MicroBio 4000 Final Exam

Pathogenicity

The ability to cause disease

Virulence

The degree of pathogenicity

Pathogenicity requirements:

Gain access to host, adhere to tissue, penetrate host defenses, damage host tissue

Virulence factors

Traits of a pathogen that help the pathogen escape the immune response and successfully establish an infection

Portals of entry

Mucous membranes, skin, parenteral route

Mucous membrane entry

Respiratory tract (easiest), GI tract (Food), Genitourinary tract (STDs), Conjunctiva (Eyes)

Skin entry

Largest organ, openings and sweat glands (fungi, worms)

Parenteral Route

Microbes deposited directly into the tissues beneath the skin or into mucous membranes through punters, bites, or wounds (HIS, tetanus)

ID50

Infectious Dose needed to cause infections in 50% of a sample population - lower the ID50 number, higher the virulence

Virulence of the microbe is dependent on

The nature of the microbe and portal of entry

LD50

lethal dose that causes death of 50% of sample population

Adhesins or ligands

Surface molecules that proteins attach to

Adhesins

Glycocalyx, fimbriae, pili, and flagella

Capsules

Organized and anchored glycocalyx, impairs phagocytosis by preventing phagocyte from adhering to bacterium, host can produce antibodies against capsule

M proteins

Found on cell surface and fimbriae, mediate attachment to bacterium, helps resist phagocytosis

Opa

Protein in cell wall, allows attachment to host cells along with fimbriae, bacteria are brought into host cell and multiply

Waxy lipid (Mycolic acid)

Resist digestion by phagocytic cells, bacteria can even multiply in phagocytes

Enzymes defense

Pathogen can wall itself off away from host defenses, produce enzyme to aid in its spread evades antibodies by degrading them

Coagulase enzyme

Coagulate fibrinogen into a blood clot, may protect bacterium from phagocytosis, isolates the bacteria from other host defense

Kinases

Digest fibrin clots, blood clots formed by the host to isolate infection, aids pathogen in its spread

Hyaluronidases

Digests polysaccharide hyaluronic acid that holds cells together, digesting action helps pathogen spread from initial site of infection

Collagenase

Breaks down collagen, helps pathogen spread

IgA proteases

destroys IgA antibodies present in body secretions

Antigenic variation

Alters surface antigen to evade the adaptive immune response

Invasins

Surface proteins produced by bacteria that rearrange actin filaments of the cytoskeleton of host cell, causes membrane ruffling of host cell which aids in pathogen entry

Actin

Allows some bacteria such as Shigella and Listeria to propel themselves through host cytoplasm, and helps pathogen stay invisible to many host defenses

Cadherin

Helps bacterial cells move between host cells

Biofilms

Microbial community that forms a slime layer on the surface that helps with adherence to host, more resistant to phagocytosis and shields antigens from EPS

Ways in which bacterial pathogens damage the host

Using host nutrients, direct damage to cells in the immediate area, produces toxins which are

Using host nutrients

Bacteria produces siderophores In order to compete with iron binding proteins in cells. Siderophores steal iron from proteins by binding to it more tightly

Direct damage

Attaches to host and uses cell nutrients, produces bacterial waste products, metabolizes and multiplies in cells causing cell rupture, penetrates into cells

Toxins

Primary contributing factor to pathogenic properties, produce toxigenicity, can be fatal if transported by blood or lymph vesicles

Intoxications

Effects of pathogenesis that is due to the toxin

Toxemia

Presence of toxins in the blood

Exotoxins

Produced inside some bacteria as part of growth and metabolism, then released outside of bacteria

Endotoxins

Toxin is part of the bacterial cell, released when cells divide or the bacteria is destroyed -

Exotoxin damage

Produced as metabolic by-products, soluble proteins, often encoded by bacteria plasmid or phage, destroys particular host cell structures, effects cause signs and symptoms

Antitoxins

Antibodies saints specific exotoxins

Toxoids

Altered toxins that can no longer cause disease, but produce immune response - vaccines that protect against bacterial toxins rather than bacteria

A-B Exotoxins

Majority of exotoxins, A (active enzyme), B (binding)

Membrane Disrupting exotoxins

Cause lysis of cell by disrupting the membrane by protein channels/pore forming, or disruption of phospholipids

Superantigens

Antigens that provoke intense immune response, combine with macrophages and stimulate T cell production, T cells release excess cytokines which induce fever and symptoms

Endotoxin damage

Toxin is part of bacterial cells, Lipid A on outer portion of cell walls, gram negative only, released when cells divide or when bacteria are destroyed, all produce same symptoms, low toxicity

Plasmids

Small circular pieces of DNA that carry genes useful to the bacteria that harbor them

R factor

Plasmids that carry resistance factors and help bacteria be resistant to some antibiotics

Lysogenic bacteriophages

Viruses that infect bacteria, some are lysogenic and can incorporate DNA into bacterial host

Lysogenic conversion

Bacterial hosts that can exhibit new properties because of incorporated viral DNA

Pathogenic effect of viruses

Virus penetrates host cell and reproduces intracellularly, death of host cell is immediate, cell damage occurs

Cytopathic effects (CPE)

visible effects of viral infection, stop protein synthesis or stop mitosis, lysosome releases enzymes, antigenic changes on surface of host, target cell for destruction, chromosomal changes in host cell

Cytocidal effects

effects that result in death

Noncytocidal effects

Result in cell damage but not death

Inclusion bodies

Granule structures that contain viruses or parts of viruses

Syncytium

Large multinucleated cells that formed from cytopathic effects

Fungi pathogenic properties

Grow on skin and help with attachment, metabolic byproducts (exotoxins) cause symptoms, capsules help resist phagocytosis, release toxins

Protozoa

Hate products cause host symptoms, can reproduce within host cells causing damage or rupture, attach to host cells and digest cells and tissue fluid, antigenic variation

Helminths

Can use host tissue for their growth or to produce parasitic masses - results in host cell tissue damage

Algae

Can produce neurotoxins

Most common portal of exit

Respiratory tract (Coughing and sneezing) and GI tract

Upper Respiratory System

Nose, pharynx, larynx, Middle ear, Eustachian tubes

Lower respiratory tract

Trachea, brachial tubes, alveoli, pleura

Sinus ducts and lacrimal apparatus empties into

Nasal cavity

Auditory tubes empty into

Upper part of the throat

Alveoli

Air sacs that make up lung tissue. Where O2 and CO2 are exchanged between lungs and blood

Pleura

Double layered membrane enclosing the lungs

Alveolar macrophages

Locates, ingests and destroys microorganisms in lung tissue

Pharyngitis

Infection and inflammation of mucous membranes of the pharynx (throat) - sore throat

Laryngitis

Infection of the larynx (voice box) - alters ability to speak

Tonsillitis

Microbes causing pharyngitis can also infect tonsils and inflame tonsils

Sinusitis

Infection of the sinuses, involves heavy mucous discharge

Epiglottitis

Inflammation of the epiglottis (flap like structure that covers the larynx when you swallow) - most life threatening of the upper respiratory diseases

Streptococcal Pharyngitis (Strep Throat)

Etiological Agent: Group A Streptococcus, Gram +
Signs and Symptoms: Local inflammation, Fever, Tender lymph nodes, sometimes earache
Pathogenesis: Resistant to phagocytosis, Cytotoxic tissue cells, RBCs and leukocytes
Detection: Rapid diagnostic test

Scarlet Fever

Etiological Agent: Streptococcus progenies strain - produces eryhtogexic toxin
Signs and Symptoms: Red skin rash due to circulating toxin, fever, red enlarged spotted tongue, tongue loses upper membrane
Pathogenesis: Only the strain is lysogenized by a bacteriophage able to produce toxin
Detection: Needs antibiotics to prevent rheumatic fever

Diphtheria

Etiological Agent: Cornybacterium diphtheriae, Gram +, Pleomorphic
Signs and Symptoms: Sore throat, fever, malaise, swelling of neck, tough grayish membrane at back of throat
Pathogenesis and Virulence factors: Non-invasive bacterium, strain carrying lysogen produces exotoxin that interferes with protein synthesis
Prevention: DTaP vaccine, triple vaccine

Otitis media

Etiological Agent: Streptococcus pneumoniae
Signs and Symptoms: Formation of pus which builds up behind the eardrums, inflamed ear drums, pain, fever
Pathogenesis and Virulence factors: Common in early childhood

Common Cold

Etiological Agent: Rhinoviruses, Coronaviruses
Signs and Symptoms: Sneezing, excessive nasal secretions, congestion, no fever, easily spreads to throat, sinuses, middle ears
Prevention: Treating symptoms, runs course in about a week

Pertussis (Whooping Cough)

Etiological Agent: Bordetella pertussis, Gram -, obligate aerobe
Signs and Symptoms: Initial stage, paroxysmal stage, Convalescence stage
Pathogenesis and Virulence factors: Capsules, two toxins, tracheal cytotoxin, pertussis toxin which enters bloodstream
Prevention: aP vaccine is given, triple vaccine, boosters

Tuberculosis

Etiological Agent: Myobacterium tuberculosis, obligate aerobe
Signs and Symptoms: Host usually not aware of infections, coughing, weight loss and loss of vigor, can result in death
Pathogenesis and Virulence factors: Acquired by inhalation, myopic acids stimulates inflammatory response, organisms phagocytize by alveolar macrophages, can escape phagocytosis, replicates in phagocytes
Prevention: Skin test, rapid blood test, PCR test

Bacterial pneumonia

Typically caused by streptococcus pneumoniae, Atypically caused by other microorganisms, inflamed pleural membranes

Pneumococcal

Etiological Agent: Streptococcus pneumoniae, Gram +, Human reservoir
Signs and Symptoms: High fever, breathing difficulty, chest pain, reddish lungs, sputum is rust colored
Pathogenesis and Virulence factors: Brochi and alveoli, dense capsule
Prevention: Agglutination test, broad spectrum antibiotic, 2 vaccines

H. influenzae

Etiological Agent: Haemophilus influenzae, Gram -, Human resevoir
Signs and Symptoms: Symptoms resemble pneumococcal pneumonia
Pathogenesis and Virulence factors: Involves bronchi and alveoli, dense capsule
Prevention: Gram stain of sputum will differentiate from pneumococcal pneumonia, special media for nutritional requirements, preventative vaccines

Mycoplasmal

Etiological Agent: Mycoplasma pneumoniae, no cell walls, known as walking pneumonia, human reservoir
Signs and Symptoms: Mild but persistent respiratory symptoms, low grade fever, cough, headache
Pathogenesis and Virulence factors:
Prevention: PCR, 'Fried eggs' appearance, tetracycline

Legionellosis

Etiological Agent: Legionella pneumophila, aerobic, Gram -, water reservoir
Signs and Symptoms: High fever, cough, potentially fatal, Gerald pneumonia
Pathogenesis and Virulence factors: Can replicate within macrophages, forms biofilms
Prevention: Culture of selective media, serological tests

Viral pneumonia

Occurs as complication of influenza, measles, or chickenpox, and recently covid

Respiratory Syncytial Virus (RSV)

Etiological Agent: Most common in infants, almost all children infected by age 2
Signs and Symptoms: pneumonia in infants, coughing and wheezing for weeks
Prevention: Serological test for viruses and antibodies, causes cell fusion in cell culture

Influenza

Etiological Agent: Influenzavirus, eight RNA segments and protein capsid
Signs and Symptoms: Fever, chills, headache, muscle ache, no intestinal symptoms
Pathogenesis and Virulence factors: Glycoproteins on surface of the envelope are spies, HA and NA spikes

Antigenic drift

Point mutation in genes encoding HA or NA spikes, may involved 1 amino acid change, allows viruses to avoid immune system, leads to change in strain, cause of season flu epidemics

Antigenic shift

Occurs when a flu strain from an animal reservoir can infect human, due to genetic recombination between different viral strains infecting the same cell, cause changed in HA and NA spikes giving rise to major change in strain, may lead to pandemics