micro_mod_6

Escherichia coli is the most likely cause of repeated episodes of cystitis (bladder infection)

Staphylococcus saprophyticus is associated with urinary tract infections in young, sexually active female

Proteus contributes to stone formation in bladder and kidney by splitting urea that forms NH3OH and “pH or urine

Helicobacter pylori

Enterobacter

Bacillus anthracis

Clostridium spp

NOT – Erysipelothrix rhusiopathiae

STREP PNEUMONIA

Causes Typhoid Fever:

Humans are the only known host/reservoir (2)

Chronic carrier state – resides in gallbladder

Facultative intracellular pathogen that typically multiplies in macrophages -->’’ CMI is important

Systemic spread of pathogen

Rose spots may occur

Escherichia

Shigella

Salmonella

Klebsiella

NOT – Vibrio [this belongs to the family Vibrionaceae ]

Vibrio vulnificus

CELL WALL CARBOHYDRATES

Peptidoglycan fragments can be released that are cytotoxic for ciliated epithelial cells involving IL-1 and nitric acid

Pili promote adherence to host cells

Antigenic variation explains the occurrence of repeated infections

Pelvic inflammatory disease (PID)

Disseminated gonococcal infection (DGI)

Arthritis

Opthalmia neonatorum

C5a þ complement activation

Leukotrienes þ lipid product of membrane metabolism

IL-8 þ product of monocytes and macrophages; once macrophages are activated they produce IL-1 which activates neutrophil

-naked DNA assimilates into recipient cell and is incorporated in genome

-when a cell lyses, the exposed, fragile DNA breaks into small pieces; other cells can absorb this DNA- these cells are deemed competent

-a single cell may not be competent at all times; frequently cells are only competent during the stationary growth phase

Gram positive transformation: (e.g. Streptococcus pneumoniae)

-competence factor is produced by a competent cell and secreted into environment, inducing neighboring cells to produce transformation-specific proteins (membrane DNA-binding protein, enzymes)

-competent cells will indiscriminately bind and absorb any DNA encountered

-if DNA strand is homologous, recombination occurs; if non-homologous, DNA is degraded

-electroporation can induce normally non-competent cells to assimilate DNA via an electrical pulse

Gram negative transformation: (e.g. Haemophilus, Neisseria)

-do not produce competence factor; competent cells always express a few DNA-binding proteins on outer membrane (* easy to remember if you consider G+ cells do not possess outer membrane, therefore they must produce competence factor to induce)

-DNA binding on surface is indiscriminate, but, to be taken into cell, a competence protein confirms DNA is a very specific (10-14 b.p.) sequence; this assures homology

-transformation occurs only if DNA is integrated into chromosome

-movement of bacterial DNA from donor to recipient via bactriophage

Bacteriophage facts:

-phage (bacteriophage) is a virus that infects bacteria

-can be ds or ss; DNA or RNA; virulent (lytic) or temperate (prophage)

• virulent phage- always operates a lytic cycle, replicating soon after infection, producing many copies of genome and proteins, assembling, then either lysing
• the cell or budding through membrane

temperate phage (prophage)- can undergo a lytic cycle or lysogenic cycle; during lysogenic cycle phage genes are integrated into host chromosome (therefore temperate phages are always dsDNA)

-host cell genome increases in size proportionate to size of viral genome; host genome now contains a prophage; when carrying a prophage, host cell is called a lysogen

-bacterial phenotype changes from integration of prophage is a lysogenic conversion

• -Corynebactrium diphtheriae is the classic example of lysogenic conversion; this bacterium will not produce
• diphtheriae toxin, and therefore will not be virulent, unless infected and lysogenized by phage b, which carries a tox gene

-usually mediated by temperate phages; can be generalized or specific

• generalized transduction:
• -host DNA can be degraded during phage lytic activity; during phage packaging, host DNA may accidentally be packaged into capsid instead of phage genome

-this pseudovirion is non-virulent, however, it can still attach to a cell and inject DNA

-if bacterial DNA is incorporated into host genome, recipient is a stable transductant with new genome

-this is a random process, capable of incorporating any portion of bacterial DNA

• -phage P1 infects E. coli, and can produce a
• generalized transduction

• specialized transduction:
• -process begins when lysogen (bacteria infected by temperate phage) enter lytic cyle

-prophage (phage genome incorporated into bacterial genome) is excised and expressed, leading to replication and lysis

-if excision is imprecise, bacterial genes flanking the prophage can be incorporated

-l phage for E. coli integrates on a specific cellular chromosome location, so flanking genes are predictable

-m phage integrates anywhere on E. coli genome, thus the flanked genes are variable

-phages may infect new cells, and bacterial genes will incorporate into genome

-requires a plasmid (dsDNA replicon) which possess their own origin of replication, regulatory proteins, thus replicate separate from the bacterial genome

-plasmids do not encode essential functions, therefore are unnecessary for bacterial growth; they often confer antibiotic resistance or toxin production

• -conjugation is also called mating since
• cell-to-cell contact is required

-bacterium must possess a conjugative plasmid to initiate conjugation; all the proteins necessary for conjugation are located on the genome of the plasmid

• Gram negative conjugation:
• -in E. coli, the F plasmid (fertility) encodes for the F pilus necessary for conjugation; this sex pilus is different from normal cellular pili

-the F pilus is produced by the donor (F+) to communicate with the recipient (F-); it attaches to an outer membrane protein produced from ompA gene

• -the cellular communication via the F pilus creates a cytoplasmic bridge; one strand of the F plasmid is sent to the recipient, beginning from a unique origin and
• leading in a 5’--> 3’ direction

-ss plasmid is completed with complementary strand in donor and recipient

• -F plasmid may be incorporated into bacterial genome; the F factor of plasmid catalyze the transfer of any attached DNA, thus incorporation into host
• genome allows transfer of bacterial DNA to neighbor

• -the result is an Hfr (high frequency
• recombinant) cell which can:
• a) transfer bacterial DNA- when transfer occurs at unique origin near F factor, this factor is often the last portion of DNA transferred, up to two hours after conjugation begins; obviously, cells cannot always maintain this two-hour connection; DNA closest to origin is most likely to be transferred; since F plasmid is not transferred, recipient frequently remains F-

b) transfer F plasmid- if F factor is precisely excised from bacterial genome, F plasmid is transferred to new cell, producing F+

• c) transfer F plasmid plus bacterial gene- imprecise excision; a few bacterial genes are excised and transferred along with F plasmid- hybrid is F’,
• indicating the plasmid contains some bacterial DNA

-R plasmids confer antibiotic resistance by degradation or by preventing permeability; R plasmids may be conjugative, containing genes specifying their transfer by conjugation; non-conjugative R plasmids do not carry genes promoting their transfer by conjugation

• Gram positive conjugation:
• -G+ cells do not have sex pili; instead, they conjugate by clumping together

-all G+ cells have receptors located on cell surface; cells produce pheromones to induce production of adhesins by plasmid-containing cells

-cells aggregate from adhesin-receptor interaction, forming conjugation bridges for plasmid transfer

Enterococcus faecalis- capable of producing several pheromones, encoded by chromosomal genes, each for a specific plasmid

-once a cell received the desired plasmid, it ceases production of the corresponding pheromone, but may still produce other pheromones

Homologous Recombination a.k.a. generalized or rec-dependent recombination

-one method of integration is homologous (generalized) recombination w/cross-over events; exogenote must possess regions of nucleotide sequence homology to endogenote

-success of recombination is predicted by the extent of sequence homology

• -RecA enzyme is necessary for homologous
• recombination in E. Coli; it coats the exogenote ssDNA and catalyzes reaction with endogenote at
• homologous sequence

-other enzymes (endonucleases, ligases) complete the process

-if the exogenote DNA enters the cell as ssDNA (transformation, conjugation), it does not need further preparation

• -if, however, it arrives as dsDNA, RecBCD will begin at an end or break in the ds, unraveling the ds until it reaches the the chi sequence (crossover hotspot
• initiator) and cuts the strand, which is then coated by RecA

-the target dsDNA endogenote will also undergo ss diplacement to clear room for the recombinant sequence; the two ssDNA segments removed from the exogenote and endogenote will switch places to the endogenote and exogenote, respectively

-recombination and replication of each DNA molecule will produce one progeny with the parent’s genome, and one with the recombinant genome

antigenic variation- primary example of homologous recombination, enables some bacteria to evade host response

Specialized Recombination a.k.a. site-specific or rec-independent recombination

-mechanism of recombination for most prophages, as well as insertion sequence elements and transposons

-requires specific enzymes which recognize specific DNA sequences for recombination

-does not require sequence homology, can recombine drastically different sequences

-e.g. lphage in E. coli has only 15b.p. homology at site of recombination, otherwise not similar

CATALASE

COAGULASE

ADHESINS

CAROTID PIGMENT (golden color)- STAPHYLOXANTHIN, INACTIVATES MICROBICIDAL EFFECTS OF SUPEROXIDES (oxy free radicals)

b-LACTAMASE ENCODING PLASMID - PEN RESISTANCE (penicillinase)

ALTERED PEN-BINDING PROT (TRANSPEP) VIA mecA - RESIDES ON CHROM AND RESISTANT TO ALL b-LAC DRUGS

VanA GENE - MODIFIED CELL WALL FROM (D-ALA D-ALA) TO (D-ALA D-LACT). FROM VANCOMYCIN RESISTANT ENTEROCOCCI

PROT A - IN CELL WALL & BINDS TO Fc PORTION OF IgG AND PREVENTS OPSONIZATION

TEICHOIC ACID - PLAY ROLE IN SEPTIC SHOCK

POLYSACCHARIDE CAPSULE - 12 SEROs BUT 85% FROM 5&8. POORLY IMMUNOGENIC

a-TOXIN AND P-V LEUKOCIDIN -- KILL LEUKOs AND CAUSE NECROSIS

b-TOXIN -- DEGRADES SPHINGOs

HYALURINIDASE -- SPREADING FACTOR, BREAKS DOWN PROTEOGLYCANS IN CONNECT. TIS.

TSST-1 -- SUPERANTIGEN

ENTEROTOXIN -- 50% OF S. AUREUS, CARRIED ON CHROM OR PLASMID. SIMILAR TO ROTO VIRUS NSP4 TOXIN.

EXFOLIATIVE TOXIN -- DESQUAMATION (SYMP OF TSS)

CW PEPTIDOGLYCAN - BAC

CM STEROLS - EUK

INTERNAL MEMBRANES - EUKs

PEN - PEPTIDOGLYCAN

STREP - INH PROT SYNTH BY BINDING TO 30S RIBO

SULF - INH FOLIC ACID SYNTH

• COCCUS - ROUND
• PAIRS NEISSERIA
• CHAINS STREP
• CLUSTERS STAPH

• ROD STRAIGHT
• SHORT SALMON

• ROD BRANCHED
• NOCARDIA

• ROD CURVED
• RIGID VIBRIO
• FLEXIBLE TREPONEMA

IRREGULAR

• CELL WALL:
• + LESS COMPLEX; PEPTIDOGLYCAN
• - MORE COMPLEX, LITTLE PEPTIDO AND OUTER MEM

• RESISTANCE TO PHYSICAL DISRUPTION:
• + MORE
• - LESS

• PEN SENSITIVITY:
• + MORE
• - LESS

• RESISTANCE TO CELL WALL LYTIC ENZYMES:
• + LESS
• -MORE

• DYE INHIBITION:
• + INH BY CRYSTAL VIOLET
• - NOT INH

• SPORE FORMATION:
• + SOME
• - NONE

• TOXIN PRODUCTION:
• + EXOTOXIN IN SOME
• - LARGELY ENDOTOXIN

• + TEICHOIC ACID
• - O ANTIGEN

REPEATING DIMERS OF N-ACYLGLUCOSAMINE AND N-ACYLMURAMIC ACID LINKED BY TETRAPEPTIDE "TAILS"

JOINED BY TRANSPEPTIDASE - TARGET FOR PEN

GRAM-

HYDROPHOBIC MEM ANCHOR OR LPS

ESSENTIAL FOR CELL VIABILITY

TOXIC COMPONENT OF LPS

O ANTIGEN ----- CORE POLYSACCHARIDE ---- LIPID A

30-37*C

ORGANIC - HETEROTROPHIC

CO2 - AUTOTROPHIC

MESOPHILIC (30-37*C)

HETEROTROPHS (ORGANIC CARBON)

CHEMOSYNTHETIC (OXIDATION OF ORGANIC/INORGANIC)

DIFFER USE OF OXYGEN

MUST REGEN OXIDIZED COFACTORS WITHOUT OXYGEN

USE PYRUVATE AS ACCEPTOR, REDUCING IT AND RELEASING PRODUCTS INTO ENV (LACTATE)

THIS IS FERMENTATION

I PERIOD - CELL MASS INC

C PERIOD - DNA REP AND SEPARATION (copy)

D PERIOD - TRANSVERSE SEPTUM FORMATION/ CELL SEPARATION (divide)

• FINAL # CELLS (N2) =
• ORIGINAL # CELLS (N1) x 2^{(# OF GENS)}

n = 3.3 x LOG(N2/N1)

HAPLOID

1 CHROM

SUPERCOILED x2 DNA

REPs SEMICONSERVATIVELY

SOLUBLE DNA FROM DONOR CELL BINDS TO SURFACE OF RECIPIENT AND IS INTERNALIZED

CROSS REACTING MATERIAL

GENE DETECTION USING Ab REAGENTS THAT CAN STILL REACT AGAINST MUTATIONS FROM ORIGINAL SEQUENCE

MUTATED GENE PROD IS FUNCTIONAL UNDER PERMISSIVE CONDITION (ex LOWER TEMP)

DO NOT RESTORE THE EXACT NUCLEOTIDE SEQUENCE OF WILD TYPE LIKE REVERTANTS BUT ULTIMATELY RESTORE FINCTION EITHER PARTIALLY OR COMPLETELY

INTRA/INTERGENIC

METHOD TO DETERMINE IF 2 MUTATIONS ARE IN SAME OR DIFF GENES

+ CAN BIND ANY x2 DNA, ONE IS INTERNALIZED AND THE OTHER IS DEGRADED AT CELL SURFACE

IF HOMOLOGOUS WITH RECIPIENT DNA, IT CAN BASE PAIR AND RECOMBINT INTO CHROM

- DO NOT PROD SOLUBLE COMPETENCE FACTORS, HAVE FEWER BINDING SITES AND ONLY RECOGNIZE DNA FROM RELATED SPECIES

RECOGNIZE RELATIONAL DNA BY PRESENCE OF MULTI COPIES OF UNIQUE SHORT (10bp) SEQUENCE DISPERSED THROUGHT CHROM.

LIKE +, ONLY ONE STRAND OF DNA ENTERS

VIRULENT (LYTIC) -- VIRAL NUC REPLICATES SOON AFTER ENTERING CELL. LYSIS

TEMPERATE (LYSOGENIC) -- DEPENDING ON ENV, MAY ALSO HAVE LYTIC CYCLE OR MAY GO THROUGH LYSOGENY, WHERE SPECIAL PHAGE REGULATORY PROTS REPRESS BULK OF PHAGE GENES. INTEGRATED AND ALWAYS CONTAIN x2 DNA

INTEGRATED PHAGE GENOME CALLED PROPHAGE

CELLS CARRYING PROPHAGE CALLED LYSOGENS

• GEN:
• TRANSFER OF BAC GENES BY PSEUDOVIRIONS

ANY REGION OF BAC GENE COULD BE TRANSFERED

PHAGE P1 MOST COMMON

• SPEC:
• TRANSFER OF PARTICULAR REGION OF BACTERIUM'S GENOME

DEPEND ON BACTERIOPHAGE AND SITE PROPHAGE RESIDES IN CHROM

LAMBDA PHAGE OF E.COLI

Mu PHAGE CAN INTEGRATE AT MANY SITES

2 COMPONENT REGULATORY SYSTEM

PILI

2 COMPONENT REGULATORY SYSTEM

Bvg

EARLY/LATE GENE EXPRESSION

FLAGELLA PHASE VARIATION

VARIATION OF PILI

RECOMBINATION

POST-TRANSCRIPTIONAL MODIFICATION

CLASSIC EXPERIMENT

PROVED TRANSFORMATION POSSIBLE

LYSOGENIC CONVERSION

TOXIN GENERATION THROUGH ACQUIRED VIRAL DNA

GENTLY LYSE CELL

MORE EFFECTIVE AT 70 THAN 100%

GAS STERILIZATION OF HEAT SENSITIVE INSTRUMENTS

X-RAYS ALSO STERILIZE

INACTIVATES SULFHYDRYL CONTAINING ENZYMES

SKIN ANTISEPTIC

INACTIVATES SULFHYDYL CONTAINING ENZYMES

HEAVY METALS

INACTIVATES SULFHYDYL CONTAINING ENZYMES

FOUND IN BLEACH

HEAT FOLLOWED BY RAPIC COOLING

USED TP STERILIZE SURGICAL ROOMS WHILE NOT IN USE

PORE SIZE THAT GUARENTEES PHYSICAL REMOVAL OF ALL BAC & SPORES

PHYSICAL REMOVAL OF BAC FROM HEAT SENSITIVE EQUIP

• G-; DIPLOCOCCI
• OXIDASE +

THAYER MARTIN + (CHOC AGAR)

GLUCOSE ONLY

DISSEMINATED GONOCOCCAL INFECTIONS (DGI): KNOWN FOR INFECTING MUCOSA OF URETHRA AND VAG

PHARYNGITIS

OPTHALMIA NEONATORUM

SERUM RESISTANT DUE TO SIALATION OF ENDOTOXIN LOS;

PROT A - INHIBITS C3b

IgA PROTEASE

ARTHRITIS AND SKIN LESIONS WHEN DISSEMINATED. LEADING CAUSE OF SEPTIC (PURULENT) ARTHRITIS IN ADULTS

OPTHALMIA NEONATORUM: VIA BIRTH CANAL OF MOM WITH GONO. TREAT WITH .5% ERYTHROMYCIN OINTMENT

ADHERENCE TO HOST CELLS: PILI FOR INITIAL BINDING. PHASE VARIATION, PILI --> NO PILI, OVER 100 SEROTYPES

OUTER MEM PROTS CALLED OPA (OPACITY-ASSOCIATED OUTER MEM PROTS) ALSO HELP. PATH DIRECTED ENDOCYTOSIS.

OPA BINDS HEPARIN SULFATE PROTEOGLYCAN (HSPG) RECEPTOR --> ENCLOSED IN VACULE

OPA INVOLVED IN CLUSTERING OF BAC

NO POLYSACC CAPSULE

PEN RESISTANT, USE CEFTRIAXONE

G-, OXIDASE +

THAYER MARTIN AGAR +

GLUCOSE AND MALTOSE

LPS, LIPO PROT A

IgA

VIRULENT POLYSACC CAP ANTI-PHAG, GROUPS A, C, W135, E. GROUP B NO CAPSULE BUT SIALIC ACID (NOT IMMUNOGENIC)

INFECT BLOODSTREAM

HEAVILY ENCAPSULATED; SERUM RESISTANT

PURPURA FULMINANS CAUSED BY DISSEMINATED INTRAVASCULAR COAGULATION (DIC). THROMBI IN SMALL VESSELS DEPRIVE OX SUPPLY IN KIDNEYS, BRAIN, LUNG, & ADRENALS (WATERHOUSE-FRIDERICHSEN SYND, ADRENAL INSUF RAPID DEATH)

CAPSULE SPECIFIC Ab RESIST INVATION OF BLOODSTREAM

AIRBORNE DROPS --> URT --> BLOOD

COLLEGE STUDENTS; MILITARY

SECOND TO S. PNEUM IN CAUSE OF BAC MENINGITIS, BUT #1 AGES 2-18

TREAT PEN G

VACCINES FOR POLYSACC GROUPS ONLY

•Menactra: conjugated, T-dependendent immunity, must be given from 2-18 years, polysaccharides A,C,Y,W135 attached to carrier protein (DIPTHERIA TOXOID)

•Menomune-unconjugated - NO CARRIER PROT, SAME TITER RESPONSE AS MENACTRA IN ADULTS

RESEMBLES STREP. PNEUM AND FLU-B

THAYER MARTIN+ (EXCEPT N. SICCA)

OXIDASE+, REACTS WITH CYTOCHROME C CREATING PURPLE-BLACK COLOR

CATALASE- (STAPH IS +)

a-HEMO: GREENISH. VIRIDANS & PNEUM

OPTICHIN: VIRIDANS(R) PNEUM(S)

b-HEMO: GAS & GBS

BACITRACIN: GAS(S)

BAC(R) --> cAMP GBS(+)

ANTISTREPTOLYSIN O ASSAY: GAS (NO HEME LYSIS IS +)

PNEUM: BILE SOLUBLE; QUELLUNG REACTION

ESCULIN: ENTEROCOCCI (BLACK+)

• GRAM+, IN CHAINS, b-HEMO, EXTRACELLULAR, CATALASE-

BACITRACIN (S)

• S. PYOGENES

• 3 ADHESINS:

– F PROTEIN: BINDS FIBRONECTIN ON PHARYNGEAL EPITHILEAL CELLS

– LIPOTEICHOIC ACID: BINDS FIBRONECTIN ON EPITHILEAL CELLS

– M PROTEIN: BINDS KEROTINOCYTES IN HUMAN SKIN AND MEDIATES INTERNALIZATION

• ANTI PHAGOCYTIC FATORS:

• – M PROTEIN: MAJOR VIRULENCE FACTOR; BINDS SERUM FACTOR H --> DESTROYS C3 CONVERTASE --> BLOCKS C3B OPSONIN --> NO PHAGOCYTOSIS;
• ANTIBODY AGAINST M IS PROTECTIVE BUT MORE THAN 100 SEROTYPES MAKES REPEATED GAS INFECTION POSSIBLE

– HYALURONIC ACID CAPSULE: NO ANTIBODIES MADE AGAINST BECAUSE COMPONONENT OF BASEMENT MEMBRANE

– C5A PEPTIDASE: DEGRADES C5A THAT ATTRACTS PHAGOCYTES

• TOXINS:

– ERYTHROGENIC TOXIN: SCARLET FEVER RASH; SUPERANTIGN; DEPENDENT ON LYSOGENIC PHAGE CONVERSION; BACTERIA DOESN’T NORMALLY CARRY; TOXEMIA AND NOT BACTEREMIA

• SCARLET FEVER --> ACUTE RHEUMATIC FEVER (MAJOR CAUSE OF DEATH BECAUSE WEAK HEARTS FROM SCARLET FEVER)

– STREPTOLYSIN O: BETA HEMOLYSIS; REQUIRES LOW OXYGEN; ANTIBODY AND ASO TITERS DEVELOPS

– STREPTOLYSIN S: BETA HEMOLYSIS; NOT INACTIVATED BY OXYGEN

• – PYOGENIC EXOTOXIN A: SPE-A -->
• TOXIC SHOCK SYNDROME; SUPERANTIGEN, SYSTEMIC SPREAD OF STREPTOCOCCI VERSUS STAPH WHICH HAS A LOCALIZED INFECTION AND TOXEMIA; SOLUBLE VIRULENCE FACTOR; LEADS TO HYPOTENSION, SHOCK, AND MULTIPLE ORGAN FAILURE

– EXOTOXIN B: PROTEASE FROM FLESH EATING S. PYOGENES CAUSING NECROTIZING FACIITIS

• SPREADING FACTORS

– HYALURONIDASE, DNASE, PROTEASE (EXOTOXIN B): LEAD TO FLESH EATING BY DISSOLVING SKIN; ONLY CURED BY CUTTING ABOVE

• • APSGN: OCCURS MORE COMMONLY AFTER SKIN INFECTIONS THAN PHARYNGITIS; SOMETIMES Ab FORM AB-AG COMPLEXES WHICH TRAVEL TO AND DEPOSIT ON GLOMERULAR BM -->
• COMPLEMENT CASCADE --> SEQUELLAE NOT AN INFECTION

– ANTIBIOTICS NOT EFFECTIVE BECAUSE NOT DIRECTLY RELATED TO DISEASE

• ARF: OCCURS AFTER PHARYNGITIS; AB TO M PROTEIN CROSS-REACT WITH HEART; SEQUELLAE NOT AN INFECTION

– AUTOIMMUNE DISEASE; REPEATED EPISODES EXACERBATE

• TREATMENT: PENICILLIN G (100% SUSCEPTIBLE)

– SHOULD BE GIVEN SOON TO AVOID PRODUCTING OF AB --> ARF OR APSGN

LANCEFIELD FACTOR -- ANTIGENIC C-CARB IN CELL WALL DETERMINES GROUP

S. AGALACTIAE, FAC ANAEROBE

GRAM+, CATALSE-, b-HEMO,

BACITRACIN (R), cAMP+

HYDROLYZES HIPPURATE

• MAJOR VIRULENCE FACTOR IS THE POLYSACHARRIDE CAPSULE

• FREQUENT CAUSE OF INFECTION IN NEONATES

• EARLY ONSET: FETUS EXPOSED VIA BIRTH CANAL; SEPSIS AND PNEUMONIA IS EVIDENT WITHIN FIRST WEEK OF LIFE

– TREAT WITH PENCILLIN

– CAN BE PREVENTED WITH PROPHYLACTIC IV PENCILLIN FOR MOTHER

• LATE ONSET: SEPSIS AND MENINGITIS FROM FIRST WEEK TO THREE MONTHS

– ACQUIRED EXOGENOUSLY

– ANTIBODIES AGAINST THE CAPSULE ARE PROTECTIVE

HSV & HHV-3 VZ

GRAM+, CATALSE-, a-HEMOLYSIS

OPTOCHIN SENSITIVE

AMIDASE POSITIVE --> BILE SOLUBILITY,

DIPLOCOCCI, LANCET SHAPED

•MUCOID APPEARANCE OF POLYSACHARRIDE CAPSULE

– POLYSACHARRIDE CAPSULE IS MAJOR VIRULENCE FACTOR/ ANTI-PHAGOCYTIC. >85 SEROTYPES

– MORE THAN 90 SEROTYPES; AB PROTECTIVE AND OPSONINZING

• • MOST FREQUENT CAUSE OF BACTERIAL PNEUMONIA, ALSO CAUSES SINUSITIS AND
• OTITIS MEDIA (BABIES)

• ACTIVATION OF ALTERNATE COMPLEMENT PATHWAY

– 1) PNEUMOCOCCAL TEICHOIC ACID AND PEPTIDOGLYCAN FRAGMENTS: LEADS TO INFLAMM RESPONSE IL-1 AND TNF-ALPHA ABD C5a

– 2) PNEUMOYLSIN: HEMOLYSIN, PORE FORMER, ALTERS CILIA MOVEMENT AND DAMAGES RESPIRATORY EPITHELIAL CELLS AND ENDOTHELIAL CELLS; DISRUPTS PULMONARY TISSUE BARRIERS

– 3) C-SUBSTANCE --> CRP: ACUTE PHASE PROTEIN INDICATIVE OF NONSPECIFIC INFLAMMATION

• IgA PROTEASE: COLONIZES IN MUCOSA OF UPPER RESPIRATORY TRACT

• LACK OF SPLEEN --> HIGH SUSCEPTIBLITY OF CAPSULATED BACTERIA (PNEUMOCOCCUS)

• INVASIVE PNEUMOCOCCAL INFECTION = BACTEREMIA, SEPSIS, AND MENINGITIS

• AMIDASE --> AUTOLYSIS --> CLEAVAGE OF PEPTIDOGLYCAN LAYER

– ACTIVATED BY BILE SALTS --> CLEAR BROTH

• QUELLUNG REACTION: Ab REACT WITH CAPSULAR ANTIGENS --> SWOLLEN AND EASILY VISIBLE

• HUMORAL IMMUNITY BEST

• 2 VACCINES AGAINST SUGAR TYPES

– 1) PNEUMOVAX: T-INDEPENDENT- NOT ENGULFED BY APC AND PRESENTED USING MHC CLAS II; IMMUNE RESPONSE FROM CROSS-LINKED AB ON B CELLS; NOT USEFUL IN CHILDREN UNDER 2; RARELY ADMINISTERED

– 2) PREVNAR: T-DEPENDENT- SUGAR CROSSLINKED WITH DIPTHERIA TOXIN; COMMONLY ADMINISTERED

• TREATMENT:

– PENCILLIN- MUST GIVE HIGH DOSE TO CROSS BLOOD BRAIN BARRIER

• RESISTANCE TO PENCILLIN BINDING PROTEIN POSSIBLE

– IF PENCILLIN RESISTANT, ALSO LIKELY AMINOGLYCAN RESISTANT, MUST GIVE VANCOMYOCIN

• – PENICILLIN RESISTANCE IS DIFFERENT THAN IN STAPH (NO BETA LACTAMASE, INSTEAD INACTIVATES PENCILLIN
• BINDING PROTEIN/TRANSPEPTIDASE)

GRAM+, CATALASE-, a-HEMOLYSIS

OPTOCHIN RESISTANT

• MOST COMMON CAUSE OF ENDOCARDITIS

– SUBACUTE BACTERIAL ENDOCARDITIS

• NORMAL FLORA MANY SUBSPECIES IN OUR MOUTHS

– CAN GET MILD BACTERMIA FROM BRUSHING TEETH

– WORSE BACTEREMIA POSSIBLE POST DENTAL SURGERY

– TREAT WITH PROLONGED PEN G WITH/WITHOUT AMINOGLYCOSIDE FOR ENDOCARDITIS

AMOXICILLAN TO PREVENT ENDOCARDITIS FOR Pt W/ DAMAGED HEART VALVE BEFORE DENTAL CARE

GRAM POS COCCI IN GRAPELIKE CLUSTERS

• GOLDEN-YELLOW COLONIES (AUREAUS MEANS “GOLD”)

• CATALASE POSITIVE: ENZYME THAT CATALYZES THE CONVERSION OF HYDROGEN PEROXIDE TO WATER AND OXYGEN; IF BUBBLES ARE OBSERVED, IT´S A POSITIVE TEST. DIFFERENTIATE BETWEEN
• STAPH AND STREP, THE LATTER DOESN´T PRODUCE CATALASE

• NO SPORES

• FACULTATIVE ANAEROBE

• EXTRACELLULAR

• • COAGULASE POSITIVE: ENZYME THAT CAUSES PLASMA TO CLOT BY ACTIVATING
• PROTHORMBIN TO FORM THROMBIN. THROMBIN THEN CATALYZES THE ACTIVATION OF FIBRINOGEN TO FORM THE FIBRIN CLOT.

• CAROTENOID PIGMENT THAT IMPARTS A GOLDEN COLOR TO ITS COLONIES

• FERMENTS MANNITOL

BACTERIMIA - UNTREATED S. AUREUS IN BLOODSTREAM HAS 80% MORTALITY RATE.

MOST COMMON OVERALL CAUSE OF BONE AND JOINT INFECTIONS.

CAN CAUSE PNUEM SECONDARY TO VIRAL INFECTION (eg FLU)

• HUMANS ARE THE RESERVOIR

• NOSE IS MAIN SITE OF COLONIZATION

• SHEDDING FROM HUMAN LESIONS

• FOMITES SUCH AS TOWELS AND CLOTHING CONTAMINATED BY THESE LESIONS

• FOUND IN VAGINA OF 5% OF WOMEN

• TRANSMISSION: HAND CONTACT

• CHRONIC NASAL CARRIAGE

• SKIN IS A COMMON SITE OF COLONIZATION, ESPECIALLY OF HOSPITAL PERSONNEL AND PATIENTS

• WOMEN WHO HAVE THIS BACTERIA IN THEIR VAGINA BC IT PREDISPOSES THEM TO TOXIC SHOCK SYNDROME

• IMMUNO-COMPROMISED

• REDUCED HUMORAL IMMUNITY

• DIABETES AND IV DRUG USE

• • CHRONIC GRANULOMATOUS DISEASE (CGD), A DISEASE CHARACTERIZED BY A
• DEFECT IN THE ABILITY OF NEUTROPHILS TO KILL BACTERIA. DUE TO A PHAGOCYTE’S NADPH OXIDASE GENETIC DEFECT RESULTING IN PRODUCTION OF LESS SUPEROXIDE RADICALS AND THEREFORE LESS HYDROGEN PEROXIDE – ENOUGH TO KILL MANY KINDS OF BACTERIA, BUT NOT ENOUGH TO KILL S.
• AUREUS. CATALASE WILL DESTROY THE SMALL AMOUNT OF HYDROGEN PEROXIDE
• PRODUCES.

• FOREIGN BODIES: SUCH AS SUTURES, AND IV CATHETERS

• LACK ANTIBODY AGAINST TSST

• IMPROPER FOOD STORAGE (TOXIGENIC INFECTION)

• POOR SKIN HYGIENE (PYOGENIC INFECTION; LOCAL)

• • SEVERE INFECTIONS CAUSED BY
• COMMUNITY-ACQUIRED MRSA ESPECIALLY AMONG HOMELESS
• AND IV DRUG USERS. ATHLETES

• 90% OR MORE RESISTANT TO PEN G, PRODUCE BETA-LACTAMASE. PENICILLINASE GENE IS CARRIED ON TRANSMISSIBLE PLASMIDS WHICH RESULTED IN RAPID SPREAD AMONG STAPHYLOCOCCI.

• • 20% RESISTANT TO B-LACTAMASE-RESISTANT PENICILLINS, SUCH AS METHICILLIN AND NAFCILLIN, DUE TO CHANGES IN THE PENICILLIN-BINDING
• PROTEIN IN CELL MEM. KNOWN AS METHICILLIN-RESISTANT S. AUREUS (MRSA) OR OR NAFCILLIN-RESISTANT S. AUREUS (NRSA). ACQUIRED THE CHROM GENE MecA THAT ENCODES ALTERED PENICILLIN/BINDING PROTEIN (PBP) (A
• TRANSPEPTIDASE), RESISTANT TO ALL B- LACTAM DRUGS

• USE VANCOMYCIN (GENTAMICIN IS SOMETIMES ADDED)

•RARE STRAINS CALLED VANCOMYCIN-INTERMEDIATE S.AUREUS (VISA) HAVE EMERGED. THE VANA GENE, PRODUCING RESISTANCE DUE TO A MODIFIED CELL WALL PRECURSORS (D-ALA-D-LAC INSTEAD OF D-ALA-D-ALA) IS PLASMID-INHERITED AND IS THOUGHT TO BE ACQUIRED FROM VANCOMYCIN-RESISTANT ENTEROCOCCI (VRE) VIA CONJUGATION

• TRIMETHROPRIM-SULFAMETHOXAZOLE OR CLYNDAMYCIN CAN BE USED TO TREAT NON-LIFE-THREATENING INFECTIONS

• INTERMEDIATE RESISTANCE STRAINS (VISA) AND WITH COMPLETE RESISTANCE TO VANCOMYCIN HAVE BEEN REPORTED.

• TOXIC SHOCK SYNDROME INVOLVES ADMINISTRATION OFA B-LACTAMASE-RESISTANT PENICILLIN SUCH AS NAFICILLIN; AND REMOVAL OF THE TAMPON OR DEBRIDEMENT OF THE INFECTED SITE AS NEEDED

• • MUPIROCIN AS TOPICAL ABX IN SKIN INFECTIONS. ALSO REDUCE NASAL CARRIAGE OF THE ORGANISM IN HOSPITAL
• PERSONNEL AND PATIENTS WITH RECURRENT STAPH INFECTIONS.

• INTRANASAL MUPIROCIN

• • CEFAZOLIN IS OFTEN USED
• PERIOPERATIVELY TO PREVENT STAPH SURGICAL-WOUND INFECTIONS

•DRAINAGE FOR ABSCESS TX

PYOGENIC INFECTIONS

• • PROSTHETIC IMPLANTS SUCH AS HEART VALVES (CAUSING ENDOCARDITIS),
• VASCULAR GRAFTS, AND PROSTHETIC JOINTS (I.E. HIP JOINTS) – CAUSES MORE THAN 50% OF ARTIFICIAL DEVICE
• INFECTIONS

• IV CATHETER SITES

• MAJOR CAUSE OF SEPSIS IN NEONATES

• PERITONITIS IN PATIENTS WITH RENAL FAILURE WHO ARE UNDERGOING
• PERITONEAL DIALYSIS THROUGH AND INDWELLING CATHETER

• MOST COMMON BACTERIUM TO CAUSE CSF SHUNT INFECTIONS

• • INFECTIVE ENDOCARDITIS: OCCURS WHEN BACTERIA FROM THE BLOOD SETTLE ON AND COLONIZE NORMAL OR PREVIOUSLY DEFORMED HEART VALVES WHICH, IN TURN, MAY LEAD TO DESTRUCTION OF VALVES; DRUG ABUSERS
• ARE ESPECIALLY AT RISK. STRAINS OF THIS ORGANISM COLONIZING THE SKIN MAKE BIOFILMS THAT ALLOW THEM TO READILY
• COLONIZE IV CATHETERS; FROM THE COLONIZED CATHETER THEY INVADE THE
• BLOODSTREAM AND GAIN ENTRANCE TO THE HEART

• GRAM+ COCCI IN GRAPELIKE CLUSTERS

• CATALASE POSITIVE (STREP-)

• NO SPORES

• FACULTATIVE ANAEROBE

• EXTRACELLULAR

• COAGULASE NEGATIVE (AUREUS+)

• WHITE COLONIES (AUREUS GOLD)

• NON-HEMOLYTIC

• DOES NOT FERMENT MANNITOL (STAPH AUR DOES)

• NOVOBIOCIN SENSITIVE (SAPRO(R), USED FOR COAG- STAPH, NOT USED IN PATIENTS, TOXIC

RESEMBLE NOROVIRUS?

• HUMAN SKIN

• ENTER BLOODSTREAM AT THE SITE OF IV CATHETERS

• ALMOST ALWAYS HOSPITAL ACQUIRED (NOSOCOMIAL)

• HOSPITAL PERSONNEL ARE A MAJOR RESERVOIR FOR ABX-RESISTANT STRAINS

• • PART OF THE NORMAL HUMAN FLORA
• ON THE SKIN AND MUCOUS MEMBRANES BUT CAN ENTER THE BLOODSTREAM
• (BACTEREMIA)

• DO NOT PRODUCE PROTEIN A

• DO NOT PRODUCE EXOTOXINS

• GLYCOCALYX: ENHANCES ADHERENCE TO PROSTHETIC IMPLANT MATERIALS

•BIOFILM

• • HIGHLY ABX RESISTANT BC MOST
• STRAINS PRODUCE BETA-LACTAMASE
• AND MANY ARE METHICILLIN/NAFCILLIN-RESISTANT DUE TO ALTERED PENICILLIN-BINDING PROTEINS.

• USE VANCOMYCIN (CAN ADD RAFIMPIN OR AN AMINOGLYCOSIDE)

• REMOVAL OF THE CATHETER

• GRAM POS COCCI IN GRAPELIKE CLUSTERS

• CATALASE POSITIVE (STREP-)

• NO SPORES

• FACULTATIVE ANAEROBE

• EXTRACELLULAR

• COAGULASE NEGATIVE (AUR+)

• WHITE COLONIES

• NON-HEMOLYTIC

• DOES NOT FERMENT MANNITOL

• NOVOBIOCIN RESISTANT (STREP EPID S)

NO PROT A

NO EXOTOXINS

• • UTI: PARTICULARLY IN SEXUALLY ACTIVE YOUNG WOMEN WHO HAVE HAD SEXUAL
• INTERCOURSE IN PREVIOUS 24 HRS.

• •2ND TO E. COLI AS A CAUSE OF
• COMMUNITY-ACQUIRED UTI IN YOUNG WOMEN

• • MUCOSA OF GENITAL TRACT IN YOUNG WOMEN (CAN ASCEND INTO THE URINARY
• BLADDER TO CAUSE UTIS)

PREDISPOSING FACTORS

• BEING YOUNG, SEXUALLY ACTIVE

TX

• QUINOLONE, SUCH AS NORFLOXACIN, OR WITH TRIMETHOPRIM SULFAMETHOXAZOLE PREVENTION

• NO VACCINE

• • SUPPURATIVE (PUS-PRODUCING) DISEASES OR PYOGENIC INFLAMMATION
• (INDUCED LOCALLY AT THE SITE OF THE ORGANISMS IN TISSUE)

PHARYNGITIS CAN EXTEND TO OTITIS, SINUSITIS, MASTOIDITIS, MENINGITIS). MOST COMMON CAUSE OF BAC SORE THROAT, SECOND TO VIRAL (I.CARE - INF, CORONA, ADENO, RHINO, EB HHV-4

IMPETIGO (SUPERFICIAL SKIN INFECTION, “HONEY-COLORED” CRUSTED LESIONS.

CELLULITIS

• •ADHERE TO PHAR EPI VIA PILI COVERED WITH LIPOTEICHOIC ACID AND M
• PROTEIN.

• ENDOMETRITIS (PUERPERAL FEVER) INFECTION IN PREGNANT WOMEN, AND SEPSIS

NECROTIZING FASCIITIS, AKA STREP GANGRENE AKA “FLESH-EATING BACTERIA” M PROTS BLOCK PHAGOCYTOSIS, SWELLING, HEAT, AND REDNESS, A DAY LATER SKIN COLOR CHANGES FROM RED TO PURPLE TO BLUE AND LARGE BLISTERS FORM, LATER THE SKIN DIES AND MUSCLE MAY ALSO BECOME INFECTED (MYOSITIS)

• • SCARLET FEVER (CAUSED BY GAS
• IN KIDS), CAUSED BY SPE-A (OR PYROGENIC/ERYTHROGENIC
• TOXIN), DUE TO LYSOGENIC
• CONVERSION BY BACTERIOPHAGE
• (TRANSDUCTION); PT. GETS SCARLET
• FEVER IF HE/SHE DOESN’T HAVE ANTITOXIN. FEVER, STRAWBERRY TONGUE, RASH THAT BEGINS ON TRUCK AND NECK, THEN SPREADS TO EXTREMITIES, SPARING THE FACE, THE SKIN MAY PEEL OFF IN FINE SCALES DURING HEALING

• • TOXIC SHOCK SYNDROME-
• PYROGENIC TOXIN, STARTS AS SKIN OR WOUND INFECTION, SYSTEMIC SPREAD OF TOXIN, MULTIPLE ORGAN FAILURE,
• SIMILARITIES WITH TSST-1: SUPERANTIGENS, PROTEIN EXOTOXINS, ENHANCE TYPE IV HYPERSENSITIVITIES, SUPPRESS THE Ab RESPONSE, INDUCE IL-1 AND TNF-ALPHA, LEAD TO MULTIPLE ORGAN FAILURE DIFFERENCE: STREP TSS INVOLVES SYSTEMIC SPREAD OF THE
• STREPTOCOCCI (BACTEREMIA) THAT ARE PRODUCING THE TOXIN, STAPH IS SPREAD OF TOXIN (TOXEMIA) FROM STAPH THAT REMAIN LOCAL. STREP TSS BLOOD CULTURES ARE OFTEN POSITIVE.

ARF & APSGN: POST INFECTION

• SEPSIS AND PNEUM (EARLY
• ONSET)

• NEONATAL MENINGITIS AND SEPSIS (LATE ONSET; LEADING CAUSE). FEVER, VOMITING, POOR FEEDING, IRRITABILITY, NEED LUMBAR PUNCTURE

• CAUSE NEONATAL PNEUMONIA

• COLONIZE THE GENITAL TRACT OF SOME WOMEN

• • IN ADULTS, PNEUMONIA, ENDOCARDITIS, ARTHRITIS, OSTEOMYLITIS, POSTPARTUM
• ENDOMETRITIS. DIABETES IS THE MAIN PREDISPOSING FACTOR
• • PEN G OR AMPICILLIN AND AN AMINOGLYCOSIDE

•PREVENTION: EARLY BY PROPHYLACTIC IV PEN G OR AMPICILLIN TO GBS PREGNANT MOM NEAR TIME OF DELIVERY (35-37 WKS)

NO VACCINE. IF NO CULTURES DONE, THEN PEN G OR AMPICILLIN VIA IV AT THE TIME OF DELIVERY FOR PROLONGED (LONGER THAN 18 HRS) RUPTURE OF MEMBRANES, WHOSE LABOR BEGINS BEFORE 37 WKS GESTATION, OR FEVER AT THE TIME OF LABOR. IF ALLERGIC TO PENICILLIN, USE CEFAZOLIN OR VANCOMYCIN.

NO ORAL AMPICILLIN TO PREGOs!

• GRAM POS COCCI CHAINS

• CATALASE NEG

• • GROWS IN 6.5% NACL OR 40% BILE
• SALTS, AND HYDROLYZES ESCULIN (CRYSTALLINE GLYCOSIDE TURNS FROM COLORLESS TO BLACK) IN THE PRESENCE OF BILE. NECESSARY TO SURVIVE IN THE BOWEL AND GALL BLADDER

• USED TO BE CLASSIFIED AS GROUP D, NOW DISTINCT

• NORMAL FLORA OF THE GI TRACT

• • MAY PRODUCE ALPHA, BETA, OR
• GAMA-HEMOLYSIS

• NO SPORES

• FACULTATIVE ANAEROBE

• EXTRACELLULAR

• • HOSPITAL ACQUIRED UTI (MAIN
• CAUSE) AND BILIARY TRACT INFECTIONS

• • PREDISPOSING FACTORS: INDWELLING URINARY CATHETERS AND UT INSTRUMENTATION
• • ENDOCARDITIS (RARE) IN PT WHO UNDERWENT GI OR UT SX OR INSTRUMENTATION

• ASSOC W/ BACTEREMIA, BEDSORES, WOUNDS, AND INTRA-ABDOMINAL INFECTIONS

• • HUMAN COLON, URETHRA AND
• FEMALE GENITAL TRACT

• • CAN ENTER BLOODSTREAM
• DURING GI PROCEDURES

• NO EXOTOXINS OR VIRULENCE FACTORS IDENTIFIED

• TX: NEED 2 ANTIBIOTICS TO KILL: PEN + AMINOGLYCOSIDE, SUCH AS GENTAMICIN
• ABX SYNERGISM

• CAN USE VANCOMYCIN WITH AN AMINOGLYCOSIDE, BUT SOME VRE HAVE EMERGED. ACQUIRED A CHROM TRANSPOSON VanA THAT ENCODES A SERIES OF PROTEINS THAT MODIFY THE D-ALA-D-ALA TERMINUS OF THE PEPTIDOGLYCAN CELL WALL, CHANGING IT TO D-ALA-D-LAC, WHICH HAS A LOW AFFINITY FOR VANCOMYCIN.

• • 2 INVESTIGATIONAL DRUGS TO TREAT INFECTIONS CAUSED BY VRE: LINEZOLID
• (ZYVOX) AND QUINUPRISTIN/DALFOPRISTIN (SYNERCID)

• PREVENT: PENICILLIN + GENTAMICIN TO PTS W/ DAMAGED HEART VALVES UNDERGOING UT PROCEDURES

Respiratory-Coronavirus-Pharyngitis, cough, similar to common cold

• Orthomyxovirus-Influenza-A&B, (Reye's syndrome if
• aspirin taken), fever and myalgia (IL-1 and TNF-a)

Paramyxoviridae Parainfluenza Bronchiolitis - Infants; Croup - young children; Common cold - adults

Paramyxoviridae-Respiratory Syncitial-Bronchiolitis and pneumonia in infants

• Paramyxoviridae Measles
• virus Giant Cell Pneumonia

• Paramyxoviridae Mumps
• virus Mumps, Parotitis, Deafness,
• Orchitis, Oophoritis, Pancreatitis, myocarditis

Adenovirus-Adenovirus-(3,4,7,11,21) 5-10% URTI in children

Picornaviridae Rhinovirus Common cold

PICORNA POLIOVIRUS DIARRHEA

PICORNAVIRIDAE ENTEROVIRUS DIARRHEA

• PICORNAVIRIDAE COXSACKIEVIRUS
• B GASTROENTERITIS, MYOCARDITIS

• ADENOVIRUS ADENOVIRUS
• (40,41) INFANT GASTROENTERITIS

CALICIVIRIDAE NOROVIRUS DIARRHEA

• ASTROVIRIDAE ASTROVIRUS DIARRHEA, GASTROENTERITIS IN ADULTS AND
• CHILDREN

REOVIRIDAE ROTAVIRUS DIARRHEA

PICORNA COXSACKIEVIRUS HERPANGINA AND HAND-FOOT-AND-MOUTH

PICORNAVIRIDAE ECHOVIRUS FEBRILE AND ASEPTIC MENINGITIS

• PARAMYXOVIRIDAE MUMPS
• VIRUS MUMPS, PAROTITIS, DEAFNESS,
• ORCHITIS, OOPHORITIS, PANCREATITIS, MYOCARDITIS

PICORNAVIRIDAE POLIOVIRUS POLIOMYELITIS

• ENCEPHALITIS ARBOVIRUSES
• (TRANSMITTED VIA ARTHROPOD VECTORS, I.E. TICKS AND MOSQUITOS)

• BUNYAVIRIDAE HANTAVIRUS
• (ROBOVIRUS) HANTAVIRUS PULMONARY
• SYNDROME

• FLAVIVIRIDAE WEST
• NILE, ST. LOUIS ENCEPHALITIS, YELLOW FEVER, DENGUE VIRUSES

• TOGAVIRIDAE EASTERN/WESTERN
• (CALIFORNIA) EQUINE ENCEPHALITIS VIRUSES

• HERPESVIRIDAE Γ EPSTEIN-BARR
• VIRUS GUILLAN-BARRE SYNDROME

• HERPESVIRIDAE Α HERPES
• SIMPLEX VIRUS 1 NECROTIC
• LESION ON TEMPORAL LOBES

• HERPESVIRIDAE Α VARICELLA-ZOSTER
• VIRUS VARICELLA (CHICKENPOX) -
• CHILDREN; ZOSTER (SHINGLES) - ADULTS

• PARAMYXOVIRIDAE MEASLES
• VIRUS SUBACUTE SCLEROSING
• PANENCEPHALITIS IS A RARE LATE COMPLICATION

• RHABDOVIRIDAE RABIES
• VIRUS RABIES, HYDROPHOBIA, SEIZURES,
• PARALYSIS

PAPILLOMA VIRUS PAPILLOMAS (WARTS)

• PARVOVIRIDAE PARVOVIRUS
• B19 ERYTHEMA INFECTIOSUM

• HERPESVIRIDAE Α VARICELLA-ZOSTER
• VIRUS VARICELLA (CHICKENPOX) -
• CHILDREN; ZOSTER (SHINGLES) - ADULTS

• PARAMYXOVIRIDAE MEASLES
• VIRUS MACULOPAPULAR SKIN
• RASH, KOPLIK'S SPOTS, CONJUNCTIVITIS, COUGH, CORYZA

• EYES ADENOVIRUS
• (18,19) CONJUNCTIVITIS

HEMORRHAGIC FEVER FILOVIRUSES EBOLA/MARBURG VIRUSES

• ARENAVIRIDAE ARENAVIRUSES LASSA FEVER, HEMORRHAGIC FEVER,
• LYMPHOCYTIC CHORIOMENINGITIS VIRUS

BUNYAVIRIDAE HANTAVIRUS HEMORRHAGIC FEVER WITH RENAL SYNDROME

RSV MOST COMMON CAUSE OF BRONCHIOLITIS/PNEUMONIA IN INFANTS

CMV MOST COMMON CAUSE OF CONGENITAL ABNORMALITIES (MICROENCEPHALY) OWL EYE INCLUSION BODIES

EBV MOST COMMON CAUSE OF INFECTIOUS MONONUCLEOSIS (LYMPHOCYTOSIS) ATYPICAL T LYMPHOCYTES

HSV MOST COMMON CAUSE OF SPORADIC ENCEPHALITIS

JCV PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY (DEMYELINATING DIS.)

• HPV MOST COMMON CAUSE OF CERVICAL CANCER GENITAL WARTS
• (PAPILLOMA)

BKV KIDNEY DISEASE

• HANTAVIRUS HANTAVIRUS
• PULMONARY DISEASE (FLU SX AFTER 3 DAYS, ARDS 12 DAYS) DEER MICE