non-segmented
Picornavirus ss(+) RNA No polymerase Naked icosahedral cytoplasm Polio,
Linear Enteroviruses
Non-segmented Rhino
Coxsackie
Hepatitis A
Flaviviros ss(+) RNA No polymerase Enveloped icosahedral cytoplasm Yellow fever,
Linear dengue, St.
Non-segmented Louis
encephalitis
Hepatitis C
Togavirus ss(+) RNA No polymerase Enveloped icosahedral cytoplasm Rubella, WEE,
Linear EEE, Venez
Non-segmented encephalitis
Coronavirus ss(+) RNA No polymerase Enveloped Helical cytoplasm Cornoavirus
Linear
Non-segmented
Retrovirus Diploid RNA dep. Enveloped Icosahedral Nucleus HIV, HTLV,
ss(+) RNA DNA or Sarcoma
Linear Polymerase truncated
Non-segmented conical
Mnemonic: Call Pico and Flo To Come Rightaway
Papovaviruses:
• group of DNA viruses that produce benign & malignant tumors
• virus types:
o Papilloma: HPV types 1-58+. Causes human, cat, dog, & rabbit warts
o Polyoma: found in mice which are asymoptomatic. If induced into newborn animals results in malignant tumors
• virus structure:
o icosohedral capsid virion, dsDNA, circular, replicated & assembled in nucleus
o p53 and RB regulates cell growth but papovaviruses binds to them to promote cell growth
o T angitens regulates transcription with the p53 and RB, T antigen is found w/ viral DNA for replication to continue in cell.
• Papovaviruses:
o Papillomaviruses replicate in the squamous epithelium of skin & mucous membranes to produce warts
o Skin warts, anogenital warts (cervical cancer, 16,18 where E1 & E2 become inactivated so that E6 binds to p53 & E7 w/ RB)
§ Koliocytosis: infectious human papillomavirus of epi layer of uterine cervix or external genitals (condylomata acuminata)
§ Hyperkeratosis: inflammation w/ excess growth of prickle cells of skin
• Treatment warts:
o Remove surgically cryotherapy (liq. N2), electric, or chemical means (ex. podophyllin)
o Laryngeal warts: remove surgically but NOT w/ irradiation b/c could induce malignant changes
o Imiquimod + IFN can promote faster healing applied to topically (ex. external genital regions)
o Cidofovir: antiviral nucleoside inhibits viral DNA polyermase
Adenovirus:
• Virus structure:
o dsDNA, naked, icosahedral, linear shaped, fiber (attachment protein + hemagglutinin activity)
o 47 different types, permissive, found in human adenoids & tonsils
• Important misc facts:
o Associated with conjunctivitis, GI tract, and upper respiratory disease (common cold).
o Produce tumors in baby hamsters but NOT in humans.
o Most common infection of tonsils & adenoids in early child life is from adeno types 3 & 7 and is latent.
Parvoviruses
• The ONLY ssDNA, naked, icosahedral, linear, e-nucleated w/ mature RBC
non-defective defective
replicates only in multiplying host cells requires helper virus (Dependo virus) ex. of
helper virus is (Adenovirusand Herpes Virus)
• Disease:
o Erythema infectiosum (fifth disease) - comment: remember a 5 finger slap in the face you get this redness!
o 1 of 5 common childhood exanthems or rashes (looks like slapped cheek (facial rash)
o Chronic hemolytic anemia (ex. sickle cell anemia) leads to aplastic crisis (lytic on RBC)
o Immunodeficient can lead to chronic anemia
• transmitted:
o vertically (cross placenta) results in spontaneous abortion associated w/ HYDROPS FETALIS
Herpesviruses
• dsDNA, enveloped, icosahedral, linear shaped,
• tegument: contains viral proteins & enzymes involved in initial replication
• Lab diagnosis:
o Tsanck smear (scrapings of infection) see Cowdry Type A cells (acidophilic intranuclear inclusion bodies) see syncytia
• Virus replication:
o Virus induces synthesis of viral thymidine kinase & DNA polymerase
o Phosphonoacetic acid inhibits herpesvirus replication by inhibiting viral DNA polyermase
o Viral protein are made in cytoplasm & enters the nucleus where they assemble w/ the DNA into virus particles
o Virus buds from nuclear membrane, pickup lipid bilayer & viral proteins that have been inserted into it.
o Infection can be lytic or lead to latent infection
Latent in nerves - Herpes Type 1 & 2 (HSV-1 & HSV-2)
- Varicella-Zoster:
a) chicken pox: (varicella portion) acute infection (children)
b) shingles: reactivation of virus of chicken pox
Latent in - Epstein Barr Virus (EBV)
leukocytes-WBC a) Burkitt’s lymphoma (tumor in jaw), nasopharyngeal carcinoma
b) infectious mononucleosis
HSV-1 (usually infects above waist) HSV-2 (usually infects below waist)
- Location of latent: Trigeminal dorsal root ganglia - Location of latent: Lumbo-sacral dorsal root ganglia
- Acute herpetic gingivostomatitis: most common - Genital Herpes: lesions develop in genital organs.
infection for Type 1. Gums swollen! Similar to herpes - Neonatal Herpes: transmitted to new borns
labialis. Oral herpes. Self-limiting. - Aseptic meningitis:mild, self-limiting
- Eczema Herpeticum:(Kaposi’s similar to Herp 8) infect
fingers (herpes whitlow)
- Keratoconjunctivitis: infects eye
- Herpes labialis:(cold sores!!) NOT common cold, most
common recurrent disease.
- Encephalitis: residual neurologic defects
• Varicella-Zoster
Chicken pox (multiple crops) Shingles
- occurs in children via mucosa the upper respiratory tract - occurs in the posterior nerve & ganglia (Dorsal RG)
- swelling of epi cells, eosinophilic inclusions found in - reactivation of the chicken pox
nuclei of infected cells & end up attacking nerve cells - triggered by stress, immunocompromise, trauma
- virus replication occurs in the nucleus
- incubation time: 2-3 weeks
- symptoms: fever, fash, vesicles appear
- differs from small pox (1 crop)
• Treatment:
o Acyclovir, vidarabine, idoxiuridine, trifluoridine
Poxvirus
• Virus structure:
o Largest DNA, enucleated, complexed shape
• Virus replication:
o ONLY DNA replicates in the cytoplasm
o Replicate in enucleated cells
o Virus DNA and proteins are packaged into virus particles occurring in cytoplasm in the Guarnieri bodies
• Small pox:
o 2 variants, enters in the mucous membranes of upper respiratory tract with incubation of 12-16 days.
o Virus multiplies in lymphoid tissues with infection throughout the body. May result in scaring.
o Diagnosis: Incoluated in embyronated eggs
o Treatment: cidofovir (inhibits DNA polyermase) also it is safer w/ less side effects
• Molluscum contagiosum
o An ex. of a pox virus leads to skin infection, benign tumor, it is a nodular-wart-like growth
o Transmitted: direct contact or fomites & spread by STD
o Treatment: curettage (scrape) or liquid N2
Picornaviruses
• Enteroviruses (intestine)
o Polio and coxsackie viruses
• Rhinoviruses (nose): common cold
• Cardiovirus: in rodents
• Virus characteristics:
o (+)ssRNA, naked, icosahedral, smallest RNA virus, nucleic acid is infectious
o Poliovirus: stable in acidic environment pH 3-9. Found in GI tract & in feces
o Rhinoviruses: unstable in acidic environment pH 5-6. Found in oropharynx area
o Replicates at 33C.
• Poliovirus
o Smallest RNA, 3 serotypes (1-3): 1&2, 2&3 cross react, 1 & 3 doesn’t cross react
o Inactivated by UV, drying. 1M MgCl2 thermally stabilizes b/c of the capsid proteins.
o Immunological properties:
§ C antigencity is the empty capsid which lacks the vRNA. NO VIRUS RNA
§ D antigencity: is the native complete virus HAS VIRUS RNA
o Host: man is the ONLY natural host
o Virus replication: adsorption (complete particles) ==> penetration ==> uncoating ==> translation (replication) ==> synthesis of
vRNA ==> maturation ==> release
o Disease: Starts oral route. Multiples in tonsil, lymph nodes, Peyer’s patches in SI. Asymptomatic shedding
Infection Ingested virus
Alimentary phase Oropharyngeal, virus in throat, intestinal mucosa
Lymphatic phase Tonsils, deep cervical lymph nodes, virus in feces, peyer’s patch,
Viremic phase Blood
Neurological phase CNS, extraneural tissue, regional nerve ganglia
• Coxsackieviruses (enterovirus)
o Coxsackie A: Found mostly in respiratory region. flaccid paralysis
o Coxsackie B: Found mostly in the body region. spastic paralysis
o Diseases:
§ Nonspecific febrile illness: Can lead to polio-like paralytic disease
§ Herpangia:fever, soar throat, anorexia, vomiting, abdominal pain, vesicles in palate, uvula. Self limiting. Not herpes!
§ Pleurodynia: chest pain (Bornholm disease: Devil’s grip)
§ Hand-Foot-Mouth: oral & pharyngeal ulcers which may spread to arms & legs w/ mild fever
§ Mycoardiopathy: mycocardial disease in adults & children
§ Common cold: upper respiratory infection
§ Diabetes Melitis:abrupt onset of diabetes after infection w/ coxsackie
o Control:
§ Spread by feces, pharyngeal secretions, sewage
• Rhinoviruses
o Virus characteristics:
§ Common cold, at pH < 6-7 (unstable in acidic environment), found in nasopharyngeal cavity, not found in GI tract
§ H&M strains
o Host: man
o Control: Vaccine is not possible b/c too many serotypes!
Coronarviruses
• Associated with common cold & SARS
• Virus structure:
o (+)ssRNA virus, enveloped, naked, helical, lipid containing, 2 glycoproteins at its surface (E1 & E2 (activtes HA)
• Multiplication:
o Different in sized viral mRNAs transcribed from vRNA
o Occurs in cytoplasm: assembly by budding into ER & Golgi apparatus. Released by fusion via exocytosis
o Multiplication is max. at ~32C
• Pathogenesis:
o Aerosol and large droplets
o Coryzas (swelling of mucosal membrane of oropharynx), sneezing, nasal congestion, etc…
o Some can cause gastroenteritis
• Prevention:
o No vaccine or regulation available
Orthomyxoviruses (Myxoviruses)
• associated w/ the influenza
• Virus structure:
o (-)ssRNA, enveloped, helical, segmented, own polyermase, infectious respiratory disease, 3 forms (A,B,C)
o A type: replicate in humans & animals, B & C type: not as virulent
Hemagglutinin (HA) Neuraminidase ( NA) Ribonucleoprotein (RNP)
- glycoprotein binds to cell receptors - removes sialic acid á virus spread in - code for structural & non-structural proteins
- main antigen against neutralizing antibody respiratory tract - capsid, it goes into the nucleus
• Virus replication:
o Virus attach to receptor (HA) enters cell
o â pH change so fuses w/ membrane & release RNP
o Viral polymerase cleaves host mRNA & uses capped primer to transcribe the vRNP.
o mRNA & vRNA made in nucleus
o HA & NA made in RER ==> SER until cell membrane & gets glycosylated
o Virus made by budding from cell
Antigenic shift Antigenic drift
- re-assortment -b/c of high error of RNA polymerase
- can have co-infection
- can be pandemic
- change in nucleic acid of virus
• Complications:
o Associated w/ lung infection (pneumonia)
§ Pneumonia: primary influenza, combined viral & bacterial, secondary bacterial pneumonia,
§ Reye’s syndrome: encephalopathy & fatty liver associated w/ Influenza B
• Associated w/ Guillain-Barre Syndrome: ascending paralysis
§ Otitis media
• Treatment:
Anti-viral
- Amantadine hydrocholoride & rimantadine
- Tamiflu
- Relenza (works against NA
- drug blocks uncoating (blocks replication)
• Vaccine
§ Vaccine is prepared in eggs
Paramyxovruses
• Virus structure:
o (-)ssRNA, enveloped, helical, non-segmented, HN and F proteins (2 spikes), contain RNA polymerase
o F protein (fusion) causes lyses of rbc when mixed w/ virus
• Replication:
o Synthesis of mRNA & proteins occur at the cytoplasm
o HN & F proteins are assembled in the cell plasma membrane
• Virus types:
o parainfluenza types 1-5: Infects humans & non-humans
o mumps: paramyxovirus
o measles: morbillivirus
o respiratory syncticial virus:
• Parainfluenzas:
o Upper respiratory disease: fever, rhinitis, pharyngitis, CROUP syndrome (laryngoracheobraonch) (barking cough … difficult to
breath)
MUMPS
• Pathogenesis:
o Asymptomatic
o Acute onset of parotitis w painful swelling in salivary glands & transmitted in saliva & respiratory secretions
o Forms multinucleated cells (F protein) causes fusion of several cells (syncytia formation)
o May lead to male sterility because can’t expand due to tunica albuginea
o Stensen’s duct: parotitis
Measles (Rubeola)
• Acute highly infectious disease: w/ rash & respiratory symptoms
o 3C (cough, coryza, conjunctivitis)
o Lacks neuraminidase
o Koplik’s spots: vesicles in the mouth. Appear tiny red patches w/ white specks on buccal mucosa
o Measles can impair CMI (cell mediated immunity)
• Complications:
o Subacute sclerosing panenceophalitis (SSPE):
§ latent in individuals, brain cells have nuclear & cytoplasmic includsions of measles ribonucleoprotein, slow virus
o Herpes 6 (multiple sclerosis)
Respiratory Syncytial Virus (RSV)
o Blocks breathing respiratory tract of young children < ½ year old causes bronchitis & pneumonia .produce syncytia.
• MMR is a live attenuated virus vaccine
Reoviruses
• ONLY dsRNA, naked, icosahedral, 10 segments, double capsid
• Disease:
o Rotavirus: affects children w/ diarrhea. Looks like wheel shaped. Can see genetic re-assortment (shift in orthomyxovirus
Rhabdovirus
• Virus structure:
o bullet shaped, enveloped, made up of 5 proteins w/ 1-protein outside (glycoprotein G)
o (-)ssRNA, helical, contains RNA polymerase
o Cytoplasmic replication
• Rabies Disease
o Infection of CNS of all warm blooded animals (mammals)
o Transmitted via bite wounds with saliva
§ Rabies multiplies in muscle & connective tissue at the infection.
o 3 stages in human rabies:
§ Prodromal phase: malaise, anorexia, headache, nausea, vomiting, sore throat, & fever.
§ Excitement phase: á salivation & perspiration. Hydrophobia (fear of water) b/c fear of swallowing due to pain
§ Depressive (paralytic) phase: convulsive seizures, coma, and death
• Lab Diagnosis
o Presence of Negir bodies in nerve cells.
o Antibodies can be detected by immunofluorescence, complement fixation, or neutralization.
• Immunity & Prevention
o Passive and active immunization at the same time!
o Give promptly to build antibodies to prevent virus attacking nervous system.
o Vaccines include: human diploid cell vaccine, duck embryo vaccine, nerve tissue vaccine (brains of animals) inject into individuals.
Slow viruses
• Incubation periods are long & may appear many years later and are categorized conventional & unconventional.
o Causes: spongiform
o Symptoms include: loss of muscle control, shivering, tremors, & dementia
o There is no inflammation, no immune response, no antigencity
• Prions: Infectious protein, no nucleic acid, cause degenerative neurological disease (scrapie)
o 2 types of prions:
§ PrPc: wildform, native, found on surface
§ PrPsc: infectious form, tertiary structure
o Replication: If PrPsc interacts with PrPc in the body will interact and change confirmation and infect near nerve cell & cause
spongiform appearance.
Hepatitis Viruses
• Definition: acute infections of the liver (jaundice) may lead to liver cancer (necrosis of hepatocytes)
• Viruses: herpes simplex, herpes-zoster virus, Epstein-Barr virus, coxsackieviruses
o Viruses replicate primarily in the liver (viral hepatits):
§ Hep A (HAV): infectious hepatitis w/ short incubation
§ Hep B (HBV): serum hepatitis w/ long incubation due to blood/fluid exchange
§ Hep C (HCV): non-A and non-B
§ Hep D: super infection, more severe than other Hep, found mostly in pregnant women
• HAV: Picornovirus
o (+)ssRNA, no envelop, enterovirus, spread by fecal-oral route (water, shellfish(raw clams)), infect liver, no cross react w/ Hep B
o Disease: acute infection
• HBV: Hepadnavirus
o dsDNA, enveloped, icosahedral, circular, variable in length.
o Made up of 2 major proteins and 1 minor protein.
o Can be seen as: Dane particle (complete virus), Sphere, or Filament with surface (s antigen)
o Risk in drug abusers, transfusions, high promiscuous populations, infected blood, breast milk, saliva, nasopharyngeal, semen,
menstrual fluid, blood.
o Disease: acute & chronic infection
o Replication: vRNA (pregenome RNA) copied into DNA by reverse transcriptase. Enzyme removes original vRNA and a double
stranded DNA is formed. Virus is formed by budding.
• HCV: Flavivirus
o (+)ssRNA, enveloped, icosahedral, lipid virus, related to plant virus, may cross a mammalian & plant virus
o called non-A & non-B hepatitis
o Disease: acute & chronic infection
• HDV: delta agent (viroid like) Fulminant hepatitis
o ssRNA contains HBV surface protein. HDV is defective virus needs a helper fxn ex w/ HBV
o super infection, intensify and becomes severe mostly in pregnant women
Oncogenes Virus
• RNA or DNA the cancer originates from a single cell
• Function of oncogene: protein kinases codes for tyrosine kinase that phosphorlyates proteins at tyrosine & causes fibrin network
• Human Leukemia-Sarcoma Virus:
o Human Trophic cell leukemia virus HTLV-I and HTLV-II
§ They are diploid cells, w/ 2 copies of genome, NOT segmented
§ HTLV-1 via tax (transcriptional activation) activates IL-1, IL-2 receptor
o HIV
§ Binds to CD4 and chemokine receptor
§ Treatment :
§ AZT (azido-dideoxythymidine)
• Used for viral reverse transcriptase to prevent DNA replication, competes thymidine & terminates DNA
growth. âWBC
• Chain termination which does not allow anything to attach to the genome
§ Anti-protease drugs: (ex. Saquinavir or Ritavir)
• Inhibit protease from cleaving the polyprotein into the virus.
• Protease cleaves the gag & pol to produce nucleocapsid proteins inhibits production of infection but does NOT
cure infection.
• Replication:
o Virus enters, cytoplasm is where the reverse transcriptase copies vRNA into complementary DNA
o DNA is called PROVIRUS & is found in linear & dsDNA form.
o DNA provirus gets into nucleus w/ pregenome chromosome, transcribes w/ infected virus
o mRNA translated into polyprotein (pp) ==> pp cleaved by proteus & assembled in plasma membrane
o virus buds from cell
Glycoprotein (glycosylated)
• gag = group specific antigen, capsid proteins
• pol = polymeras, protease, integrase
• env = enveloped glycoproteins
• LTR = aka long term repeats, these are promoters to enhance transcription factor binding sites
Misc:
What replicates in the cytoplasm? Which viruses do you see coryza?
• pox virus • Coronavirus
• cornovirus • paramyxovruses - Measles (Rubeola) which includes the 3C’s
• paramyxovirus
• rhabdovirus
What is the treatment for polio?
Guillan Baire Syndrome found in? • aridone
• EBV – herpes
• Influenza (ortho)
Plasmodiasis periodic fever, chills, blood, cyclical drug resistant in Chloroquine PO4,
Malaria, plasmodium hepatosplenomegaly, plasmodial falciparum malaria primaquine PO4, quinine
vivax, ovale, anemia forms in RBC for falciparum malaria
malariea, falciparium
Toxoplasmosis - primary infection ingestion oocyts, serum, tissues, definitive host cat pyramethamine +
Toxoplasma gondii asymptomatic or mild meat containing organism not family sulfadiazine
- congenital infections tissue cysts readily
(anomalies of CNS, eyes) observed or
- immunocompromised: cultured from
disseminated infection humans
involving CNS
Babesiosis / Babesia Nantucket fever, resembles bite of nymph of blood & important infection of clindamycin + quinine
microti malaria hard tick, Ixodes organism in domestic & wild
sacapularis RBC animals & deer mice,
field mice important
reservoir
Cryptosporidiosis profuse, watery diarrhea oocysts, feces of stool, gut Immunocompromised, antibiotics not effective,
animals, human tissue, oocyts fatal diarrhea, immunocompetent self
feces & respiratory observed via dehydration, limiting, supportive care,
secretions phase contrast parenteral nutrition, paromomycin (some
microscopy, supportive success)
acid-fast
stained
material
Additional materials
- Levine’s last lecture on parasitology
- Enterococcus
- M. Marium (Group I)
- IMVIC (relevant lactose & gas), pg 33
- UPEC
- Bortonella Quintana
- Coxsacckie
- Coronavirus
- Orthomyxovirus
- West Nile Virus (arbo virus) ==> What family does it belong to? Flavivirus
- Oncogene
What is the difference btw the measles (rubeola) vs. German measles (rubella)?
measles (rubeola) German measles (rubella)
- acute infectious disease w/ rash & respiratory - subcategory of toga virus
- 3C - (+)ssRNA, enveloped
- no neuraminidase - rash on face
- Koplik’s spot - congenital anomalies
- impair’s CMI
- SSPE
- RSV: blocks resp. tract in young children