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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
ad