Chapter 13  Viruses, Viroids, and Prions

 

 

General characteristics of Viruses

 

A.  Unique characteristics

1.  Filterable – very small (go through filter)

2.  Obligate intracellular parasites – require host cells in order to multiply

3.  Contain single type of nucleic acid, DNA or RNA

4.  Have protein coat surrounding nucleic acid

5.  Uses cell’s machinery to multiply

 

B.  Host Range

Viruses infect all organisms, but usually specific

Viruses that infect bacteria à bacteriophages

 

C.  Viral size (Fig. 13.1)

20 – 1000 nm in length

 

 

Viral Structure

DRAW

 

 

 

 

 

 

A.  Components of viruses

 

1.  Nucleic Acid – consists of one of the following

ds-DNA

ss-DNA

ds-RNA

ss-RNA

 

2.  Capsid

protein coat

made of capsomeres (protein subunits)

 

3.  Envelope

Usually lipid bilayer obtained from host plasma membrane

Contains both host and viral proteins

 

B.  Two types of viruses

1.  Nonenveloped (naked) viruses (Fig. 13.2)

2.  Enveloped viruses (Fig. 13.3)


General Morphology of Viruses

 

A.  Helical Viruses

Long rods

Ex:  Ebola virus (Fig. 13.4)

 

B.  Polyhedral viruses

Many sided

Most common à icosahedral (20-sided)

Ex:  Adenovirus (Fig. 13.2b)

 

C.  Complex viruses

Complicated structures

Ex:  T-even bacteriophage (Fig. 13.5a)

 

 

The isolation cultivation, and identification of viruses

 

A.  Growing bacteriophages in the lab

1.  Infect bacterial culture with bacteriophage

2.  Put on agar plate

3.  Plaques form (areas of destroyed bacteria) (Fig. 13.6)

 

B.  Growing Animal viruses in the lab

 

1.  In Living animals

mice, rabbits, guinea pigs, etc.

 

2.  In embryonated eggs

Inject into fertile chicken egg

 

3.  In cell cultures

Put virus on monolayer of cells à plaques form

 

 

Multiplication of bacteriophages

 

A.  Lytic cycle (by lytic phages, ex: T-even bacteriophages) (Fig 13.10)

 

1.  Attachment

Phage attaches to host cell

 

2.  Penetration

Phage penetrates host cell and injects its DNA

 

3.  Biosynthesis

Phage DNA directs synthesis of viral components by host cell (viral enzymes, nucleic acids, Capsid proteins)


4.  Maturation

Viral DNA and capsids are assembled into complete virions (infectious particles)

 

5.  Release

Viral enzymes (lysozymes) cause host cell lysis

New virions are released

 

B.  Lysogenic Cycle

Performed by temperate phages

Ex: Bacteriophage Lambda (Fig 13.12)

 

1.  Lysogenic Cycle

(* indicates a step different from the bacteriophage lytic cycle)

 

a.  Attachment

Phage attaches to host cell

 

b.  Penetration

Phage penetrates host cell and injects its DNA

 

c.  Phage DNA integration* 

Phage DNA is spliced into bacterial chromosome à prophage

Most viral genes repressed à no viral activity

 

d.  Host cell replication*

Each new cell carries prophage

 

e.  Induction* (onset of productive lytic cycle)

Occurs spontaneously or as a result of injury (UV, chemicals)

Phage DNA excised

Lytic cycle proceeds (Biosynthesis à Maturation à release)

 

2.  Three results of lysogeny

 

a.  Immunity

Lysogenic cells immune to reinfection by the same phage

 

b.  Phage conversion

Host cell may exhibit new properties

Ex:  Corynebacterium diphtheriae

C. diphtheriae à non pathogenic

C. diphtheriae + lysogenic phage à diphtheria

(phage carries gene for a toxin, bacteria expresses gene)


c.  Specialized transduction (Fig. 13.13)

Certain bacterial genes are transferred from one bacterium to another via a phage.

During induction, some of the adjacent bacterial genes can be excised from host chromosome and packaged in capsid. 

When phage infects new cell, bacterial genes are also transferred

 

 

Multiplication of Animal Viruses

(* indicates a step different from the bacteriophage lytic cycle)

 

1.  Attachment

Virus attaches to host cell

 

2.  Penetration*

Capsid enters by

a.  Endocytosis (Fig. 13.14)

Occurs with naked and enveloped viruses

b.  Fusion

Occurs with some enveloped viruses

Viral envelope fuses with plasma membrane

DRAW

 

 

 

 

 

 

 

 

3.  Uncoating*

Capsid removed by enzymes

 

4.  Biosynthesis

Viral nucleic acid directs synthesis of viral components by host cell (viral enzymes, nucleic acids, Capsid proteins)

 

5.  Maturation

Viral DNA and capsids are assembled into complete virions

 

6.  Release*

a.  Nonenveloped viruses à rupture of plasma membrane

b.  Enveloped viruses à budding (Fig. 13.20)


HIV (Retroviridae) multiplication (Fig. 13.19)

 

1.  Attachment

 

2.  Penetration

 

3.  Uncoating

 

4.  Biosynthesis

 

a.  Reverse transcription

Viral ss-RNA    viral reverse transcriptaseà     Viral ds-DNA

 

b.  Integration           

Viral ds-DNA integrates into host cell DNA (provirus)

 

c.  Provirus latent

No viral activation

Provirus replicates with cell

 

d.  Provirus expression

Viral components synthesized

 

5.  Maturation

 

6.  Release (by budding)

 

 

Viruses and Cancer

Oncogenic viruses

Viral nucleic acid integrates into host DNA à mutation à cancer

Capable of inducing tumors

10 % of cancers are induced by viruses

Ex:      Epstein-Barr virus à Burkitt’s lymphoma, Nasopharyngeal carcinoma

Hepatitis B virus à liver cancer

Human Papilloma virus (HPV) à cervical cancer

 

 

Latent Viral infections

Viral infection but no disease for long period, then disease appears suddenly

Ex:  Herpes simplex virus

Inhabits host’s nerve cells, no symptoms

Stimulus activates virus à cold sore


Persistent Viral infections

Viral infection that causes viral load and disease that develops gradually over long period

Ex:  Subacute sclerosing panencephalitis (SSPE)

Caused by measles virus

Results in mental deterioration

 

 

Prions (proteinaceous infectious particle)

Causes spongiform encephalopathy (“spongy brain”) (Fig. 22.17)

Loss of motor control à mental deterioration à coma à death

 

Ex:  in animals à Scrapie, “mad cow disease”

Ex:  in humans à Kuru, Creutzfeldt-Jacob disease (Fig. 22. 18)

Can have very long incubation times (> 20 years)

 

Disease mechanism:  (Fig. 13.21)

PrPC is a normal protein in brain

PrPSc is an abnormal protein, same primary structure but folded differently

PrPSc contacts PrPC à causes PrPC to refold into PrPSc

PrPSc taken in by endocytosis and accumulates in lysosomes

Actual cause of cell damage unknown

 

 

Viroids

Cause plant disease (including important crops)

Short pieces of naked RNA that do not code for protein

Host cell makes many copies of RNA à plant growth stunted


Chapter 14  Principles of Disease and Epidemiology

 

 

Pathology 

Scientific study of disease

Includes

Etiology – the cause of disease

Pathogenesis – the manner in which disease develops

Final effects on body

 

Infection – invasion or colonization of the body by pathogens

 

Disease – Change in health, may be due to infection

 

Normal Flora (Fig. 14.1, 14.2)

Harmless microbes in body

Benefit host by preventing overgrowth of harmful microorganisms

We carry 10 times the bacterial cells as we have normal cells

 

 

Symbiosis – relationship between Microbiota and host

 

A.  Commensalism

One organism benefits, the other unaffected

Ex:  Corynebacteria inhabit surface of eye

 

B.  Mutualism

Both organisms benefit

Ex:  E. coli inhabiting human intestine

E. coli gets nutrients

Human gets Vitamin K, some Vitamin B, and proteins that inhibit growth of pathogens

 

C.  Parasitism

One organism benefits at the expense of another

Ex:  disease-causing bacteria

 

 

Opportunistic Microorganisms

Cause no disease in normal person but might in different environment

Ex:     Gain access through broken skin à cause disease

Host is immune suppressed à cause disease


The Etiology of Infectious Diseases

 

A.  Koch’s postulates (Fig. 14.3)

Used to determine the etiology of an infectious disease

 

1.  The same pathogen must be present in every case of the disease.

 

2.  The pathogen must be isolated from the diseased host and grown in pure culture.

 

3.  The pathogen from the pure culture must cause the diseases when it its inoculated into a healthy, susceptible lab animal.

 

4.  The pathogen must be isolated from the inoculated animal and must be shown to be the original organism.

 

B.  Exceptions to Koch’s postulates

 

1.  Some microorganisms will not grow on artificial media

Ex:  Treponema pallidum cannot be grown on artificial media

 

2.  The same disease may be caused by several different pathogens

Ex:  pneumonia à caused by many pathogens

 

3.  The same pathogen may cause several different diseases

Ex:  Steptococcus pyogenes causes sore throat, scarlet fever, skin infections, ….

 

4.  May not be ethical to test

Ex:  HIV only grows in humans, not ethical to test HIV on humans

 

 

Classifying Infectious Diseases

 

A.  Definitions

 

Symptoms

Subjective changes in body function

Not apparent to observer

Ex:  pain, malaise

 

Signs

Objective changes in body function

Can observe and measure

Ex:  lesions, swelling, fever, paralysis

 

Syndrome

Group of symptoms or signs that accompany a particular disease

Ex:  Acquired Immunodeficiency Syndrome (AIDS)


B.  Classification based on how disease is transmitted

 

1.  Communicable disease

Spreads from one host to another

Ex:  chickenpox, measles, tuberculosis, typhoid

 

Contagious diseases

Easily spreads from one host to another

Ex:  chickenpox, measles

 

2.  Noncommunicable disease

Not spread from one host to another

Caused by

a.  Normal Flora

b.  Microbes that normally are outside body but are introduced into the body

Ex:  Clostridium tetani in soil

àIntroduced through wound or abrasion

à Tetanus

 

C.  Classification based on the frequency of occurrence of disease

 

1.  Sporadic disease

Occurs only occasionally

Ex:  typhoid fever

 

2.  Endemic Disease

Constantly present in the population

Ex:  common cold

 

3.  Epidemic disease

Many people acquire in a short amount of time

Ex:  gonorrhea

 

4.  Pandemic disease

Epidemic disease that occurs worldwide

Ex:  influenza, AIDS

 

D.  Classification based on severity or duration of a disease

 

1.  Acute disease

Develops rapidly, last a short time

Ex:  influenza

 

2.  Chronic Disease

Develops more slowly

Likely to be continual or recurrent for long periods

Ex:  infectious mononucleosis, TB


3.  Latent disease (sequelae)

After initial infection, causative agent remains inactive, then becomes an active disease, producing symptoms

Ex:  Shingles

 

E.  Classifications based on the extent of host involvement

 

1.  Local infection

Microorganisms limited to small area of the body

Ex:  boil or abscesses

 

2.  Systemic infection

Microorganisms or products spread throughout body by blood or lymph

Ex:  measles

 

3.  Blood infections

 

a.  Bacteremia – bacteria in blood

 

b.  Septicemia – bacteria multiplying in blood

 

c.  Toxemia – toxins in blood (Ex:  tetanus)

 

d.  Viremia – viruses in blood

 

4.  Primary infection

Acute infection that causes initial illness

 

5.  Secondary infection

Caused by opportunistic pathogen after primary infection weakened body’s defenses

Ex:  streptococcal pneumonia (secondary)  following influenza (primary)

 

6.  Subclinical infection

No apparent disease

Ex:  poliovirus, hepatitis A carriers

 

 

The stages of a disease (Fig. 14.5)

 

A.  Incubation period

Time between initial infection and first appearance of signs or symptoms

 

B.  Prodromal Period

Early mild symptoms, such as general aches and malaise

 

C.  Period of Illness

Overt signs and symptoms of disease

Immune response overcomes pathogens or death occurs


D.  Period of Decline

Signs and symptoms subside

Patient vulnerable to secondary infections

 

E.  Period of Convalescence

Person regains strength

Body returns to prediseased state

 

 

The Spread of Infections

 

A.  Reservoirs of Infection – continual source of disease organisms

 

1.  Human Reservoirs

People that harbor pathogens, often asymptomatic carriers

Is principle living reservoir of human disease

Ex:  people infected with measles

 

2.  Animal Reservoirs

Wild or domestic animals that harbor pathogens

Zoonoses – diseases that can be transmitted from animals to humans

Ex:  rabies, Lyme disease

 

3.  Nonliving Reservoirs

a.  Soil

Ex:  Soil that contains fungi, C. botulinum, C. tetani

b.  Water

Ex:  fecally contaminated water

Vibrio cholerae à cholera

c.  Food

Ex:  Food that contains Salmonella typhimurium

 

B.  The Transmission of Disease (Fig. 14.6)

 

1.  Contact Transmission (Fig. 14.7)

 

a.  Direct Contact Transmission

Person to person transmission

Ex:  touching, kissing, sexual intercourse

Ex of diseases transmitted:  common cold, influenza, STD’s

 

b.  Indirect contact transmission

Transmitted from reservoir to host by means of a nonliving object (Fomite)

Ex. Of Fomite:  tissues, towels, toys, syringes

Ex. of diseases transmitted:  Hepatitis B

 

c.  Droplet Transmission (Fig. 14.8)

Spread in mucus droplets that travel short distances

Ex:  Produced in sneezing, coughing

Ex. of diseases transmitted:  influenza, pneumonia


2.  Vehicle Transmission

Transmission of disease agent by medium

Ex:  by water, food, air, blood, body fluids

 

Types of vehicles

 

a.  Waterborne transmission

Contaminated water

Ex. of diseases transmitted:  Cholera

 

b.  Foodborne transmission

Unsanitary or incompletely cooked food

Diseases trans:  Food poisoning, tapeworm infestation

 

c.  Airborne transmission

Droplet nuclei in dust that travel more than 1 m

Ex. of disease trans.:  measles, TB

Also fungal spores

Ex. of diseases trans.:  histoplasmosis

 

3.  Vector Transmission

Transmission via animals, esp. arthropods

 

Types of vector transmission

 

a.  Mechanical Transmission

Passive transport of pathogen on feet or body parts

Ex:  houseflies transfer infected feces to food

Diseases trans:  typhoid fever, shigellosis

 

b.  Biological Transmission

Active process

Arthropod bites infected host à arthropod infected

Infected arthropod bites uninfected host à host infected

Ex:  Anopheles mosquito is vector for malaria

 

 

Nosocomial Infections

Infections acquired as a result of a hospital stay

5-15% of hospital patients acquire

 

A.  Examples of nosocomial infections

Staphylococcus aureus and E. coli à surgical would infections, pneumonia

Clostridium difficile à diarrhea

 

B.  Causes of Nosocomial infections (Fig. 14.9)

 

1.  Microorganisms in the hospital

Hospitals are a major reservoir for pathogens


2.  The compromised host

Resistance to infection impaired by …

Broken skin

Suppressed immune system

 

3.  The chain of transmission

Patient to patient

Staff to patient

 

C.  The control of nosocomial Infections

Reduce number of pathogens

à aseptic techniques, hand washing, etc,

àkeep areas clean and disinfected

 

 

Emerging infectious diseases

Diseases that are new, or changing, or showing an increase in incidence

(Table 14.6)

Know three of these disease, including the etiology

 

 

Epidemiology

Study of when and where diseases occur and how transmitted

Central source of epidemiological info. in U.S.

à The Centers for Disease Control and Prevention (CDC)


Chapter 15  Microbial Mechanisms of Pathogenicity

 

 

How Microorganisms enter a host à portals of entry

 

A.  Portals of entry

 

1.  Mucous Membranes

a.  Respiratory tract

Diseases:  cold, pneumonia

b.  Gastrointestinal tract

Diseases:  poliomyelitis, Hepatitis A

c.  Urogenital tract

Diseases:  AIDS, syphilis

d.  Conjunctiva

Diseases:  conjunctivitis

 

2.  Skin

Impenetrable by most microorganisms

Diseases:  Hookworms, fungi

 

3.  The Parenteral Route

Deposit microorganisms directly into tissues

Punctures, injections, bites, wounds

 

B.  Factors that determine if infection causes disease

(microorganisms in body à may or may not cause disease)

 

1.  The preferred portal of entry

Many pathogens only cause disease through one portal of entry

Ex:  Streptococci,     inhaled à pneumonia

swallowed à no disease

 

2.  Numbers of invading microbes

As number of microorganisms increase, probability of disease increases

 

3.  Adherence

For most pathogens….       adhere to host cells à disease

no adherence à no disease

Adhesins on microorganism bind to receptors on host cells (Fig. 15.1)


How Bacterial Pathogens penetrate host defenses

 

A.  Capsules

Outer gelatinous cover on some bacteria

Can resist host defenses …

à Phagocytic immune cells can’t adhere

à can’t phagocytize

Ex:  Steptococcus pneumoniae

with capsule à Pneumococcal pneumonia

w/o capsule à harmless

 

B.  Components of the cell wall

May contain chemicals that enhance virulence

Ex:  S. pyogenes produces M-protein

à helps attachment to host cells

à resists phagocytosis by white blood cells

Ex:  Mycobacterium tuberculosis has waxes (Mycolic acid) in the cell wall

à resists digestion by phagocytes

 

C.  Enzymes

Some bacteria produce harmful extracellular enzymes

Ex:  Clostridium perfringens

à produces collagenase