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MICROBIOLOGY. Prepared by: Dr. D. Boyd, DDS Oral & Maxillofacial Pathologist Associate Professor Reference: Kaplan Review Notes . INTRODUCTION. NORMAL MICROBIAL FLORA Properties: Population of microbes that usually reside in the body.

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Microbiology

MICROBIOLOGY

Prepared by: Dr. D. Boyd, DDS

Oral & Maxillofacial Pathologist

Associate Professor

Reference: Kaplan Review Notes


Introduction
INTRODUCTION

  • NORMAL MICROBIAL FLORA

  • Properties:

    • Population of microbes that usually reside in the body.

    • Resident flora: fixed population that will repopulate if disturbed, e.g S mutans (caries)

    • Transient flora: from environs & reside in body without invasion, & prevent infection by more pathogenic organisms (bacterial interference)


Distribution of normal microbial flora
Distribution of Normal Microbial Flora

  • LocationMajor Organism

  • Skin Propionibacteria acnes, Staph epidermis & aureus, diptheroids

  • Oral cavity viridians Streptococcus, Prevotella melaninogenicus, Actinomyces, Peptostreptococcus, other anaerobes

  • Nasopharynx:oral microbes, Staph pneumonia, Hemophilus, Nisseria meningitis

  • Vagina Childbearing age: Lactobacillus, yeast, Streptococcus


Microbial virulence factors
Microbial Virulence Factors

  • Gene products required for establishment in the host.

  • Gene products located on chromosomes, or plasmid or transposons (mobile genetic material)

  • Primary pathogens virulence factors disease.

  • Opportunistic pathogens (environ or normal flora)  disease ONLY if host is immunocompromized


Categories of virulence factors
Categories of Virulence Factors

  • Enzyme production

    Hyaluronidasebreaks down Hyaluronic acid digestion of tissue

    Protease digests protein  spread of infection

    Coagulase allows coagulation of fibrinogen  clot

    Collagenase breaks down collagen (connective tissue)


Categories of virulence factors1
Categories of Virulence Factors

  • 2. Toxins

  • Exotoxins

    • heat-labile proteins with specific enzymatic activities

    • Produced by both Gram positive & negative microbes

    • Released extracellularly

    • Often sole cause of disease


Categories of virulence factors2
Categories of Virulence Factors

  • Exotoxins:

    • Domains with discrete biologic functions  maximal toxicity

    • A - B toxins

      • B subunit bind to host tissue Glycoproteins

      • A subunit enzymatically attack susceptable


Categories of virulence factors3
Categories of Virulence Factors

  • Endotoxins

    • Heat-stable lipopolysaccharide molecule

    • Located on outer membrane of Gram negative microbes

    • When released by cell lysis  Lipid A portion  septic shock (fever, acidosis, hypotension, complement consumption, and disseminated intravascular coagulation DIC)


Categories of virulence factors4
Categories of Virulence Factors

  • 3.Surface components

    • Protect organism from immune response

    • Polysaccharide capsule of H influenzae

    • Acidic polysaccharide capsule of Streptococcus pneumoniae

    • Adhesins  attach microb to cell of host

    • Filamentous appendages (fimbriae, pili)  attach microb to cell of host

    • Flagella  motility


Classification identification of bacteria
Classification & Identification of Bacteria

  • General properties

  • Prokaryotic = single –cell organism

  • 70 S ribrosomes

  • Naked, single, circular chromosome of double stranded DNA the replicates bi-directionally)

  • No true nucleus (no nuclear membrane)

  • No membrane bound organelles

  • Cell wall is rigid, peptidoglycan layer  Gram positive or negative, Acid fast (resist acid de-coloration e.g Mycobacteria)


Classification identification of bacteria1
Classification & Identification of Bacteria

  • Mycoplasma + Ureaplasm

    • Only bacteria that do NOT have cell walls

  • Chlamydia’s cell wall lack muramic acid

  • Both resistant to beta-lactam antibiotic (penicillin + cephalosporins)

  • Prokaryotic flagella do NOT have:

    • 9 + 2 microtubles arangement

    • microtubules


Classification of bacteria
Classification of Bacteria

  • Biomedical characteristics

    • Bordetella pertussis grows only onBordet- Gengou agar)

    • E. coli ferment only Lactose sugar

    • M. tuberculosis produces Naicin

  • Serologic reactivity with specific Antibodies in diagnostic immunoassays

  • Bacteriophage typing used in tracing source of epidemics

  • Animal pathogenicity & Antibiotic sensitivity


Bacterial structure
Bacterial Structure

  • 1. CELL ENVELOPE

  • Gram positivesmooth surface with 3 layers

    • Cytoplasmic membrane = smooth surface

    • Thick layer of:

      • Peptidogylcan

      • Lipoteichoic acids

      • Polysaccharides

      • Teichoic acid (sometimes

    • Outer capsule (sometimes)


Bacterial structure1
Bacterial Structure

  • Gram negative (complex cell envelope)

    • Cytoplasmic membrane (inner membrane)

    • Periplasmic space (containing peptidoglycan

    • Outer membrane

      • Tri-layered anchored to cell membrane by lipoprotein

      • Endotoxin (LPS, somatic O antigen, core polysaccharide)

      • Protein porin channels

    • Capsule (sometimes)


Bacterial structure2
Bacterial Structure

2. PLASMA (cell) MEMBRANE

Function as osmotic barrier

60 – 70% protein

30 – 40% lipid (fat)

Carbohydrate (small amounts)

Bacterial electron transport chain (cytoplasmic membrane)

Membrane polyribosome-DNA

Mesosomes = convoluted structures of cell membrane important in cell division)


Bacterial structure3
Bacterial Structure

  • 3. CYTOPLASMIC STRUCTURES

  • 1. Nucleoid region = circular chromosome of double-stranded DNA

    • Lack introns, histones, nuclear membrane

  • 2. Ribosomes

    • 70% RNA (ribonucleic acid), 30% protein

    • 70S ribosome attached to messenger RNA  proteins

    • 70 S complex  subunits 50S + 20S


  • Bacterial structure4
    Bacterial Structure

    • 3. Polyamines located in Ribosomes

      • Prevent dissociation of the 70S ribosome

  • 4. Cytoplasmic granules store:

    • Glycogen

    • Lipid (poly-bete-hydroxybutyrate)

    • Phosphate (volutin granules)


  • Bacterial structure5
    Bacterial Structure

    • Spores (endospores):

      • Bacillus & Clostridium species

      • Promote survival

      • Resit heat + drying

      • Highly dehydrated + refractile

      • Convert to vegetative state via germination when environ favorable

  • Bacillus species used to check Autoclave used in Sterilizing instruments


  • Bacterial growth
    Bacterial Growth

    • Depends on

      • Available nutrients

      • External environs e.g Temperature

      • Growth rate of specific species

    • Lag phase = period of no growth, adapting

    • Exponential phase

      • Steady state of growth,

      • Continues until nutrients are depleted or toxic wastes products accumulate

      • Antibiotics maximally effective


    Bacterial growth1
    Bacterial Growth

    • Stationary phase occurs when nutrients are exhausted or toxins accumulate (cell loss = cell formation)

    • Phase of decline occur when death rate increases due to cell starvation or sensitivity to toxins


    Survival in oxygen
    Survival in Oxygen

    • Used to classify bacteria

    • All bacteria produce Superoxideion (O2-) in the presence of Oxygen.

    • Superoxide dismutase + O2- Hydrogen peroxide (H2O2)

    • Catalase or Peroxidase + H2O2 H2O + O2

    • Obligate Anaerobeslack these enzymes therefore Oxygen is toxic to them. (Clostridium & Bacteroides)

    • Facultative organisms grow with or without oxygen.


    Energy production
    Energy Production

    • Requires a source of Carbon

    • Fastidious bacteria lost their metabolic machinery and need many additional requirements.

    • Siderophores = Iron (Fe3+) chelating compound essential for bacterial growth.


    Mechanisms of energy production
    Mechanisms of Energy Production

    • 1. Fermentation

      • Anaerobic degradation of glucose to obtain ATP

      • Less efficient than respiration

      • Used by most Obligate Anaerobes & all Streptococcus species


    Mechanisms of energy production1
    Mechanisms of Energy Production

    • 2. Respiration

      • Completely oxidizes Organic fuels

      • Requires an Electron Transport Chain to drive the synthesis of ATP

      • Produces 20 times as much ATP

      • Requires terminal electron acceptor (TEA)

        • Oxygen, nitrate, fumarate

    • Obligate Aerobes

      • Uses respiration only

      • Must use O2 as TEA (M. tuberculosis)


    Sporulation
    Sporulation

    • Spore

    • Dormant structure capable of surviving long period of unfavorable environs.

    • Capable of re-establishing the vegetative state.

    • Resistant to radiation, drying, disinfectants.

    • Thermal resistance due to high content of Calcium & Dipicolinic acid in the core.


    Sporulation1
    Sporulation

    • Bacillus & Clostridiumspecies.

    • Inhibition of sporulation related to Guanosine Tri-phosphate (GTP) pool.

    • Carbon & Nitrogen important

    • Germination & Outgrowth occur when environs & nutrition (glucose, nucleic acid, amino acids) allow.


    Genetic transfer
    Genetic Transfer

    • Movement of genetic material into Host

    • 1. Transformation

      • Uptake & Integration of naked DNA

      • Once inside the cell homologous re-combination with chromosome of the recipient must occur

      • Induced in the Lab with Salt & Heat shock, which force cells to take up plasmids carrying genes of interest.

      • Streptococcus, Haemophilius, Neisseria gonorrhea, Helicobacter pylori (stomach ulcers)


    Genetic transfer1
    Genetic Transfer

    • 2. Transduction

      • Phage-mediated transfer of bacterial DNA

    • Generalized:

      • bacterial DNA mistakenly packaged into empty phage head

      • Recombination occur


    Genetic transfer2
    Genetic Transfer

    • Transduction (cont)

    • Specialized:

      • Lysogenic phage integrated into bacterial chromosome excises itself

      • Accidentially takes up chromosomal DNA

      • Phage replicates  bacterial gene picked up replicates

      • Genes carried into cells that the progeny virus infected

      • Occurs most often


    Genetic transfer3
    Genetic Transfer

    • 3. Conjugation (bacterial sex)

    • Direct transfer of bacterial DNA

    • Requires cell to cell contact

    • Most important mechanism for widespread transfer of genetic information between bacteria.

    • Plasmid mediated. (Extrachromosomal piece of circular DNA that can replicate itself)

      • Carries genes that encode resistance to antibiotics + virulence factors

      • Narrow-host-range, broad-host-range plasmids


    Genetic transfer4
    Genetic Transfer

    • 3. Conjugation (continued)

    • Narrow-host-range exist in single species

    • Broad-host-range transfer between different genera

    • Conjugated plasmid code for genes involved in transfer between cells

    • Non-conjugated plasmids require help of conjugated plasmid


    Genetic transfer5
    Genetic Transfer

    • 4. Insertion Sequences are small pieces of DNA that code for the enzyme Transposase which allow pieces to jump into & out of DNA

    • Transposons consist of:

      • Two insertion sequences flanking an antibiotic resistance genes

      • Frequently associated with mutiple drug resistance plasmids


    Dental clinic microbiology
    Dental Clinic Microbiology

    • Sterilization

      • Most commonly used

      • Bacteria + Fungi + Viruses + Spores killed

    • Disinfection

      • Killing of pathogenic organisms + most microbes in general.

      • Will NOT kill spores

      • Disinfected instruments are NOT sterile but safe to use


    Classification of instruments
    Classification of Instruments

    • Critical Instruments

      • Pierce mucous membrane or enter sterile tissues

      • Scalpel blades, Periodontal scalers, Endodontic files, Handpieces

      • Must be Sterilized or Disposable

    • Semi-critical Instruments

      • Touch mucous membrane

      • Mouth mirrors, Explorers, Xray instruments


    Sterilization methods
    Sterilization Methods

    • Autoclave (Steam)dull or corrode sharp edges

      • 121 degrees F for 20 – 30 minutes, 15psi

    • Dry Heat (Driclave) – maintain sharp edges

      • 160 degrees F for 1 – 2 hours

    • Ethylene oxide (Chemiclave) 8 – 12 hours

      • Used for heat-sensitive instruments

    • “Cold Sterilization (misnomer)

      • Uses long-term disinfectants

      • Spores are NOT killed unless placed in Glutaraldehyde 12 – 15 hours


    Sterilization methods1
    Sterilization Methods

    • All instruments must be clean & free of debris

    • Failure to Strelize due to:

      • Autoclave over packed

      • Time insufficient (wrapped instrument need more time)

      • Autoclave cycle interrupted (power cut)

      • Tissue (protein) left on instruments


    Material method action
    Material Method & Action

    • Material/Method Action

    • Steam Heat & Protein denaturation

      Disinfectants

      Alcohol & Phenols Protein denaturation

    • Glutaraldehyde Alkylation protein / DNA & Ethylene oxide

    • Detergent Membrane disruption

    • Chlorohexidine Membrane disruption

    • Peroxides & Hg & I Oxidize Sulfhydryl bond

    • Soap Emulsifcation of Fat


    Disinfectant guidelines
    Disinfectant Guidelines

    • Must be Environmental Protection Agency (EPA) approve

    • Must kill “benchmark” organism Mycobacterium tuberculosis

    • Must have Dental Association seal of approval for use on dental instruments

    • Disinfectants used on materials & surfaces

    • Antiseptics used on live tissue

    • Hepatitis A & Mycobacterium hard to kill on surfaces


    Sterilization monitors
    Sterilization Monitors

    • Sterilizers should be checked weekly

    • Process Indicator(Does NOT show sterilization)

      • Shows that sufficient Temperature was reached for a specific period of time.

      • Color change strip or section on autoclave bag.

    • Biological Monitors (Legal requirement)

      • Spore strips of Bacillus sp loaded with instruments & cultured after autoclaving.

      • “Control strip” used to show viability of spores.


    Universal precautions
    Universal Precautions

    • All patients are assumed to be infectious.

    • Equal Disinfectant/Sterilization/Cleaning procedures for all patients

    • Preparation of Rooms Instruments & Materials depend on Procedure NOT Patient.

    • Hand Washing:

      • Single most effective measure for infection control

      • Arrival & leaving work, before & between patients, before & after going to restroom


    Procedures included in universal precautions
    Procedures Included in Universal Precautions

    • Sterilization of MOST instruments.

    • Disinfection of semi-critical instruments + “Touch and Splash” surfaces.

    • Barrier methods (Gloves, Masks, Face Shields, Plastic Chair Covers, Light Handle Covers)

    • Disposable instruments (Saliva Ejectors, Prophy angles, etc)


    History of universal precautions
    HISTORY OF UNIVERSAL PRECAUTIONS

    • 1970s: Hepatitis B “clusters”traced to dental offices

    • 1980s: HID disease refocused dental profession

    • Much easier to contract HBV than HIV

    • Approximate conversion rate after needle stick:

      • HBV 30%

      • HCV 3%

      • HIV 0.3%


    Vaccination
    VACCINATION

    • Hepatitis B vaccination MUST be offered Free to all Dental Health Care Workers

    • Three injections (0 month, 1 month, 6 months)

    • Cannot contract disease from vaccination, not made from human blood products.

    • Recombivax:

      • Made HBsAg

      • Produced by Yeast


    Gram positive cocci staphlococcus streptococcus
    Gram Positive CocciStaphlococcus & Streptococcus

    • STAPHLOCOCCUS

    • Genus Characteristics & Classification

    • Gram positive

    • Divide in perpendicular plane  Clusters

    • Relatively resistant to Heat & Drying

    • Metabolically

      • Facultative organism

      • Possess Superoxide dismutaese & Calalase


    Staphylococcus cont
    Staphylococcus (cont)

    • Clinically:

    • S. aureus only is pathogenic

      • +ve Coagulase Test identifies S. aureus

    • S. epidermidis most numerous on the Skin

      • Coagulase test negative

        • Also S. Saprophyticus

          • Urinary tract infection in sexually active women

          • Treatment: Penicillin


    Staphylococcus aureus
    Staphylococcus aureus

    • Common infectious agent in humans

    • NOT part of normal flora

    • Transient in Nasopharynx, Skin, Vagina (30%)

    • Host defense = PMNs

    • NO protective immunity  repeated infection

    • Virulence factors include:

      • Protein A Binding protein Coagulase

      • DNAse Staphylokinase Lipase

      • Hyaluronidase Exotoxins (hemolysis)


    Staphylococcus aureus cont
    Staphylococcus aureus (cont)

    • Conditions Commonly Caused by S. aureus

    • Direct Infection of Skin:

      • Folliculitis Furuncle Carbuncle Abscess

      • Cellulitis Wound infection

    • Systemic Infection:

      • Osteomyelitis Endocarditis

      • Lung abscess pneumonia

    • Toxic-mediateddisease:

      • Food poisoning Scalded skin syndrome

      • Bullous impetigo Toxic shock syndrome


    Staphylococcus aureus cont1
    Staphylococcus aureus (cont)

    Treatment:

    • Penicillinase-resistant penicillin:

      • Amoxicillin, Methicillin, Nafcillin

    • Cephalosporin (first generation)

    • Vancomycin (methicillin-resistant S. aureus)

      • VRSA have been discovered


    Staphylococcus epidermidis
    Staphylococcus epidermidis

    Common nosocomial pathogen (Hospital based)

    Associated with:

    IVs Catheters Prosthetic devices

    Major virulence factor:

    Exopolysacharidebiofilm (slime)

    Difficult for Immune system to detect

    Treatment = Vancomycin


    Streptococcus know very well
    Streptococcus Know Very Well

    • Genus Characteristics

    • Gram positive cocci, grow in Chains

    • Metabolically:

    • Aerotolerant Anaerobes (facutative anaerobes)

    • Energy from fermentation only (lackcytochromes)  Lactic acid

    • Lack Catalase (cytochrome-containing enzyme degrades Hydrogen peroxide  oxygen + HOH

    • Medically most important Streptococcus are auxotrophs (require vitamin, amino acids for growth, not free living in the environs)


    Streptococcus cont
    Streptococcus (cont)

    • Classification

    • Based on reaction in Blood agar

    • Alpha Hemolytic

      • RBCs intact, partial breakdown of heme green (viridans) pigment

    • Beta Hemolytic

      • RBCs completely lysed

      • Group A clinically most important

    • Gamma Hemolytic: no effect on RBCs


    Alpha hemolytic steptococcus s pneumoniae viridans
    Alpha Hemolytic SteptococcusS. pneumoniae & Viridans

    • STREPTOCOCCUS PNEUMONIAE

    • Grow inshort chains

    • Inhibited by Optochin or Bile

    • Transmission via aerosol droplets from person to person

    • 20 – 40% of normal people colonized in Nose

    • Clinical Manifestations:

      • Most common cause of bacterial pneumonia

      • Otitis media Sinusitis Bronchitis

      • Bacteremia Meningitis (#1 cause in elderly)


    Streptococcus pneumoniae cont
    STREPTOCOCCUS PNEUMONIAE (cont)

    • Risk Factors for infection with S. pneumoniae

      • Poverty Debilitated state of Health

      • Absence of Spleen Sickle cell anemia

      • Hodgkin’s disease Multiple myeloma

      • AIDS

    • Most important virulence factor = carbohydrate capsule


    Streptococcus pneumoniae cont1
    STREPTOCOCCUS PNEUMONIAE (cont)

    • Prevention

    • Vaccination with its polysaccharide antigen (Pneumovax)

      • Should be given to:

        • Elderly, Splenectomy, smokers, alcoholics, children

    • Treatment

      • Penicillin (resistant forms)

      • Vancomycin Erythromycin


    Viridans streptococcus non beta hemolytic streptococcus
    Viridans Streptococcus (non-beta-hemolytic Streptococcus)

    • Found in oral flora, non-hemolytic Strep

    • S. mutans - tooth surface

    • S. mitis

    • S. sanguis - tongue

    • S. salivarius

    • Facultative anerobes. Gram positive


    Streptococccus mutans
    Streptococccus mutans

    • Chief etiologic agent for caries

    • Characteristics:

      • Aciduric

      • Attaches to pellicle [glucan (dextrans)]  Plaque  caries + Periodontal disease

      • Produces Glucosyltransferase  Glucans

      • Preferred substrate Sucrose (Energy + Glucans)

      • pH in Plaque < 5  demineralize Teeth


    Caries cont
    Caries (cont)

    • Other Aciduric Bacteria:

      • Lactobacillus species:

        • Colonize late carious lesions

        • Acid produced eliminate other bacteria + dissolve Enamel


    Caries cont1
    Caries (cont)

    • Effects of Fluoride on S. mutans & Caries:

      • Makes enamel more resitant to acid

      • Changes Hydroxyapatite to Fluorapatite by substituting F- for –OH ion

      • Shifts Remineralization – Demineralization equilibrium towards Remineralization

      • Toxic to bacteria, interferes with Glucosyltransferase

      • In high concentration (topical gel) will kill bacteria

      • 1 part per million (1mg/L)

      • Absorbed into developing teeth


    Viridans streptococcus subacute bacterial endocarditis
    Viridans Streptococcus & Subacute Bacterial Endocarditis

    • Caused due to bactermia with lodgement on artifical or defective Heart valves

    • Occur when:

      • Susceptible conditions:

        • Replacement valves

        • Previous history of Endocarditis

        • Mitral valve prolapse with regugitation

        • Rhematic heart disease


    Viridans streptococcus subacute bacterial endocarditis1
    Viridans Streptococcus & Subacute Bacterial Endocarditis

    • Occur when: (cont)

      • Colonization by bacteria  valve damage

      • Procedure involving bleeding (extractions, scaling, periodontal probing, endodontics)

    • Antibiotic Premedication: Patients with Heart Murmurs:

      • Amoxicillin (First choice)

      • If allergic to penicillin:

        • Clindamycin Azithromycin

        • Clarithromycin Cephalexin Cephadroxil


    Beta hemolytic steptococcus
    Beta Hemolytic Steptococcus

    • Subdivide into groups A – D, F & G

    • Based on antibodies to heat-labile, acid-stable Carbohydrate in cell wall

    • Antigen called C carbohydrate or Lancefield antigen

    • GROUP A STREPTOCOCCUS (GAS)

    • STREPTOCOCCUS PYOGENES

    • Most important

    • Growth inhibited by antibiotic Bacitracin


    Beta hemolytic steptococcus1
    Beta Hemolytic Steptococcus

    • Clinical Manifestations:

    • Suppurative(pus) complications of pharyngitis:

      • Otitis media Peritonsillar cellulitis

      • Erysipelas (skin) Scarlet Fever

      • Meningitis Pneumonia

      • Peritonsillar & Retropharygeal abscess

      • Pyoderma (impetigo)

      • Bacteremia Perianal abscess

      • Lymphangitis Emphyema

      • Meningitis Pneumonia


    Group a streptococcus streptococcus pyogenes cont
    GROUP A STREPTOCOCCUSSTREPTOCOCCUS PYOGENES (cont)

    • Clinical Manifestations (cont)

    • Non-suppurative

    • Occur weeks after initial Skin infection

      • Glomerulonephritis

        • Edema, Hypertension, Hematuria)

      • Rheumatic fever: (Post Pharngeal infection)

        • Fever, Endocarditis, Polyarthritis

        • 7 – 28 days after Pharyngitis)


    Group a streptococcus streptococcus pyogenes cont1
    GROUP A STREPTOCOCCUSSTREPTOCOCCUS PYOGENES (cont)

    • Transmission & Epidemiology

    • Obligate parasite in humans

    • Spread from person to person via air droplets or direct contact with Skin or Fomites

    • Pharyngitis most common in Winter & Spring

    • Highest incidence in Adolescents

    • Contaminated Milk & Eggs causes for food- borne epidemics

    • Impetigo-like Skin infection mostly in summer due to Insect Bites.

    • Virulence Factor: most important is M protein


    Group b streptococcus streptococcus agalactiae
    Group B Streptococcus (Streptococcus agalactiae)

    • Part of normal flora of Vagina + GIT (25%)

    • Resistant to Bacitracin

    • Virulence factor = antiphagocytic polysaccharide capsule

    • Infants more susceptible, aspirate organism during passage thru Birth Canal, lack passive resistance from maternal IgG antibodies

    • Clinical Manifestations: pneumonia, sepsis, meningitis

    • Treatment: penicillinase-resistant penicillin


    Group b streptococcus enterococcus
    Group B Streptococcus (Enterococcus)

    • Previously group D Streptococcus

    • Enterococcus faecalis and E. Faecium

    • Part of normal Fecal flora

    • Cause infection when spread to Urinary Tract in Hospital Patients  Abscess

    • Cause 10% Subacute Endocarditis

    • Inhibited by Penicillin

    • Vancomycin-resistant Enterococci (VRE)


    Gram positive bacilli
    Gram Positive Bacilli

    • Listeria – NO Spores

    • Corneybacterium - NO Spores

    • Bacillius – Spores

    • Clostridium - Spores


    Listeriia monocytogenes
    Listeriia monocytogenes

    • Small Gram positive coccobacillus. No spores

    • Microscopically resemble non-pathogenic Corynebacterium genus, part of normal Skin flora

    • Transmission:

      • Facultative intracellular pathogen

      • Infects phagocytic cells

      • Prduces listeriolysis O  beta-hemolysin

      • Contaminated Meat or unpasteurized Milk


    Listeriia monocytogenes cont
    Listeriia monocytogenes (cont)

    • Risk Factors

      • Neonates (transmission across placenta or during delivery

      • Pregnancy (Bacteremia)

      • Alcoholics (Meningitis)

      • Immunosuppression: (AIDS, Steroids, Chemotherapy, Transplants)  Meningitis


    Cornybacterium diphtheriae
    Cornybacterium diphtheriae

    • Non-motileClub-shaped No Spores

    • Diphtheria toxin (encoded by lysogenic phage)

    • Clinical Manifestations:

      • Upper Respiratory tract infection

      • Tonsillar gray pseudo-membrane

      • Compromised airway

      • Diphtheria toxin especially toxic to Heart

    • Treatment: anti-toxin & Erythromycin ASAP

    • Prevention: Vaccine (diphtheria toxoid) during 1st year. Boosters every 10 years


    Bacillius anthracis
    Bacillius anthracis

    • Spores persists in Soil for many years

    • Encoded on Plasma is Anti-phagocytic capsule

      composed of D-glutamate

    • 3 Virulence Factors (Anthrax toxin)

      • Protective antigen (PA)

      • Lethal factor

      • Edema factor

    • Anthrax toxin = combination of all three

    • Transmission via Skin cuts or Inhalation


    Bacillius anthracis cont
    Bacillius anthracis (cont)

    • Clinical Manifestations

    • Cutaneous antrax:

      • 95% of all infections

      • Papules  Ulcers with necrotic centers

      • Regional Lymphadenopathy

      • Edema major complication  death 20%

    • Systemic anthrax

      • Acquired thru Inhalation or GIT  Lymphadenopathy  death

    • Treatment: penicillin Killer vaccine


    Bacillus cereus
    Bacillus cereus

    • Two Enterotoxins

    • Grows on Food, especially Cereal Grain (rice)

    • Clinical Manifestations: Food Poisoning

      • Short incubation ( 1- 6 hours – emetic type)  severe nausea & vomiting

      • Long incubation (10 – 24 hours – diarrheal type)  abdominal cramps + diarrhea

    • Treatment& Prevention:

      • Fluids. Vancomycin if indicated.


    Clostridium
    Clostridium

    • Large obligate anaerobe

    • Spore forming

    • Found in Soil or human GIT

    • 4 major pathologic species

      • C. perfringens C. tetani

      • C. diffcilie C. botulinum

    • Destructive Enzymes + Toxins

      • Collagenase Protease

      • Hyaluronidase Lecithinase


    Clostridium perfringens
    Clostridium perfringens

    • Fast growingNon-motile Soil & GIT

    • Alpha toxin (Lecithinase)  Lysis of RBC & other cells

    • Transmission thru disrupted:

      • Skin GIT Other Epithelial tissues

      • Due to Trauma Surgery (septic abortion)

      • Spores found in Soil


    Clostridium perfringens cont
    Clostridium perfringens (cont)

    • Clinical Manifestations

    • Gas gangrene (myonecrosis)

      • Life threatening (muscle & CT necrosis)

      • Gas is end product of Fermentation  crepitation

      • 80% of cases of Gas gangrene.

    • Food Poisoning

    • Third most common cause of bacterial food-borne epidemics (1stS. aureus, 2nd Salmonella)

    • Abdominal pain & diarrhea for 24 hrs. No Rx


    Clostridium perfringens cont1
    Clostridium perfringens (cont)

    • Clinical Manifestations (cont)

    • Skin & Soft tissue infections localized

    • Suppurative infection usually polymicrobial

    • Intra-abdominal infection  Bowel perforation + emphysematous cholecystitis

    • Pelvic infection  Tubo-ovarian abscess + Shock

    • Treatment: Surgical Debribment + Penicillin


    Clostridium difficile
    Clostridium difficile

    • Normal bowel flora(small percentage of adults)

    • 2 Heat-labile toxins:

    • Enterotoxin (exotoxin A) Cytotoxin (exotoxin B

    • Clinical Manifestations:

    • Cause 25% ofantibiotic-associated diarrhea

    • Cause 95% of pseudomembranous colitis

      • Associated with Clindamycin & Ampicillin

      • Nausea Vomiting Abdominal pain Voluminous green diarrhea

    • Treatment: Vancomycin or Metronidazole


    Clostridium tetani
    Clostridium tetani

    • Spores abundant in the Soil

    • Spores inoculated into wounds

    • 50% of case no history of a wound

    • Produces tetanospasim a plasmid encoded neurotoxin that blocks the normal inhibition of Spinal motor neurons  spastic paralysis  Death

    • Tetanospasim prevents release of the inhibitory neurotransmitter glycine & gamma-amino butyric acid  spastic paralysis.


    Clostridium tetani cont
    Clostridium tetani (cont)

    • Four Clinical Manifestations:

    • Local infection local muscle contraction

    • Cephalic infection can follow chronic Otitis media.

    • Generalized Tetanus infection(60% mortality)

      • Pain “Lock-jaw” Death

      • Opisthotonos (head & heels bent backwards & body bowed forward)

    • Neonatal tetanus: infection of umbilical stump & major cause of infant mortality in developing countries.


    Clostridium tetani cont1
    Clostridium tetani (cont)

    • Treatment:

      • Surgical Debridement of wound

      • Human Tetanus anti-toxin

      • Respiratory support

      • Muscle relaxants (curare-like drugs)

      • Metronidazole

    • Prevention:

      • Immunization with Tetanus toxoid

      • Booster shots every 10 years

      • No natural immunity


    Clostridium botulinum
    Clostridium botulinum

    • Ubiquitous in Soil

    • Produces powerful heat-labile neurotoxin

    • Ingested in improperly canned food

    • Toxin blocks release of Acetylcholine from neurons in the peripheral nervous system  Flaccid paralysis

    • Clinical Manifestations:

    • Dilated un-reactive pupils (bulbar paralysis)

    • Descending paralysis starting with Cranial Ns

    • Progressive respiratory weakness

    • Dry mucous membranes (mouth)


    Clostridium botulinum cont
    Clostridium botulinum (cont)

    • Clinical Manifestations (cont)

    • Infant botulism (floppy baby syndrome)

      • Failure to thrive

      • Progressive muscular weakness

      • Poor motor development

      • Infants should not be fed Honey

      • Unexpalined Hypotension No Fever

    • Treatment:

      • Human anti-toxin

      • Respiratory support


    Gram negative cocci
    Gram Negative Cocci

    • NEISSERIA

    • Non-motile Non-spore-forming

    • Gram negative cocci

    • Arranged in pairs (diplococci) with flattened adjacent sides facing each other (“coffee beans)

    • Fastidious organisms

    • Very susceptible to Heat Cold Drying


    Neiseeria meningitis
    Neiseeria meningitis

    • Key virulence factors:

      • Anti-phagocytic capsule

      • Endotoxin

      • IgA protease

    • Transmission:

    • via Respiratory droplets

    • Carriage rate in adult Nasopharynx is 10-30%

    • Most carriers are asymptomatic

    • Greatest risk in those with late complement (C6 – C8) deficiencies


    Neisseria meningitis cont
    Neisseria meningitis (cont)

    • Clinical Manifestations:

    • Meningitis usually sudden & fulminant onset

    • Waterhouse-Friderichsen syndrome: (coagulopathy, Hypotension, Adrenal cortex necrosis, sepsis, death)

    • Diagnosis:

    • Identifying Gram negative cocci in Spinal fluid

    • Demonstrate production of oxidase & maltose fermentation.

    • Treatment: Penicillin G.

      • Carriers & Close contacts Rifampin


    Neisseria gonorrhoeae
    Neisseria gonorrhoeae

    • Produce beta-lactamase

    • Transmission:

      • Venereal contact Fomites

      • Increased incidence in:

        • Sexually active young adults (15-30 y o)

        • Non whites Low socio-economic class

        • Urban settings


    Neisseria gonorrhoeae cont
    Neisseria gonorrhoeae (cont)

    • Clinical Manifestations:

    • Primarily uro-genital tract

    • Men:

      • Acute urethritis & yellow purulent discharge

      • 90% will be symptomatic

      • Common complications:

        • Urethral stricture Epididymitis

        • Prostatitis Proctitis (homosexuals)


    Neisseria gonorrhoeae cont1
    Neisseria gonorrhoeae (cont)

    • Women:

      • Asymtomatic in 20 – 80% of cases

      • Inability to observe discharge

      • Complications;

        • Pelvic inflammatory disease (15 – 20%)

        • Generalized Peritonitis

        • Infertility


    Neisseria gonorrhoeae cont2
    Neisseria gonorrhoeae (cont)

    • Disseminated disease observed as:

      • Meningitis Arthritis

      • Subacute bacterial endocarditis

    • Ophthalmic neonatorum:

      • Maternal transmission during birth

      • Ophthalmic Tetracycline, Erythromycin, Silver nitrate for prevention

    • Pharyngitis:

      • Oral manifestation of gonorrhea

      • More common with oral sex


    Neisseria gonorrhoeae cont3
    Neisseria gonorrhoeae (cont)

    • Diagnosis;

    • Men : Gram negative diplococci in Urethral discharge

    • Women: Culture + Biochemical Tests

      Treatment & Prevention:

    • No longer susceptible to penicillin

    • Ceftriaxone

    • plus Doxycycline (anti-chlamydial drug)

    • Safe sex decrease incidence of gonorrhea


    Gram negative bacilli enterobacteriaceae
    Gram Negative BacilliEnterobacteriaceae

    • Gram negative Non-spore forming

    • Facultative Motile

    • Many are normal GI flora (symbiotic relation)

    • Synthesize Vitamin K

    • Deconjugate Bile & Sex hormones  recirculated in the Liver

    • Prevent colonization by primary pathogens

    • Escherichia Citrobacteria Klebsiella

    • Enterobacteria Serratai Proteus

    • Klebsiella not motile


    Enterobacteriaceae
    Enterobacteriaceae

    • Mostly lack virulence factors

    • Act as Opportunistic pathogens when break thru normal anatomical barriers or in cases of Immunosuppression

    • Most common cause for Intra-abdominal sepsis + UTI

    • Those with Virulence Factors:

      • Shigella sp Salmonella sp

      • Yersinia sp (not in GIT)

      • Escherichia col

        Shigella + Salmonella only pathologic in Humans


    Enterobacteriaceae1
    Enterobacteriaceae

    • Physiology:

    • Facultative Ferment or Respire

    • Easily destroyed by Heat + Disinfectants

    • Sensitive to Drying or Desiccation

    • Survive best in High Moister environ

    • Respiratory + Anesthesia equipment common causes for Nosocomial infections

    • Ice machines + Water supply  Epidemics


    Enterobacteriaceae2
    Enterobacteriaceae

    • Pathogenicity:

    • Due to Endotoxin (LPS)  Fluid into GIT  Diarrhea

    • Toxicity due to Lipid A portion of LPS

    • LPS may cause Endotoxic Shock

      • Blood pools in Microcirculation  Hypotension

      • Vital organs reduced Blood  decreased perfusion  Acidosis + Ischemia + Hypoxia

      • Disseminated Intravascular Congestion


    Shigella
    Shigella

    Obligate human pathogen Not motile

    S. Dysenteria S. flexneri S. sonnei S. boydi

    • Transmission by fecal-oral route

      • Not killed in stomach, < 100  disease

    • Pathogenesis

    • Colon site of disease  destroys GI lining

    • Virulence factors (Adhesin, Toxins, Invasins)

    • Endotoxin  increased local inflammation


    Shigella1
    Shigella

    • Clinical Manifestations:(Shigellosis)

    • Bacillary dysentery:

      • Abdominal cramps

      • Diarrhea (Blood + PMNs + Mucus)

      • Carrier state 1 – 4 weeks after disease

    • Treatment

    • Hydration Electrolyte replacement

    • Fluoroquinolones

    • Prevention thru personal hygiene, proper garbage disposal & water purification.


    Enterotoxigenic escherichia coli e coli
    Enterotoxigenic Escherichia coli (E. coli)

    • Pathogenicity (virulence factors)

    • K 1 capsular antigen (inhibits phagocytosis)  neonatal meningitis + urinary tract infection

    • Hemolysin  Kidney infection

    • Clinical Manifestations:

    • Major cause of infant death (persistent watery diarrhea)

    • Most common cause of “Traveler’s diarrhea”

    • Acquired via fecally contaminated water

    • Most common cause of Urinary Tract Infections. Treatment = Bactrin


    Salmonella
    Salmonella

    • Motile LPS  inhibit Complement-mediated killing

    • Non-Typhoidal Salmonella infection

      • Inflammatoey Diarrhea & Fever

      • Acquired thru Eggs + Chicken + Food + HOH

      • Large inoculum (> 1 million cells) needed

      • More severe under age 10

    • Cause Osteomyelitis in Sickle Cell Anemia patients


    Salmonella cont
    Salmonella (cont)

    • Typhoidal Salmonella infection

    • Caused byS. typhi(only Human Colon)

    • Thyphoid (Enteric) Fever

    • Progressive Subacute Fibrile-wasting

    • Common in developing countries

    • Worst in young children

    • Transmission:

    • Large inoculum in Fecally contaminated Food or Water

    • Ulcers & perforation of GIT


    Typhoid fever cont
    Typhoid Fever (cont)

    • Clinical Manifestations (3 phases)

    • First week: fever, lethargy, constipation, pain

    • Second week bacteremia occur

      • High fever : Low Pulse Abdominal pain

      • “Rose” spots Skin Diarrhea

    • Third week: Exhaustion Less fever

    • Complicatons:

      • Relapse (20%) Bleeding Abscess

    • Treatment: Chloroamphenicol (1st choice) Cephalosporins


    Common opportunistic enterobacteriaceae
    Common Opportunistic Enterobacteriaceae

    • Klebsiella sp

    • Non-motile Lactose fermenting Rods

    • Laboratory: colonies appear large + mucoid due to large Capsule

    • Klebsiella pneumonia = major pathogen

    • Clinical Manifectation:

    • Severe Lobar pneumonia (Aspiration, Abscess)

      • Sputum “currant jelly”

      • Alcoholics Diabetics COPD


    Common opportunistic enterobacteriaceae1
    Common Opportunistic Enterobacteriaceae

    • Proteus sp

    • Highly Motile Cause UTI

    • Produce Urease  increase pH  Struvite (stones)  obstruct UT  hiding place

    • Citrobacter  Pyelonephritis

    • Enetrobacter  Pneumonia

    • Serratia  Pneumonia + UTI


    Gram negative bacilli additional enteric pathogens vibrio chlolerae cholera
    Gram Negative Bacilli: Additional Enteric PathogensVibrio chlolerae (Cholera)

    • Gram negative bacillus “Comma” shape

    • Fresh & Salt Water, Cold blooded animals.

    • Pathogenecity

      • Pili  adherence to GIT (small intestine)

      • Non-invasive infection, clinical effets due to enterotoxin (choleragen)

    • Transmission: fecal-oral (food/water)

    • Clinical: severe watery (“rice water”) diarrhea (20 liters/day). Loss of Na, Cl, K, Bicarbonate)

    • Treatment: Hydration & Doxycycline


    Gram negative bacilli additional enteric pathogens
    Gram Negative Bacilli: Additional Enteric Pathogens

    • Campylobacter

    • Small Curved Gram negative Rods

    • Reservoirs = Domestic animals

    • C. jejuni:

      • Transmission via Fecal-Oral (Food/HOH)

      • Clinical Manifestations: (Enterocolitis)

        • Bloody diarrhea Fever Malaise

        • Painful Abdominal cramps

    • C. fetus:Bacteremia + Metastatic Infections(IC)


    Gram negative bacilli additional enteric pathogens helicobacteria pylori
    Gram Negative Bacilli: Additional Enteric PathogensHelicobacteria pylori

    • Spiral shaped motile Rod

    • Produces urase Alkaline environ

    • Reservoir possibly Humans only

    • Older patients + Families

    • Lives in close proximity to Gastric Epithelial cells

    • High association with Antral gastritis & Duodenal ulcers (90%)

    • Treatment: Bismuth salts, Tetracycline, Amoxicillin, Metronidazole


    Gram negative bacilli additional enteric pathogens pseudomonas
    Gram Negative Bacilli: Additional Enteric PathogensPseudomonas

    • Gram negstive Rod

    • In Soil + HOH

    • Component of Bowl flora

    • Human very resistant

    • P. aeruginosa

      • Important Nosocomal infection in immunocompromised + chronically ill


    Gram negative bacilli additional enteric pathogens pseudomonas1
    Gram Negative Bacilli: Additional Enteric PathogensPseudomonas

    • P. Aeruginosa (cont):

      • Groups at Risk:

        • Radiation treated patients

        • Burn patients

        • Patients with Metastatic + Metabolic diseases

        • Prolonged Immunosupression (Steroids) + Antibiotics

        • Prior instrumentation + manipulation

        • Cystic fibrosis


    Gram negative bacilli additional enteric pathogens pseudomona
    Gram Negative Bacilli: Additional Enteric PathogensPseudomona

    • P. Aeruginosa (cont):

      • Clinical Manifestations:

        • Wound + Burn infetions

        • Ecthyma gangrenosum

          • Skin lesions with vascular invasion

        • Ear infections:

          • Otitis externa – swimmers (mild)

          • Malignant Otitis externa – Diabetics


    Gram negative bacilli additional enteric pathogens pseudomona1
    Gram Negative Bacilli: Additional Enteric PathogensPseudomona

    • P. Aeruginosa (cont):

      • Clinical Manifestations: (cont)

        • Pulmonary infections

          • Cystic fibrosis + Immunocompromised

        • Corneal infections –Contact Lens wearers

        • UTI

      • Treatment: Antipseudomonal penicillin: Gentamicin, Ticaricillin, Piperacillin

        • Aminoglycosides (Tobramycin)


    Respiratory pathogens
    RESPIRATORY PATHOGENS

    • HEMOPHILUS

    • Small pleomorphic coccobacillus

    • Many species are normal flora of Nasopharynx

    • Hemophilus influenzatype b (major pathogen)

    • Clinical Manifestations:

      • Meningitis (30 mo – 6yo) Otitis media

      • Acute epiglossitis: rapid onset, compromised airway

    • Treatment: Cefotaxime Amoxicillin

    • Prevention: vaccine for H. influenza type b.


    Respiratory pathogens1
    RESPIRATORY PATHOGENS

    • H. ducreyi

      • Associatedwith Chancroid:

        • Venereal disease

        • Painful Non-indurated ragged ulcer

        • Genitalia + Perianal

    • Presence of beta-Lactamase in both H. influenza and H. ducreyi result in high resistance to treatment with Penicillin


    Respiratory pathogens cont
    Respiratory Pathogens (cont)

    • BORDETELLA PERTUSSIS

    • Small Gram negative fastidious coccobacillus

    • Strict Aerobe

    • Cause of Whooping cough

    • Virulence factor:

    • Attach to host via pili

    • Toxins:

      • Pertussis toxin Adenylate cyclase toxin

      • Tracheal cytotoxin Lipopolysaccharide


    Bordetella pertussis cont
    Bordetella pertussis (cont)

    • Clinical Manifestations of Whooping Cough

    • Highly communicable via respiratory route

    • Humans only known reservoir

    • Incubation period = 7 – 10 days 3 Stages:

    • Catarrhal or prodromal: mild URT infection

    • Paroxysmal cough followed by “whoop” on inspiration

    • Convalescence: decline in “whoop” over mos.

    • Treatment & Prevention: Erythromycin (catarrhal stage) & Immunization (DPT)


    Respiratory pathogens cont1
    Respiratory Pathogens (cont)

    • LEGIONELLA PNEUMOHILIA

    • Gram negative Facultative Aerobe

    • Intracellular parasite

    • Widely distributed in aquatic environments

    • Requires Fe & Cystine to grow

    • Uses Complement receptor to infect Macrophages

    • Transmission: (Aerosol)

    • Air conditioning units Humidifiers

    • Respiratory devices, Shower head, Whirlpools


    Legionella pneumohilia cont
    LEGIONELLA PNEUMOHILIA (cont)

    • Clinical Manifestations:

    • Can be asymptomatic

    • Pontiac fever: mild, febrile illness without pneumonia

    • Legionnaires’ disease: severe often fatal pneumonia

    • Treatment: Erythromycin


    Anaerobes
    ANAEROBES

    • Obligate anaerobes require a reducing agent (substance able to donate electrons, reducing a 2nd substance & itself being oxidized {combined with Oxygen or lose an electron})

    • Obligate anaerobes cannot survive in Oxygen since they cannot detoxify the Superoxide ion.

    • Include: Gram positive & negative, cocci & bacilli

      • “coil-shaped” Spirochetes


    Obligate anaerobes cont
    Obligate Anaerobes (cont)

    • Greatest natural defense is tissues with high oxidation-reduction potential no growth.

    • Normal inhabitants of:

      • Oral cavityVaginaGIT

    • Can cause opportunistic infections in tissues adjacent to their normal habitat due to tissue injury or vascular compromise.


    Obligate anaerobes cont1
    Obligate Anaerobes (cont)

    • Pathology

    • Primarily purulent abscess formation

    • Culture most often reveal polymicrobal infection with multiple facultative & anaerobic species.

    • Treatment:

      • Surgical drainage Penicillin G

      • Clindamycin Metronidazole

      • Chloroamphenicol Cefoxitin


    Anaerobic gram negative bacilli
    Anaerobic Gram Negative Bacilli

    • BACTEROIDES:Primary organism of Colon

    • Bacteroides fragilis:

    • Most frequent cause of anaerobic infection

    • Gram negative No Spore Non-motile

    • Inhabits GIT & Genital tract

    • 4 virulence factors:

      • Polysaccharide capsule(antiphagocytic + chemotactic)

      • Endotoxin

      • Superoxide dismutase  survive in Oxygen

      • Beta-lactamase  resistance to Penicillin


    Bacteroides fragilis cont
    Bacteroides fragilis (cont)

    • Clinical Manifestations:

    • Intra-abdominal infections:

      • Appendicitis Abscesses

      • Peritonitis

    • Treatment:

      • Metronidazole Clindamycin

      • Chloroamphenacol

      • Incision & Drainage (I & D)


    Prevotella bacteroides melaninogenicus
    Prevotella (Bacteroides) melaninogenicus

    • Small coccobacillus

    • Primarily found in Oropharynx

    • Black pigmented colonies grown on Blood agar

    • Virulence factors:

      • Anti-phagocytic capsule Collagenase

    • Important agent in Oral & Lung infections

    • Associated with Chronic Periodontal Disease (periodontitis)


    Fusobacterium nucleatum
    Fusobacterium nucleatum

    • Pleomorphic Gram negative Rod (tapered end)

    • Normally inhabit:

      • Mouth GIT Female Genital Tract

    • Possess potent Endotoxin

    • Most common isolate in Oral & Lung infections

    • With Spirochetes  Acute Necrotizing Ulcerative Gingivitis (ANUG)

    • F.necrophorum (Liver abscess)

    • Treatment: Penicillin, Cephalosporins, Clindamycin


    Anaerobic gram postive bacilli
    ANAEROBIC GRAM POSTIVE BACILLI

    • Spore Forming:

      • Clostidium sp – see Gram positive bacillus section

    • Non-spore Forming:

      • Propionibacteria

        • Skin  infect Shunts + Prosthetic devices

        • Skin  Acne

      • Actinomyces – to come later


    Anaerobic cocci
    ANAEROBIC COCCI

    • ANAEROBIC GRAM POSITIVE COCCI

    • Peptosteptococci:

      • Found in Mixed infections

        • Skin Oral URT

        • Female Genital tract

      • Treatment:

        • Penicillin Cephalosporins

        • Clindamycin Metronidazole


    Anaerobic cocci1
    ANAEROBIC COCCI

    • ANAEROBIC GRAM NEGATIVE COCCI

    • Veillonella sp

      • Resemble Neissera sp

      • Normal Flora of:

        • Mouth Nasopharynx Vagina

      • Rarely cause infection

      • Can be confused with Neissera on Gram Stain


    Periodontal pathogens
    PERIODONTAL PATHOGENS

    • Part of Normal flora of Sulcus (not teeth)

    • Mostly Gram Negative (LPS)

    • Mostly Anaerobic

    • Mostly Capnophilic (loves Carbon Dioxide)

    • Examples:

      • Prevotella melaninogenicus

      • Porphyromonas gingivalis

      • Spirochetes Borrelia Fusobacteria

      • Campylobacter rectus Eichenella corrdens


    Periodontal pathogens1
    PERIODONTAL PATHOGENS

    • Examples:

      • Actinobacillus actinomycetemcomitans (A. a)

      • Veillonella

    • Periodontal disease (PDD)  Collagen Attachment loss + Bone destruction

    • Juvenile Periodontitis:

      • Mainly associated with A.a

      • Very little Plaque clinically

      • Young patients (Blacks) Very aggressive

      • Hyper-responsive Immune state


    Mycobacteria actinomycetes
    MYCOBACTERIA & ACTINOMYCETES

    • MYCOBACTERIA

      • Acid-fast Bacilli

      • High Lipid Content in Cell Wall

      • Cause Tuberculosis & Leprosy

    • ACTINOMYCETES

      • Gram Positive with Branching growth pattern

      • Abundant in Soil


    Mycobacterium tuberculosis
    Mycobacterium tuberculosis

    • Obligate anaerobe Acid-fast bacillus (AFB)

    • Cell wall contains Mycolic acid, Lipoproteins & Glycolipoproteins essential for Tuberculin activity and confers the ability to induce Type 1V Hypersensitivity Reactions.

    • Slow growing 20 – 60 day to see colonies

    • Antigenicity: Purified-protein derivative (PPD) antigenic material for Skin Testing.


    Mycobacterium tuberculosis cont
    Mycobacterium tuberculosis (cont)

    • Pathogenicity

      • Cord factor: (Virulence)

        • Serpentine grouping pattern

        • Inhibits PMN migration

        • Elicit Granuloma formation

        • Attacks Mitochondrial membranes

      • Sulfatides protect against attack from hosts Lysosome hydrolytic enzymes


    Mycobacterium tuberculosis cont1
    Mycobacterium tuberculosis (cont)

    • Epidemiology:

    • Only found in Humans

    • More common in lower socio-economic groups

    • Rapid rise due to HIV/AIDS + Immigration

    • Transmission:

    • Primarily air droplet inhalation

    • Most infectious are those with untreated cavitary lung TB  actively expel bacilli.

    • Risk of infection greater than risk of disease.


    Mycobacterium tuberculosis cont2
    Mycobacterium tuberculosis (cont)

    • Pathogenesis:

    • 1st : Delayed-type Hypersensitivity (T-cell), 3-4wks after infection  positive Tuberculin reaction.

    • Acquired cellular immunity with resistance or protection from re-infection.


    Mycobacterium tuberculosis cont3
    Mycobacterium tuberculosis (cont)

    • Primary infection:

    • Exudative type:

      • Organism inhaled spreads to:

        • Macrophages LNs Blood

      • Signs of infection minimal

      • Immune competent host limit organism to Lung.

    • Productive type:

      • Granuloma tubercles & calcified lesion (Ghon complexes) form.

      • PPD test positive


    Mycobacterium tuberculosis cont4
    Mycobacterium tuberculosis (cont)

    • Secondary infection (re-activated):

    • Usually localized in apex of Lung (high Oxygen tension)

    • Granuloma with caseation necrosis & fibrosis

    • Results from quiescent focus or new infection insipte of immunity.

    • Clinical manifestations:

    • Fatigue Weight loss Anorexia

    • Weakness Fever Night sweats


    Mycobacterium tuberculosis cont5
    Mycobacterium tuberculosis (cont)

    • Clinical Manifestations (cont)

    • Pulmonary TB (80%)

      • Hemoptysis (cough + blood)

      • pneumonitis

    • Miliary (disseminated) TB

      • Mostly:

        • Bone & joints Brain Kidney

        • Peritonium Lymph nodes


    Mycobacterium tuberculosis cont6
    Mycobacterium tuberculosis (cont)

    • Diagnosis of TB:

    • Abnormal Chest X-ray

    • Acid-fast bacteria in Sputum, culture M. tuberculosis

    • Skin Testing:

    • PPD-S injected into Skin, read at 48-72 hrs

    • Diameter of Induration (> 10 mm = positive)

    • FalseNegative if injection too deep into skin

    • False positive due to previous immunization

    • Positive PPD test does NOT = active disease


    Mycobacterium tuberculosis cont7
    Mycobacterium tuberculosis (cont)

    • Treatment:

    • Period of 6 - 9 months

    • Combination of at least 3 anti-tuberculosis drugs

    • If HIV-positive treat for 9 – 12 months

    • Multiple-Drug-Resistant TB (MDRTB)

      • Do Sensitivity Testing

    • Isoniazid Rifampin

    • Ethambutol Pyrazinamide


    Mycobacterium tuberculosis cont8
    Mycobacterium tuberculosis (cont)

    • Prevention:

    • INH (Isonicotine hydrazine) prophylaxis if:

      • Contact with patient with active disease

      • Recently converted PPD-positive person

    • BCG (Bacille Calmette-Guerin):

      • Used to establish cell-mediated immunity

      • PPD negative persons

      • Positive PPD skin test.


    Mycobacterum bovis
    Mycobacterum bovis

    • TB in cattle Present in Soil Positive PPD

    • In humans with Ingestion of unpasteurized contaminated milk, or Inhalation (dairy farmers)

    • Clinical Manifestations:

    • Pulmonary disease:

      • Elderly with Bronchitis + Emphysema

      • M. kanasasii, M. avium-intracellulare,

      • M. forttuitum-chelone


    Mycobacterum bovis1
    Mycobacterum bovis

    • Clinical Manifestations: (cont)

    • Lymphadenitis: M. scrofulaceum, Children

    • Cervical & Mesenteric Lymphadenopathy

    • Cutaneous leasion: M. marinum

      • Open wound (“swimming pool” granuloma

    • Disseminated disease: HIVD

      • M. kansasii M. avium-intracellulare

    • Dissemination to Bones & Joints will give positive PPD Skin test

    • BCG vaccine from live attenuated M. bovis


    Mycobacterium leprae
    Mycobacterium leprae

    • Cannot grow in vitro on any culture media

    • Acid fast Delayed-type Hypersensitivity

    • Leprosy (Hansen’s disease):

    • Endemic (Africa, South & SE Asia, S. America)

    • Transmission:

    • Contact with Nasal secretions or Ulcer exudates of infected cases.

    • Lesions involve cooler parts of body (Skin of Nasopharynx, Cartilage, Eyes, Testicles & Larynx)

    • Incubation = 5 – 7 years


    Mycobacterium leprae cont
    Mycobacterium leprae (cont)

    • Disease Forms:

    • Tuberculoid Leprosy:

      • Indolent (causing little pain, slow growing)

      • Non- progressive

      • Mature granulomas in Skin

    • Lepromatous Leprosy:

    • Progressive & Invasive

    • Foamy Histiocytes, no Eiptheliod or Giant cells

    • Schwann cell (neural) infected  nerve damage

    • Skin lesions are invasive & nodular


    Mycobacterium leprae cont1
    Mycobacterium leprae (cont)

    • Immunity:

    • Mediated by CD4 T-helper cells

    • Low infectivity rate

    • Treatment:

    • 3 – 5 years

    • Dapsone + Rifampin

    • Close contacts should also be treated


    Actinomycetes
    ACTINOMYCETES

    • Filamentous shape & causes Actinomycosis

    • Actinomyces, Nocardia, Steptomyces

    • Actinomyces israelii & A. naeslundii

    • Anaerobic Gram positive bacilli

    • Part of normal oral flora

    • Pathogenic only after trauma (surgery)


    Actionmycetes israelii cont
    Actionmycetes israelii (cont)

    • Clinical Manifestations:

    • Cervicofacial actinomycosis:

    • Mandibular infection following dental caries(50%)  PulpitisExtractions

    • Pyogenic abscess  swelling, pain, erythema

    • “Yellow” sulfur granules expelled from fistula

      • Mycelial filaments surrouned by Eosinophils

    • Osteomyelitis may occur post Extractions


    Actionmycetes israelii cont1
    Actionmycetes israelii (cont)

    • Thoracic Actinomycosis:

      • Extension of Cericofacial infection (20%)

    • Abdominal Actinomycosis

      • Traumatic perforation of GIT mucosa

      • Ruptured Appendix Ulcers

    • Pelvic Actionmycosis

      • Women using Intrauterine devices

    • Traetment: Penicillin or Ampicillin for several weeks + surgical drainage


    Nocardia asteroides
    Nocardia asteroides

    • Soil + Aquatic Environs

    • Aerobic Gram positive Filamentous AFB

    • Clinical Manifestations (Nocardosis)

    • 50% have underlying disease e.g. Diabetes

    • Opportunistic infection with Hematologic malignancies e.g. Leukemia

    • Begins as Chronic Lobar Pneumonia

    • CNS Most Common site for Metastatic infection  Abscess formation

    • Treatment: Sulphonmides + Surgical drainage


    Rickettsiacae chlamydia
    Rickettsiacae & Chlamydia

    • RICKETTSIACEAE

    • Genera:

    • Rickettsiia, Bartonella, Coxiella, Ehrlichia

    • Obligate intracellular parasites in Endothelial cells.

    • Small pleomorphic Gram negative coocobacilli

    • Transmitted by Arthropods (except Bartonella, Cociella burnetti)

    • Treated with Tetracycline (Doxycycline)


    Rickettsial diseases
    Rickettsial Diseases

    • Rocky Mountain Spotted Fever (RMSF)

    • Caused by Rickettsia rickettsi (90% of cases )

    • Epidemiology: S Central & Eastern USA

    • Transmission:Ticks (reservoir =rodents, dogs)

    • Clinical Manifestations:

    • After 1 – 3 day incubation  malaise, frontal headache & fever

    • Skin  maculo-papular rash on palms & soles within 2 –4 days of unset of symptoms  spreads centripetally on Trunk


    Rickettsial diseases cont
    Rickettsial Diseases (cont)

    • Epidemic Typhus (louse-bourne typhus)

    • Caused by Ricketsia prowazkii

    • Transmission by human body Louse

    • Clinical Manifestations:

    • Similar to RMSF but not as severe

    • NO rash on sole or palms

    • Brill-Zinzzer disease: recurrent form

    • Endemic (Murine) Typhus:R. typhi

    • Cycled by Rats & its Ectoparasites (Fleas) thru Feces


    Rickettsial diseases cont1
    Rickettsial Diseases (cont)

    • Q FeverCoxiella burnetii No RashNo Arthropod vevtor

    • Transmission:

      • Inhaling infected Dust

      • Handling infected Hides or Tissue

      • Drinking contaminated Milk

    • Reservoirs: Ticks, wild animal, Sheep, Cows, Goats

    • Clinical Manifestations: Fever Chills Headache

      • Malaise, Myalgia, mild Pneumonia


    Chlamydiae
    CHLAMYDIAE

    • Obligate intra-cellular parasite. Humans only

    • Infects Birds + Mammals

    • Possess gram negative envelope (LPS)

    • EB (Elementary Body) infectious form

    • Reticular Body (RB) non-infectious form

    • Infected cells develop oval vacuolar inclusions containing Glycogen (stain with Iodine)

    • Chlamydia trachomatis

    • Transmitted by:

      • Fomites Sexually Perinatally


    Chlamydia trachomatis cont
    Chlamydia trachomatis (cont)

    • Treatment: Erythromycin Tetracycline

    • Prevention: safe sexual practices

    • Clinical Manifestations:

    • Ocular trachoma blindness (developing countries)


    Chlamydia trachomatis cont1
    Chlamydia trachomatis (cont)

    • Sexually Transmitted Diseases:

    • Number one cause of STD

    • In Men:

      • non-gonococcal Urethritis

      • Epididymitis

      • Prostatitis

      • Proctitis


    Chlamydia trachomatis cont2
    Chlamydia trachomatis (cont)

    • Sexually Transmitted Diseases (cont)

    • In Women:

      • Cervicitis Urethritis Salpingitis PID

    • Lymphogranuloma venereum

    • Venereal disease

    • More common in Black Males

    • Primary lesion painless, vesicular on Penis, Anus or Rectum

    • Then becomes painful, suppurative & spread into Inguinal & Femoral LNs


    Chlamydiae cont
    CHLAMYDIAE (cont)

    • C, psittaci

    • Transmission: Inhalation of infected Bird Droppings Pneumonia

    • C. pneumonia

    • Human-only pathogen believed to be transmitted by Inhalation

    • Clinical Manifestations:

      • Pharyngitis Bronchitis

      • Mild Atypical Pneumonia


    Spirochetes
    SPIROCHETES

    • Motile Helical Coiled

    • Divide by Transverse Fission (splitting along the short axis)

    • Contain axial fibril (flagella) , outer sheath, protoplasmic cylinder (cell wall & membrane) and cytoplasm.

    • Three Genera:

      • Treponema (syphilis, yaws, pinta, bejel)

      • Borrelia (Lyme disease, Relapsing Fever

      • Leptosipra (leptospirosis)


    Spirochetes1
    SPIROCHETES

    • Treponema pallidum

    • Most important species

    • Highly motile

    • Does not grow on artificial media therefore can not be grown in the Lab

    • Agent of Syphilis


    Syphilis cont
    Syphilis (cont)

    • Transmission:

    • Sexually Across Placenta

    • Blood Transfusion

    • Risk groups:

      • People with multiple sex partners

      • Infants born to infected mothers


    Syphilis cont1
    Syphilis (cont)

    • Clinical Manifestations:

    • Primary syphilis:

    • Arise within 2 – 10 weeks of exposure

    • Organism spread to LNs & Blood

    • Chancre forms at site of innoculation:

      • Firm Painless Reddish

      • Raised border Center ulcerated

      • Heals within 3 – 6 weeks without scarring

      • Contains numerous spirochetes (highly infectious)


    Syphilis cont2
    Syphilis (cont)

    • Secondary syphilis:

    • Occur 1 – 3 months after primary syphilis

    • Symptoms:

      • Skin rash Fever Sore Throat

      • Headache

      • Generalized lymphadenopathy especially Epitrochlear region (inner condyle of Humerus).

      • Mucous patch on mucous membrane Orally & Genital. Highly infectious.


    Syphilis cont3
    Syphilis (cont)

    • Latent syphilis:

    • 30 – 40% of cases. Mucocutaneous relapses

    • Lesions remain infectious

    • Tertiary syphilis: (30% of untreated cases)

    • Benign tertiary syphilis

      • Gumma in Skin (not infectious)

    • Cardiovascular syphilis aneurysms

    • Neurosyphilis  Tabes dorsalis (wide-bases gait with long “slapping” motion of Legs

      • Argyll-Robertson pupils(fail to react to light)


    Syphilis cont4
    Syphilis (cont)

    • Congenital syphilis:

    • Transplacental transmission  fetus

    • Mother has Primary or Secondary syphilis

    • 25% mortality if left untreated

    • Manifestations in Newborn:

      • Hepatosplenomegaly Hemolytic anemia

      • Pneumonia Skin lesion

      • “Snuffles” (obstructed nasal breathing)


    Syphilis cont5
    Syphilis (cont)

    • Congenital syphilis (cont)

    • Hutchinson’s Triad:

      • Teeth:

        • “barrel (screw-driver)” shaped Incisors

        • “peg-shaped” Lateral Incisors

        • “mulberry” Molars

      • Eye: interstitial keratitis

      • Nerve: Eight Nerve Deafness

      • Nose: ”Saddle nose” deformity


    Syphilis cont6
    Syphilis (cont)

    • Serology Diagnosis:

    • Darkfield Microscopy

    • VDRL (Venereal Disease Experimental Laboratory)

    • RPR (Rapid Plasma Reagin)

    • VDRL & RPR uses cardiolipin as a antigen as Complement Fixation (CF)or Flocculation Tests.

    • FTA (Fluorescent Treponemal Antibody) Test

    • Treatment: Penicillin

    • Prevention: Safe sex


    Other treponemal disease
    Other Treponemal Disease

    • Yaws (T. pertenue)

    • In the Tropics Direct contact Mainly Children

    • Lesion = painless, erythematous (Arm or Leg)

    • Pinta (T. carateum)

    • Person to person Sexually Transmited

    • Bejel (T. pallidum)

    • Poor hygiene Transmission by direct contact

    • Skin lesions highly infectious


    Borrelia
    BORRELIA

    • Transmitted by Arthropods

    • Coarse, irregular Coils, very flexable, motile

    • Lyme Disease

    • Caused by Borrelia burgdorferi

      • Reside in Tick vectors (Ixodes) that feed on infected Deer or Mice reservoirs

    • First described in Lyme, Connecticut (USA)

    • Now thru out USA, Europe, Australia


    Borrelia1
    BORRELIA

    • Lyme Disease (cont)

    • Clinical Manifestations:

    • Erthymatous Chronicum Migrans

      • Red macule  annular erythema with cental clearing (“bull-eye’) at site of Tick bite

    • Rash within 10 days, fades within 3 – 6 weeks

    • Infection still active  Fever, Headache, Malaise, Myalgia, Adenopathy, Meningeal irritation.


    Borrelia2
    BORRELIA

    • Lyme Disease (cont)

    • Clinical Manifestations:

    • Untreated  Neurologic + Cardiac disease

    • Neurolgic Symptoms:

      • Severe Headache Meningitis

      • Cranial nerve palsies

      • Painful peripheral neuropathies


    Borrelia3
    BORRELIA

    • Lyme Disease (cont)

    • Clinical Manifestations:

    • Cardiac Symptoms:

      • Cardiac Arrhythmias (resolve after several weeks)

      • Myocarditis Pericarditis

    • Diagnosis: Clinical Hx Tick bite Serology

    • Relapsing Fever:Borrelia recurrentis

      • Transmitted by Human Body Louse


    Mycoplasma ureaplasma
    MYCOPLASMA & UREAPLASMA

    • Smallest free-living organisms

    • Prokaryoitic cells looking like Gram negative bacteria

    • Ability to Hydrolyze Urea

    • Clinically Important:

      • Mycoplasma pneumoniae

      • Mycoplasma hominis

      • Ureaplasma urealyticum


    Mycplasmataceae
    MYCPLASMATACEAE

    • Characteristics & Physiology:

    • Filamentous Pleomorphic

    • Facultative Uses Fermentation for Energy

    • Require Sterols for growth, because cell membranes contain Cholesterol

    • Lack cell wall, therefore resistant to beta-lactam antibiotics (Penicillin)

    • Mycoplasma pneumoniae

    • Found word wide

    • Transmitted by Aerosol Droplets


    Mycoplasma pneumoniae
    Mycoplasma pneumoniae

    • Clinical Manifestations:

    • Most common cause for Pneumonia in Young Adults (“walking pneumonia”)

      • Non-productive Cough

      • Low-grade Fever Insidious Headache

      • Non-purulent Otitis media in 20% of cases

      • Bullus myringitis in 20% of cases

    • Treatment: Macrolides (Erythromycin, Azithromycin), Tetracycline, Fluoroquinolones

    • Diagnosis using cold agglutinins (IgM)


    Mycoplasma hominis
    Mycoplasma hominis

    • Sexually transmitted

    • Major cause of postpartum women

    • Clinical Manifestations:

    • Postabortal & Postpartum Fever + Bactaremia

    • Pelvic Inflammatory Disease (PID)


    Ureaplasma urealyticum
    Ureaplasma urealyticum

    • Sexually transmitted

    • Produces Urea

    • Minor cause for non-gonococcal Urethritis


    Virology
    VIROLOGY

    • Smallest agents of infection (20 – 300 nm dia)

    • RNA or DNA surrounded by protective protein shell (capsid).

    • Shell surrounded by an envelope containing lipid & protein.

    • Multiplication occur intracellularly.

    • Can become latent & integratetheir Genome into host cell and transmitted to each daughter cell


    Viral classification identification
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Morphology:

    • Terminology:

      • Viron: complete virus particla

      • Capsid:

        • Protein shell encloses / protects Nucleic Acid Genome (DNA or RNA)

        • Protein units = Capsomeres

        • Control host range & cell tropism

        • Adsorb to cell surface


    Viral classification identification1
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Morphology:

    • Terminology: (cont)

      • Nucleocapsid: Protein Shell + Nucleic Acid

      • Peplomeres: Protein Spikes on Envelope


    Viral classification identification2
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Morphology: (cont)

    • Nucleocapsid:

      • Helical Nucleocapsid:

        • Extended Nucleic Acid cavity, surrounded by Helical arranged Proteins

        • Outer Lipid Envelope

        • Orthomyxoviruses Paramyxoviruses

        • Rhabdoviruses


    Viral classification identification3
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Morphology: (cont)

    • Nucleocapsid:

      • Icosahedral Nucleocapsid

        • Condensed Nucleic Acid forming a Cuboidal shape (Hexagonal)

        • Enveloped or Naked

        • Parvoviruses Adenoviruses

        • Herpesviruses Picornaviruses


    Viral classification identification4
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Morphology: (cont)

    • Envelope:

      • Lipid structures

      • Derived from Nuclear or Plasma cell Membrane acquired during viral maturation when the Nucleocapsid buds thru the Host’s membrane

      • Not rigid, appear heterogeneous


    Viral classification identification5
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Morphology:

    • Envelope: (cont)

      • Viral Glycoproteins Peplomeres:

        • Viral Attachment Proteins (VAP)

        • In Outer Envelope

        • Important role in Antigenic structure + Host Immune response

        • Mediate viral Binding + Entry in Host cell

    • Antibodies to gp120 GP of HIV used to tell course of disease & viral load


    Viral classification identification6
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Morphology: (cont)

    • Viral Classification

      • Based on Nucleic Acid composition

        • Single or double-strand DNA or RNA

        • Positive-sense RNA (+RNA) serve as mRNA

        • Negative-sense RNA need a RNA polymerase to synthesize a complementary positive strand to serve as mRNA


    Viral classification identification7
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Morphology: (cont)

    • Viral Proteins:

      • Important in initial contact with Host cell

      • Dictate which cell is infected

      • Hemagglutinins: Vaccine Antigens

      • Enzymes:

        • Neuraminidase:

          • Release viral particles from cells  continue infection


    Viral classification identification8
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Morphology:

      • Enzymes: (cont)

        • RNA polymerase

          • Needed for viral Replication of Negative-sense RNA viruses

          • Carried into cell as part of Viron

        • Reverse Transcriptase: (Retroviruses)

          • Transcribe Single-stranded RNA into Double-stranded DNA  Integrated into Host by Intergrase


    Viral classification identification9
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Replication

    • Depend on Host cell to provide synthetic mechanism & metabolic machinery

    • Replication Cycle:

    • Lyse Host cell or form stable interaction so Host cell can survive

      • 1. Adsorption (attachment):

        • Viral Surface Protein (Capsomere or Peplomere) + Host cell Receptor

        • Host & Tissue specific


    Viral classification identification10
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Replication Cycle: (cont)

      • 2. Penetration & Uncoating:

        • Helped by Receptor-Specific Endocytosis

        • Virus loses it Coat or Envelope  separate Capsid & Envelope from Nucleic Acid


    Viral classification identification11
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Replication Cycle: (cont)

      • 3. Synthetic Stage:

        • mRNA transcribed from Viral Nucleic Acid by Host cell

        • Minus-strand RNA virus, Double-strand DNA & DNA viruses initiate Nucleic Acid synthesis  mRNA

        • Positive-strand RNA viruses initiate Protein synthesis


    Viral classification identification12
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Replication Cycle: (cont)

      • 4. Production of Viral Proteins:

        • With Positive-sense RNA (polio virus), viral RNA (mRNA) read directly by Host cell Ribosome & Enzymes for RNA synthesis produced


    Viral classification identification13
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Replication Cycle: (cont)

      • 4. Production of Viral Protein

        • With RNA viruses, viral genome (-RNA, double-strand RNA or DNA) synthesize mRNA using RNA-dependent RNA polymerase (Transcriptase) found in Viron & encoded by viral genome.

        • Others by Transcription of viral DNA to synthesize mRNA  protein synthesis


    Viral classification identification14
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Replication Cycle: (cont)

      • 4. Production of Viral Protein (cont)

        • Some Proteins = structural units (Capsomeres, Peplomeres)

        • Others = Enzymes needed for DNA synthesis (DNA polymerase)


    Viral classification identification15
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Replication Cycle: (cont)

      • 5. Replication of Viral Genome (Nucleic Acid)

        • Plus-stranded RNA viruses immediately synthesize proteins without Nucleic Acid Replication of Transcription.

        • RNA synthesis occur when enough RNA polymerase are formed, using host cell machinery

        • Minus-strand copy made from parental strand RNA  Template  Replication


    Viral classification identification16
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Replication Cycle: (cont)

      • 5. Replication of Viral Genome (Nucleic Acid)

        • Minus-strand & Double-strand RNA viruses first synthesis mRNA for the translation into viral proteins

        • Minus-strand act as negative Template for synthesis of mRNA

        • Viral genome carry RNA-dependent RNA polymerase needed to synthesize mRNA from minus-strand.


    Viral classification identification17
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Replication Cycle: (cont)

      • 5. Replication of Viral Genome (Nucleic Acid)

        • Double-strand viruses (Retrovirus) synthesize a Positive Strand from Negative Strand of parent which act as both mRNA & replicative intermediate to make Negative-sense RNA

        • Retroviruses use Negative Strand of DNA intermediate to make Positive-sense RNA


    Viral classification identification18
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Replication Cycle: (cont)

      • 5. Replication of Viral Genome (Nucleic Acid)

        • Double Strand DNA virus replicate by using each Strand as a Template for synthesis of complimentary DNA copy.


    Viral classification identification19
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Replication Cycle: (cont)

      • 5. Replication of Viral Genome (Nucleic Acid)

        • Hepatits B virus have a viral RNA-dependent DNA polymerase (reverse transcriptase) that uses viral mRNA as a template to synthesize missing portion of viral genome, which duplicate using Host DNA polymerase

        • Single-strand DNA virus (Parvovirus) synthesize Double-strand intermediate as template


    Viral classification identification20
    VIRAL CLASSIFICATION & IDENTIFICATION

    • Viral Assembly:

      • Occur at towards end synthetic period

      • Viral Genomes & Capsid Polypeptides assembly  Infectious viral offspring

    • Release: (Final Stage)

    • Enveloped virus released by Budding process

    • Nucleocapsid bud thru viral membrane patches, gaining viral specific Glycoproteins.

    • Poxvirus & Naked Capsid viruses breakout rapidly  cell disintegration


    Summary of viral growth cycle
    SUMMARY OF VIRAL GROWTH CYCLE

    • Attachment of virus to cell

    • Penetration of cell

    • Uncoating of viral genome

    • Transcription of genome into mRNA

    • Translation into proteins

    • Replication of viral genome

    • Assembly of particles into new virus

    • Release of virus


    Summary
    SUMMARY

    • All RNA viruses have Single-stranded RNA EXCEPT Reovirus

    • All RNA viruses have an Envelope EXCEPT Reovirus, Calicivirus, Picornavirus

    • All DNA viruses have a Double-stranded DNA EXCEPT Parvovirus (ss); Hepadnavirus has ss in its DNA.

    • All DNA viruses have Icosahedral Nucleocapsid EXCEPT Poxvirus


    Summary1
    SUMMARY

    • All viruses with Helically Symetrical Nucleocapsid are RNA viruses

    • Positive-sense RNA viruses are mRNA, so can directly encode proteins needed for replication.

    • Other viruses require enzymes (RNA-dependent or DNA-dependent RNA polymerase), to produce mRNA for replication

    • NOTE: Non-enveloped viruses are resistant to Disinfectants


    Summary2
    SUMMARY

    • All DNA viruses replicate in the Nucleus EXCEPT Poxvirus

    • All RNA viruses replicate in the Cytoplasm EXCEPT Influenza virus & Retroviruses


    Dna viruses hhappp
    DNA Viruses (HHAPPP)

    • ADENOVIRUSES:

    • Double stranded DNA

    • Naked icosahedral nucleocapsid

    • Transmission:

    • Person to person via respiratory & ocularsecretions

    • Infects mucous membranes & LNs

    • Humans only known Host


    Adenoviruses cont
    ADENOVIRUSES (cont)

    • Clinical Manifestations:

    • Acute Respiratory Disease:

      • Tonsils Adenoids LNs

      • Most infections acute & self-limiting

      • Influenza-like illness in late Fall & Winter

      • Pharyngitis, fever, cough, malaise

      • Conjunctivitis “pink-eye”

      • Diarrhea & Gastroenteritis

      • Treatment: Supportive (fluids etc)

        Vaccine with live non-attenuated virus


    Papovaviruses
    PAPOVAVIRUSES

    • Papiloma Polyoma Vacuolating viruses

    • Double stranded circular DNA

    • Naked icoahedral nucleocapsid

    • HUMAN PAPILLOMAVIRUS: (HPV)

    • World wide distribution

    • Cause Skin “warts” (Papilloma) & Genital “warts (Condyloma Acuminata)

    • Lesions pedunculated

    • Most common cause of viral STD


    Papillomavirus cont
    Papillomavirus (cont)

    • Transmission via contact with “warts”

    • Associated with:

      • Laryngeal papillomas

      • Oral, Laryngeal, Penile & Cervical Cancer

    • Treatment:

    • Electrocautery Cryocautery

    • Excision Chemicals

    • Recurrence common (auto-inoculation)


    Herpesviruses
    HERPESVIRUSES

    • Double stranded DNA

    • Enveloped icosahedral nucleocapsid

    • Latent infection with recurdescence of disease

    • HERPES SIMPLEX VIRUS, TYPE 1 & 2

    • Cause Oral & Genital vesicular lesions

    • Epithelial cell are infected & destroyed

    • Upon resolution of acute illness, virus migrates to ganglions where they reside, later to migrate down neuron to re-infect Epithelial cell giving rise to new lesion.


    Herpes simplex virus type 1 2 cont
    HERPES SIMPLEX VIRUS, TYPE 1 & 2(cont)

    • Humans are only known host

    • Transmission: direct contact with vesicular lesions (infectious) or secretions

    • HSV 1:

    • Clinical Manifestations:(“fever blisters”)

    • Usually acquired early in life (< 5 y o)

    • Oral lesions on all mucosal surfaces

    • Pain, Fever, Lymphadenopathy (PrimaryHerpetic Gingivostomatitis)

    • Intraoral Recurrent lesions on Keratinized, bound down mucosa(Hard Palate + Gingiva)


    Herpes simplex virus type 1 2 cont1
    HERPES SIMPLEX VIRUS, TYPE 1 & 2(cont)

    • HSV-2

    • Transmission: sexual contact

    • Clinical Manifestations;

    • Genital vesicular lesion + neurologic disease

    • Pain

    • Vesicular lesion  superficial ulcers  heal with “yellow” crusting

    • Recurrent infection at site of primary infection

    • Activation of latent virus by stress, menses, fever, sunlight, trauma, immune suppression


    Herpes simplex virus type 1 2 cont2
    HERPES SIMPLEX VIRUS, TYPE 1 & 2(cont)

    • Diagnosis:

    • Identification of clinical lesion

    • Tissue culture

    • Tzanck Cytologic smear show multinucleated giant cell with margination of chromatin

    • Immunofluorescent stains show intranuclearinclusion bodies

    • Treatment:

    • Primary Herpetic Gingivostomatitis:supportive

    • Acyclovir for severe disease or immunosuppression


    Herpesviruses cont
    Herpesviruses (cont)

    • VARICELLA-ZOSTER VIRUS (VZV)

    • Chicken-pox & Shingles (Herpes-Zoster)

    • CHICKENPOX (VARICELLA)

    • Clinical Manifestations: (2 weeks incubation)

    • Mild self-limiting illness

    • Fever, macular then papular eruption on Skin & mucous membranes (oral)

    • Papules are pruritic vesicular

    • Highly contagious  epidemics

    • Transmission: Respiratory secretions


    Herpesviruses cont1
    Herpesviruses (cont)

    • VARICELLA-ZOSTER VIRUS (VZV)

    • SHINGLES

    • Recurrent infect of VZV in adults

    • VZV latent in sensory ganglia of spinal nerves

    • Activated by:

      • Trauma Neoplasm Drugs

      • Imunosuppression

    • Clinical Manifestations:

    • Severe dermatomal pain with vesicular lesions

    • Treatment:Acyclovir, VZIG,attenuated Vaccine


    Herpesviruses cont2
    Herpesviruses (cont)

    • EPSTEIN- BARR VIRUS (EBV)

    • Agent for Infectious mononucleosis (IM)

    • Virus replicates in Epithelial cells infect B-lymphocytes

    • Transmission:Saliva & Respiratory secretions

    • Associated with:

      • Burkitt’s lymphoma Nasophayngeal Ca

      • Hairy leukoplakia (lesion on lateral Tongue seen with diagnosis of AIDS)


    Herpesviruses cont3
    Herpesviruses (cont)

    • EPSTEIN- BARR VIRUS (EBV) [cont]

    • Clinical Manifestations: Last for 2 – 4 weeks

    • Fatigue Tender Lymphadenopathy Fever

    • Headache Splenomegaly (rupture0 Pharyngitis

    • Histology show Warthin-Finkeldey cells + Atypical Lymphocytes with “foamy cytoplasm (Downey cells) on Cytology

    • Diagnosis:Heterophile Ab(90%) Paul-BunnelTest

      (Monospot Test)

    • Treatment: Supportive. Acyclovir severe disease


    Herpesviruses cont4
    Herpesviruses (cont)

    • CYTOMEGALOVIRUS (CMV)

    • Mononucleosis-like illness (subclinical)

    • Life-long latent infection

    • Incubation period = 4 – 8 weeks

    • Reactivation in immunosuppressed patients [cancer, transplant (esp. Kidney), AIDS]

    • CMV Retinitis in AIDS patients

    • Congenital disease transplacentally  Cytomegalic Inclusion Disease

    • Treatment:Ganciclovir in severe disease


    Herpesviruses cont5
    Herpesviruses (cont)

    • Human Herpesvirus-6 (HHV-6)

    • Lymphotrophic etiologic agent for Pediatric “sixth disease” or Roseola infection (exanthem subitum)

      • Erythematous pruritic rask on Skin, last several weeks

    • Human Herpesvirus-8 (HHV-8)

    • Associated with Kaposi Sarcoma

      • Associated with AIDS


    Poxvirus
    POXVIRUS

    • Largest of all viruses

    • Linear double stranded DNA with envelope

    • Replicate in cytoplasm of infected cell

    • Ovoid to brick-like in shape

    • VARIOLA VIRUS(smallpox virus)

    • Transmission: direct contact. Humans only.

    • MOLLUSCUM CONTAGIOSUM)

    • “wart-like” Skin lesions (face, trunk, limbs)

    • COWPOX: contact with cow udders. Fingers & Hands. Self limiting.


    Other dna viruses
    OTHER DNA VIRUSES

    • HEPADNAVIRUSES:

      • Include Hepatitis B virus (HBV)

    • PARVOVIRUSES:

    • Single-standed DNA virus

    • Serotype B19 only Human pathogen

    • Cause Erythema infectiosum (“fifth disease”) in Children  “slapped cheek” rash


    Condition with erythematous rash
    CONDITION WITH ERYTHEMATOUS RASH

    • Measles

    • Rubella

    • Scarlet fever

    • Roseeola

    • Exanthem subitum (HHV-6)


    Rna viruses
    RNA Viruses

    • PICORNAVIRUSES

    • Small single stranded RNA

    • Naked nucleocapsid

    • Positive sense (can serve as mRNA)  replicate in cytoplasm of infected cell.

    • Divided into:

    • Enteroviruses (polioviruses, coxsackie, echovirus, enterovirus)

      • Acid resistant

  • Rhinoviruses (“common cold”)


  • Rna viruses1
    RNA Viruses

    • PICORNAVIRUSES

    • ENTEROVIRUSES:

    • Poliovirus:

    • Bind to receptor in the GIT & Neurons

    • Only Primates. Majority of disease subclinical

    • Transmission: Person-person via contaminated water (virus excreted in feces)

    • Pathogenesis:

    • Virus ingested  replicates in oropharynx & GIT  drain to LNs  viremia  CNS destruction (motor neuron in Spinal cord)


    Rna viruses cont
    RNA Viruses (cont)

    • PICORNAVIRUSES

    • ENTEROVIRUSES:

    • Poliovirus (cont)

    • Clinical manifestations: Flaccid paralysis.

    • Prevention:

    • Live attenuated virus vaccine(oral: OPV, Sabin

    • Killed virus vaccine (IPV, Salk vaccine)

    • Both vaccines induce serum Ab  immunity

    • Oral vaccine  GIT immunity & sIgA synthesis


    Rna viruses cont1
    RNA Viruses (cont)

    • PICORNAVIRUSES

    • ENTEROVIRUSES:

    • Echovirus(Enteric Cytopathic Human Orphan)

    • All infect the GIT

    • Transmission:

      • Ingestion or Inhalation  Throat  GIT

    • Epidemiology: incidence increased in Summer

    • Clinical Manifestations:

    • Fever Rash Enteritis “common cold” Hemorrhagic conjunctivitis Meningitis


    Rna viruses cont2
    RNA Viruses (cont)

    • PICORNAVIRUSES

    • ENTEROVIRUSES:

    • Coxsackieviruses:

    • Coxsackievirus A  Herpangina & Hand-Foot-Mouth Disease

    • Clinical: Headache Sore throat Stiff Neck Dysphasia Fever Anorexia Abdominal pain

    • Transmission: (contact with Horses)

    • Nasopharyngeal secretions Oro-fecal

    • Epidemiology: epidemics in Summer & Fall


    Rna viruses cont3
    RNA Viruses (cont)

    • PICORNAVIRUSES

    • ENTEROVIRUSES:

    • Coxsackieviruses:

    • Coxsackie B

      • Myocarditis Pericarditis

      • Pleurodynia

    • Enterovirus 72: Etiologic agent for Hepatitis A


    Rna viruses cont4
    RNA Viruses (cont)

    • PICORNAVIRUSES

    • RHINOVIRUSES (causes “common cold”)

    • Transmission & Epidemiology

    • Over 100 Serotypes

    • Infect only Humans (Nose & Throat)

    • Incubation period = 2 – 4 days

    • Clinical Manifestations (up to a week)

    • URT irritation Headache Nasal discharge Cough Malaise Chills Myalgia

    • Treatment & Prevention: Supportive.


    Rna viruses cont5
    RNA Viruses (cont)

    • ORTHOMYXOVIRUS(Influenza virus A, B, C)

    • Medium size , negative sense, single stranded, segmented RNA + enveloped nucleocapsid.

    • Transmission: Inhalation

    • Clinical Manifestations:

    • Influenza C: Incubation period = 1 – 4 days

      • symptoms of “common cold”

    • Influenza A & B (B  Reye syndrome)

    • Fever Chills Myalgia Sore throat Headache Nasal congestion Dry cough

    • Rx: Amantadine, Rimantadine ( Type A)


    Rna viruses cont6
    RNA Viruses (cont)

    • PARAMYXOVIRUSES

    • Negative sense with Envelope Nucleocapsid

    • Genetically stable

    • Initial infection via URT (respiratory)

    • Common cause of URT infection in Children

      • PARAINFLUENZA VIRUSES:

        • Transmission: Aerosol Droplets

        • Etiologic agent for Croup (barking cough)

        • Laryngo-tracheobronchitis


    Rna viruses cont7
    RNA Viruses (cont)

    • PARAMYXOVIRUSES

      • MEASLES VIRUS (RUBEOLA)

      • Highly infectious childhood infection

      • Fever & Maculopapular exanthem (skin rash)

      • Virus multiples in the Oropharynx LNs

      • Infection  permanent immunity

      • Transmission: Respiratory secretions


    Rna viruses cont8
    RNA Viruses (cont)

    • Clinical Manifestation of Measles:

    • Koplick spots:

      • “bluish-white” specks on a”red” base found on Buccal mucosa

    • Abrupt onset of Anorexia (loss of appetite)

    • Nausea Fever Malaise Cough

    • Coryza (profuse nasal discharge)

    • Conjunctivitis

    • Maculo-papular erythematous rash, lasting 5 days, starts on the Face  Trunk


    Rna viruses cont9
    RNA Viruses (cont)

    • Complications of Measles:

    • Encephalitis (inflammation of the Brain)

    • Pneumonia (immunodeficiency)

    • Otitis media (middle Ear infection)

    • Subacute Sclerosing Panencephalitis (fatal)

    • Possible association with Multiple sclerosis (demyelination of nerves with numbness & weakness of the extremites)

    • Treatment & Prevention:

    • Live attenuated vaccine at 15 months (MMP)

    • Serum Globulin (most donors have Antibodies)


    Rna viruses cont10
    RNA Viruses (cont)

    • PARAMYXOVIRUSES

      • MUMPS VIRUS

      • Causes an acute contagious, nonsuppurative Parotitis(unlateral or bilateral)

      • Orchitis (Testicular inflammation) possible complication

      • Prevention:

      • Immunization with live attenuated virus (part of Measles-Mumps-Rubella (MMR) vaccine)


    Rna viruses cont11
    RNA Viruses (cont)

    • PARAMYXOVIRUSES

      • RESPIRATORY SYNCYTIAL VIRUS (RSV)

      • Main cause of Lower URT infection in Infants

      • Transmission: Aerooal Droplets, Fomites

      • Clinical Manifestation:

        • “common cold-like” symptoms

        • Severe Lower URT infection (Infants)


    Rna viruses cont12
    RNA Viruses (cont)

    • TOGAVIRUSES

    • Disease range from Febrile Encephalitis  severe Bleeding

    • Positive single-stranded RNA + Enveloped Nuceocapsid

      • ALPHAVIRUS

        • Include Encephalitis viruses

        • Transmission: Insects (Zoonotic agents)


    Rna viruses cont13
    RNA Viruses (cont)

    • TOGAVIRUSES

      • ALPHAVIRUS

        • Eastern Equine Encephalitis (EEC) virus

          • Abrupt Headache & Fever

          • Nuchal rigidity

        • Western Equine Encephalitis virus

          • Less severe disease

          • Mostly Childran


    Rna viruses cont14
    RNA Viruses (cont)

    • TOGAVIRUSES

    • RUBIVIRUS (rubella)

    • Cause German measles (3 day measles)

    • Only Togavirus not transmitted by arthropod

    • Disease of shorter duration & less severe

    • Infection starts in URT  throughout Body due to viremia

    • Morbilliform rash (like measles) occur 2 – 3 weeks post infection


    Rna viruses cont15
    RNA Viruses (cont)

    • Rubella (German measles )(cont)

    • Congenital rubella

    • Virus transmitted across the Placenta

    • Serious consequence if it occurs in 1st Trimester

    • Complications:

      • Mental retardation Blindness

      • Heart abnormalities Motor dysfunction

      • Encephalitis

    • Prevention: live attenuated virus vaccine (MMR)


    Rna viruses cont16
    RNA Viruses (cont)

    • FLAVIVIRUSES (arthropod-borne)

    • Yellow Fever:

    • Mosquito borne

    • Incubation period = 3 – 6 days

    • Clinical Manifestations:

    • Acute onset Fever Proteinuria

    • Jaundice (yellow skin/sclera of eye)

    • Vomiting (vomitus black) Hemorrhage

    • Prevention: attenuated vaccine


    Rna viruses cont17
    RNA Viruses (cont)

    • FLAVIVIRUSES (cont)

    • Dengue Fever (mosquito borne illness)

    • Clinical Manifestations:

    • Fever Rash Arthralgia

    • Lympadenopathy Hemorrhage

    • Death (10%)

    • Occur primarily in the Tropics


    Rna viruses cont18
    RNA Viruses (cont)

    • RABDOVIRUSES

    • Rabies virus (causes Rabies)

    • “bullet-shaped” Enveloped, single stranded, Negative sense RNA virus, with Nucleocapsid with Glycoprotein spikes.

    • Replicates within Host cell cytoplasm

    • Transmission: Bite from dog, skunk, bats, fox.

    • Pathogenesis:

    • Break in Skin  Muscle & CT (incubation period 2 – 16 weeks)  along Nerves  CNS (Basal Ganglia) & Salivary Gld


    Rna viruses cont19
    RNA Viruses (cont)

    • Rabies (cont)

    • Negri bodies in Neurons of the Hippocampus

    • Clinical Manifestations: (4 phase)

    • Prodrome symptoms:

      • Paresthesia at site of wound

      • Irritability (mood & temperament change)

      • Flu-like illness

    • Pharyngeal spasm  drooling (hydrophobia)

    • Seizures & coma  Death


    Rna viruses cont20
    RNA Viruses (cont)

    • Rabies (cont)

    • Diagnosis:

    • Direct Immunofluorescenc assay for virus

    • Immunofluorescenc assay for Nergi bodies in Nerve tissue (Ammon’ horn)

    • Treatment & Prevention:

    • Vaccine: Human & Pets with inactive virus from infected Human diploid cells

    • Human rabies immunoglobulin(HRIG) immediately in case probable infection. Very painful.


    Rna viruses cont21
    RNA Viruses (cont)

    • RETROVIRUSES

    • Diploid, positive sense, single-stranded RNA

    • Viral-encoded reverse transcriptase which produces double-stranded DNA from RNA

    • Viral genome encodes 3 groups of proteins:

      • Pol (reverse transcriptase + integrase)

      • Env (type-specific envelope protein)

      • Gag (type-specific viral core protein

    • Include Human T-cell leukemia viruses (HTLV 1 & 11) & HIV (Lentivirus)


    Rna viruses cont22
    RNA Viruses (cont)

    • RETROVIRUSES (cont)

    • ONCOVIRUSES (promote cell growth)

    • Human T-Lymphotrophic Virus 1 (HTLV 1)

    • Infects CD4 (helper) T-cells  Acute T-cell Lymphocytic Leukemia (ATLL)

    • Human T-Lymphotrophic Virus 11 (HTLV 11)

    • Causes Hairy cell leukemia


    Rna viruses cont23
    RNA Viruses (cont)

    • RETROVIRUSES (cont)

    • HUMAN IMMUNODEFICIENCY VIRUS

    • Cause Acquired Immunodeficiency Syndrome

    • AIDS initially recognized in 1981

    • HIV isolated in 1983

    • Infects helper T-cells by attachment to cell surface protein (CD4) & Macrophages.

    • Patient prone to opportunistic infections (when CD4 count drops below 200), malignancies & Wasting syndrome


    Hepatitis viruses
    HEPATITIS VIRUSES

    • HEPATITIS A VIRUS (HAV)

    • Picornavirus RNA virus

    • Transmission:

      • Fecal-orally. Incubation period = 15-40 days

      • Epidemic Endemic (institutional)

      • Childhood disease mild, adult severe

    • No chronic hepatitis or carrier state

    • Diagnosis: presence of anti-hepatitis A IgM

    • Treatment: Killed virus vaccine (food-handlers & day care workers) & gamma Globulin


    Hepatitis viruses cont
    HEPATITIS VIRUSES (cont)

    • HEPATITIS B VIRUS (HBV)

    • Enveloped double stranded DNA virus

    • Viral Antigens:

      • Surface antigen (HBsAg) found in virion

        • Indicates active viremia (infectivity)

      • Core antigen (HBcAg) found in capsid

      • E antigen (HBeAg) found in capsomere


    Hepatitis viruses cont1
    HEPATITIS VIRUSES (cont)

    HBV (cont)

    • Antibodies to HBV:

      • Ab to HBsAg

        • Protective

        • Detected after virus disappears from serum

      • Ab to HBcAg

        • Detected after appearance of HBsAg

        • Confirm infection when HBsAg & Ab to HBsAg is absent (window phase)


    Hepatitis viruses cont2
    HEPATITIS VIRUSES (cont)

    • Antibodies to HBV (cont)

      • Ab to HBeAg associated with low risk of infectivity

    • Transmission:

      • Parenteral (not by mouth) & Sexual contact


    Hepatitis viruses cont3
    HEPATITIS VIRUSES (cont)

    • Clinical Manifestations of HBV Infection:

    • Anorexia Nausea Vomiting

    • Headache Fever Dark Urine

    • Abdominal pain Jaundice

    • Arthralgia Arthritis Nephritis

    • Dermatitis (Skin)

    • 10 – 15% develop:

      • chronic hepatitis(cirrhosis & hepatocellular carcinoma)

      • Carrier state (infectious)


    Hepatitis viruses cont4
    HEPATITIS VIRUSES (cont)

    • Liver function tests for HBV:

    • Elevated Transaminase Hyperbilirubinemia

    • Elevated Alkaline phosphatase

    • Prevention of HBV:

    • Recombinant HBsAg (Health Care Workers)

    • Children 3 doses: 1st at birth, 2nd at 2 –4 mos, 3rd at 6 – 18 mos


    Hepatitis viruses cont5
    HEPATITIS VIRUSES (cont)

    • HEPATITIS C VIRUS (HCV)

    • Positive sense, single stranded RNA virus

    • Classified as a Flavivirus

    • Associated with post-transfusion hepatitis

    • HEPATITIS D (delta agent)

    • RNA virus, replicate only in cells infected with HBV.

    • HEPATITIS E VIRUS

    • Single stranded RNA. Disease similar to HAV. Severe in pregnancy. Spread oro-fecally.


    Mycology
    MYCOLOGY

    • Eukaryotic organisms (True Nucleus)

    • Cell Wall ( Glucose + Mannose polymers (chitin)

    • Cell membrane (Ergosterol)

    • Yeast: Round or oval, reproduce by budding

    • Mold:

      • Tubular structures called Hyphae

      • Grow by branching & extensions (mycelia)

    • Reproduction: sexual or asexual (mitosis)

    • Immunity: T-cell is protective in fungal disease Eosinophils also found in tissue


    Dermatophytosis cutaneous mycosis
    DERMATOPHYTOSIS (Cutaneous Mycosis)

    • Stratum corneum infections: (Ringworm)

    • Tinea corporis  body

    • Tinea cruris  groin (jock itch)

    • Tinea pedis  feet (athlete’s foot)

    • Tinea manuum  hands

    • Tinea capitis  head

    • Tinea barbae  beard

    • Tinea unguium  nails

    • Diagnosis: Skin scrapings (KOH & UV light)

    • Treatment: Miconazole or Clotrimazole


    Subcutaneous mycoses
    SUBCUTANEOUS MYCOSES

    • SPOROTRICHOSIS:

    • Etiology:Sporothrix schenckii (fungus)

    • World wide in soil, plants, plant debris

    • Classically associated with rose thorns (rose gardener’s disease)

    • Clinical Manifestations:

    • Limited to Skin

    • Regional lymphadenopathy


    Systemic mycoses
    SYSTEMIC MYCOSES

    • Deep invasion into organs

    • HISTOPLASMOSIS (Darling’s disease)

    • Etiology:Histoplasma capsulatum

    • Transmission via Bird & Bat droppings

    • Histology: Yeasts found in Macrophages

    • Clinical Manifestations;

    • Acute pulmonary histoplasmosis (5-21 days after exposure.) Headache & Fever.

    • Treatment: None, self-limiting


    Systemic mycoses cont
    SYSTEMIC MYCOSES (cont)

    • COCCIDIOIDOMYCOSIS

    • Etiology:Coccidioides immitis (fungus)

    • Deserts of SW United States & N. Mexico

    • Transmission via inhalation due to fresh diggings, dust storms)

    • Clinical Manifestations:

    • Acute pneumonia sub-clinical in 60% of cases

    • 40% develop influenza-like symptoms 7-28 days post exposure

    • Fever Malaise Dry cough Eosinophilia Erythematous rash. Rx Amphotericin B


    Systemic mycoses cont1
    SYSTEMIC MYCOSES (cont)

    • BLASTOMYCOSIS

    • Etiology:Blastomyces dermatidis (fungus)

    • Transmission via inhalation of spores associated with dust.

    • Clinical Manifestations:

    • Acute blastomycosis pneumonia

      • Asymptomatic or Severe  Death

      • “influenza-like” symptoms:

        • Fever Chills Productive cough

        • Pleuritic chest pain


    Opportunistic mycoses
    OPPORTUNISTIC MYCOSES

    • Causes disease in immunocompromised.

    • Sometimes found in Normal Flora (oral & skin)

    • CANDIDA

    • Pseudohyphae or Chlamydospores

    • Etiology:Candida albicans

    • Found on or in:

      • Mucocutaneous surfaces Soil

      • Hospitals Some foods


    Opportunistic mycoses cont
    OPPORTUNISTIC MYCOSES (cont)

    • CANDIDA (cont)

    • Clinical Manifestations:

    • Oropharyngeal candidiasis (Thrush)

      • “white plaques” on Tongue & Buccal mucosa

      • Cytology shows pseudo-hyphae (PAS stain)

      • Treatment: Nystatin Ketoconazole

        • Mycelex troches (no sugar)


    Opportunistic mycoses cont1
    OPPORTUNISTIC MYCOSES (cont)

    • CANDIDA (cont)

    • Clinical Manifestations (cont)

    • Vaginal candidiasis

      • Diabetics Antibiotic therapy

      • Pregnancy  Neonatal “Thrush”

      • Thick yellow-white discharge

      • Intense pruritis

    • Treatment: Nystatin suppositories


    Opportunistic mycoses cont2
    OPPORTUNISTIC MYCOSES (cont)

    • CANDIDA (cont)

    • Clinical Manifestations (cont)

    • Invasive candidiasis associated with:

      • Diabetes

      • Damaged mucosal surfaces (catheters)

      • Immunosuppression (AIDS, Chemotherapy (leukemia, lymphoma), long term Steroids & Antibiotics)

    • Treatment: Systemic Ketoconazole


    Opportunistic mycoses cont3
    OPPORTUNISTIC MYCOSES (cont)

    • CRYPTOCOCCOSIS

    • Etiology:Cryptococcus neoformans (yeast)

    • Found in:

      • Pigeon droppings, Soil Fruits Milk Wood products

    • Immunosuppression predisposes to disease

    • Clinical Manifestations:

      • Pulmonary Meningitis

    • Treatment: Amphotericin B


    Opportunistic mycoses cont4
    OPPORTUNISTIC MYCOSES (cont)

    • ASPERGILLOSIS

    • Etiology: Aspergillus fumigatus

    • Found in naturally in Soil, spores in the Air

    • Clinical Manifestations:

    • Allergic bronchopulmonary aspergillosis

      • Hypersensitivity reaction (IgE mediated)  bronchospasm

      • Wheezing Fever Eosinophilia

    • Treatment: Steroid for symptoms


    Opportunistic mycoses cont5
    OPPORTUNISTIC MYCOSES (cont)

    • ZYGOMYCOSIS (Mucormycosis)

    • Etiology: genera Rhizopus & Mucor (nonseptate hyphae)

    • Molds found in decaying vegetation

    • Persons predisposes:

      • Diabetics Immunosuppression

      • Malnutrition

    • Clinical Manifestations:

      • Rhinocerebral (Erode thru Nose, Palate, Sinus, Orbit  Brain

      • Pulmonary due to inhalation of spores


    Opportunistic mycoses cont6
    OPPORTUNISTIC MYCOSES (cont)

    • PNEUMOCYSTIS CARINII

    • Fungus based on rRNA homology

    • Clinical manifestation:

    • Interstitial Pneumonia in Immunosuppressed  Death

    • Treatment:

    • Trimethoprim-sulfamethoxazole (TMP-SMX)

    • Pentamidine


    Summary3
    SUMMARY

    • IN VIVO FORMS OF FUNGI:

    • Coccidioides – spherules

    • Histoplasma – intracellular yeast

    • Blastomyces – broad-base buds

    • Cryptococcus – large capsule

    • Candida – pseudohyphae

    • Aspergillus – branching septate hyphae

    • Mucor / rhizopus – broad non-sptate hyphae


    Protozoa
    PROTOZOA

    • Unicellular eukaryotic organisms

    • Usually reproduce asexually in Human host

    • GIT & MUCOCUTANEOUS PROTOZOA

    • GIARDIASIS

    • Etiology:Giardia lamblia

    • Transmission: Feces in Water or Food

    • Clinical Manifestations:

      • Diarrhea Abdominal cramps

      • Bloating Flatulence Malaise

      • Weight loss Steatorrhea


    Protozoa cont
    PROTOZOA (cont)

    • AMEBIASIS

    • Etiology:Entamoeba histolytica

    • Transmission: fecal-oral route (poor sanitation)

    • Clinical Manifestations: (Colon of Humans)

      • Diarrhea Abdominal cramps Nausea

      • Vomiting Flatulence

      • Dysentery

        • Severe abdominal pain Dehydration

        • Bloody stool Liver abscess


    Protozoa cont1
    PROTOZOA (cont)

    • TRICHOMONAS VAGINITIS

    • Etiology:Trichomonas vaginalis

    • Clinical Manifestations:

      • Dysurea Pruritis

      • Copious “yellow-frothy” discharge

      • Symptoms worse with alkaline vaginal PH

      • Dyspareunia

      • Men: Prostatitis Urethritis


    Blood tissue protozoa
    BLOOD & TISSUE PROTOZOA

    • MALARIA

    • Etiology:Plasmodium falciparum (intracellular parasite)

      • Sexual phase occur in Anopheles mosquito

      • Asexual phase occur in Humans

    • Clinical Manifestations

      • Periodic Fever & Chills (lasts up to 1 hour)

      • Diaphoresis (profuse perspiration)

      • Nausea Vomiting Malaise

    • Treatment: Chloroquine


    Blood tissue protozoa cont
    BLOOD & TISSUE PROTOZOA (cont)

    • LEISMANIASIS

    • Etiology:Leishmania species

    • Transmission: bite from Sandfly.

    • Pathogenesis: parasite invades Reticuloendothelial cells & reside in Phagolysosomes.

    • Clinical Manifestations:

      • Skin Mucocutaneous Visceral

    • Treatment: Pentostam Glucantime


    Blood tissue protozoa cont1
    BLOOD & TISSUE PROTOZOA (cont)

    • AFRICAN SLEEPING SICKNESS

    • Etiology:Trypanosoma brucei

    • Transmission: bite fro infected Tsetse Fly  CNS involvement  Death

    • Clinical Manifestations:

      • Chancre at site of inoculation

      • Parasitemia in 2 – 3 weeks  LNs

      • Fever Rash Headache Mental changes

      • CNS involvement: Anorexia, Lassitude, Fatique, Wasting, Stupor, Coma, Death

      • Treatment: Suramin Melarsoprol (CNS)


    Blood tissue protozoa cont2
    BLOOD & TISSUE PROTOZOA (cont)

    • TOXOPLASMOSIS

    • Etiology:Toxoplasma gondii

    • Transmission: via secondary hosts

      • Sexual cycle in GIT of Cats  oocyst (encapsulate zygote)  Feces

      • Infested oocytes invade GIT of intermediate host  disseminate in blood  pseudocysts in tissue.

      • Tissue ingested by human in raw or undercooked meat.


    Blood tissue protozoa cont3
    BLOOD & TISSUE PROTOZOA (cont)

    • TOXOPLASMOSIS (cont)

    • Clinical manifestations:

    • Primary infection with mild mononucleosis-like illness

    • Immunodeficiency: meningoencephalitis  seizures

    • Congenital infection:

      • Chorioretinitis Hydrocephaly

      • Diffuse Intracranial Calcifications

      • Anemia Seizures

    • Treatment: Pyrimethamine Sulfadiazine


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