I. Introduction to Microbiology (15%)
A. Early History
1. Discovery of microorganisms
Aristotle (384-322) and the Greeks believed that living organisms developed from non-living materials. In 1590: Hans and Zacharias Janssen, Dutch lens grinders, produce the first compound microscope by mounted two lenses in a tube. Robert Hooke (1635-1703) published his "Micrographia" in 1660 which contained drawings and detailed observations of the biological materials. Then in 1676, Anton van Leeuwenhoek (1632-1723) was the first person to observe microorganisms, describing rods ands spheres observed in the scrapings from his teeth..
2. Disproving spontaneous generation
In 1688, Francesco Redi (1626-1678), an Italian physician, first refuted the idea of spontaneous generation through experimentation by showing that rotting meat carefully kept away from exposure to flies will not spontaneously produce maggots. Louis Pasteur's (1822-1895) now famous experiments of 1861 with his swan-necked flasks showed that microorganisms do not arise through spontaneous generation .
3. Development of germ theory of disease
Several events led to the development and proof that microbes cause disease. Hieronymus Fracastorius (Girolamo Fracastoro) wrote "On Contagion" in 1546 ("De contagione et contagiosis morbis et curatione"), which is the first known discussion of the phenomenon of contagious infection. Agostino Bassi de Lodi (1835) showed that a fungus was responsible for the disease affecting silkworms with this discovery marking the first microorganism to be identified responsible for a disease. Pasture later in 1865 identified a protozoan responsible for another silk worm disease. Ignaz Semmelweiss (1818-1865), a noted Hungarian physician, showed that doctors in Vienna hospitals were responsible for spreading puerperal (childbed) fever while delivering babies. He introduced infection control in the 1840's by having the doctors under his supervision to wash their hands between patient. contacts. In the 1860's, Joseph Lister (1827-1912), the noted English surgeon, introduced antiseptics in surgery through the use of carbolic acid to clean and kill bacteria on surgical instruments, and the wounds and dressings. His success in reduced surgical mortality due to bacterial infection resulted in this practice to readily be adopted by other surgeons..
Robert Koch (1843-1910). German bacteriologist was the first to cultivate the rod shaped anthrax bacteria, Bacillus anthrais, outside the body using blood serum (1876) and subsequently injected these bacteria into health cattle, resulting in the disease state. He subsequently published "Koch's postulates" (1884), which form the critical test method for proof that a microorganism is the cause of a disease, although it should be noted that there are a few diseases that fall outside the postulates.
Koch's postulates
1. The pathogen must be present in every case of the disease.
2. The pathogen must be isolated and cultured in vitro.
3. The disease must be reproduced when a pure culture of the pathogen is inoculated into a susceptible host.
4. The pathogen must be recoverable from the experimentally-infected host.
4. Discovery of immunity
In China by 1000 B.C., smallpox was endemic, where disease continues permanently within the population. With the understanding that survivors of smallpox were subsequently immune from reinfection, prevention was undertaken through the practice of variolation, induction of a mild form of the disease, hopefully. This involved the inhalation, sniffing, of dried crusts from a smallpox lesions, and later this practice changed to inoculation through the use of the pus from a lesion scratched into the skin.
After hearing from a milkmaid that she could not contract smallpox because she had already had cowpox, Edward Jenner, on 14th May 1796, after taking scrapings from cowpox lesions, then used these scrapings when scratching the arm of a young boy. A small bump appeared in a few days, followed by the mild illness of cowpox. On July 1st, he then directly exposed that same boy to smallpox, with the result of no smallpox disease development, confirming vaccination.
5. Discovery of viruses
6. Development of chemotherapeutic agents
B. Place of microorganisms in the world
1. prokaryotes vs. eukaryotes
2. Prokaryotes
a. Bacteria
b. Cyanobacteria
3. Archaeobacteria
4. Eukaryotes
a. Protista
(1) Protozoa
(2) Simple algae
b. Fungi
5. Viruses
C. Microbial laboratory techniques
1. Microscopy
2. Stain procedures
3. Media preparation and growth
4. Pure culture and aseptic techniques
II. Biology of Microorganisms (25%)
Microbiology is primary concerned with:
the cellular, procaryotes and eucaryotes,
bacteria,
fungi (smaller),
algae (smaller),
protozoa,
as well as, some multicellular parasites,
and, lastly, the non cellular viruses.
All cellular organisms can be divided into either procaryotes or eucaryotes. Differences between prokaryotes and eukaryotes are:
1. Nature and arrangement of genetic material.
2. The presence or lack of membrane bounded organelles.
3. Protein synthesis mechanism.
4. The cell wall chemistry.
A. Anatomy
1. Prokaryotes
Main characteristics:
1. Genetic material, DNA, is not enclosed in a membrane nucleus,
2. No membrane bound organelles,
3. The DNA is not associated with histone proteins, and
4. Cell walls that, almost always, contain complex polysaccharide peptidoglycan.
Peptidoglycan contains an unique sugar called muramic acid. It is found only in the cell walls of prokaryotes, and nowhere else in nature. Eubacteria contain muramic acid with archaebacteria containg a pseudomurein of a differing structure.
As well, cell division is usually by binary fission.
Other characteristics include:
Endospore formation for some prokaryotes.
Gas vesicles exist for some prokaryotes, and
Flagellum structure/function.
Two groups, eubacteria, true bacteria, and archaeobacteria; which although they look similar, differ in their chemical composition.
a. Bacteria
Eubacteria, or true bacteria - (includes all bacteria that infect man)
(1) Gross morphology - cell size, shape, and arrangement
cell size,
most range between 0.20 to 2.0 �m in their diameter with the lenght from 2 to 8 �m
shape, and arrangement
coccus - spherical - (plural cocci, means berries) - upon division, cocci remain attached to each other, as
diplococci, form pairs after dividing
streptococci, form chainlike patterns after dividing
tetrads, form grups of four after dividing
sarcinae, form cubelike groups of eight after dividing, and
staphylococci, which form braod sheets or grapelike clusters after dividing.
bacilli - rods - divide only across their diameter, thus form fewer arrangements
most bacilli are single rods in a group
diplobacilli, form pairs after division
streptobacilli, form chains after division, with
some bacilli looking like straws,
some bacilli look like cigars, and
coccobacilli, are oval and look much like cocci
spirilla and spirochetes with vibrios are curved and spiral bacteria
vibrios are curved and look like commas
spirilla are helical and look like a corkscrew
spirochetes are helical but have flagella and an axial filament for movement
Stella and Haloarcula,are star and square shaped respectively
Most bacteria are monomophic, retaining their single shape,; however, some are pleomorphic, having many shapes.
(2) Component parts - name, chemistry, function, and importance
(a) Cell envelope
The cell envelope differentiates the two groups of bacteria; gram positive and gram negative.
i) capsule
Many bacteria have a capsule. The presence of a capsule may be related to the virulence of the bacteria. Usually it is polysaccharide that the layer is made from; however, some bacterial use a polypeptide (polyglutamic acid).
External to the cell wall, the capsule is organized and firmly attached to the cell wall; however, when it is not unorganized and only loosely attached it is termed a slime layer. Both a capsule or slime layer can be described with the general term of glycocalyx.
Capsules protect against phagocytosis.
Streptococcus pneumoniae that are the polysaccharide capsulated strains produce pneumococcal pneumonia; however, uncaspulated strains fail to produce pneumonia.
Bacillus Anthracis has a D-glutamic acid capsule.
Other bacterial of note with capsules:
Hemophilus influenzae - pneumonia and meningitis especially in children
Klebsiella pneumonia - bacterial pneumonia
Yersinia pestis - bubonic plague
The sticky glycocalyx helps the bacteria attach to surfaces
Streptococcus mutans attaches to the surface of teeth - an important cause for dental caries
Klebsiella pneumoniae attach in the respiratory tract
S. mutans, when sugar stores are low, may use the polysaccharide capsule for a nutrient and energy source.
ii) Cell wall - chemical and structural differences, Gram stain
iii) Cell membrane
(b) Cytoplasm
i) Chromosome and plasmids
ii) Ribosomes
iii) Cell inclusions
(c) Spores
d) Appendages
i) Flagella
ii) Pili
b. Cyanobacteria - special features
2. Eukaryotes (fungi, algae, and protozoa)
Main characteristics:
1.
2.
3.
4.
a. Fungi
(1) Cellular and vegetative structures
(2) Reproductive structures
b. Algae
(1) Cellular structure
(2) photosynthetic apparatus
c. Protozoa
(1) Structures for locomotion - flagella, cilia, pseudopodia
(2) Vacuoles
B. Growth and nutrition
1. Patterns of nutrition
2. Requirements for growth (increase in numbers/mass)
a. Physical - pH, temperature
b. Chemical - N, C, energy sources; vitamins; trace elements
c. Gaseous - anaerobic, aerobic, facultative
3. Cultivation
a. Selective, enrichment, and differential media
b. Mixed and pure cultures
c. Culture techniques - solid and liquid media
4. Dynamics of populations
a. Growth mechanisms - binary fission, mycelial growth, budding
b. Growth rates, generation times
c. Growth curve: lag, exponential growth, and stationary phases
d. Enumeration of cell numbers and culture mass - viable and total counts; turbidity
C. Metabolism - basic mechanisms of metabolism and energy conversion
1. Enzymes (mediators of all reactions)
a. Structures and functions
b. Factors that influence enzyme activity
2. Photosynthetic vs. Chemosynthetic metabolism
3. Cellular respiration
a. Aerobic
b. Anaerobic
c. Fermentation
4. Photosynthesis
5. Biosynthetic mechanisms
a. Macromolecular synthesis
(1) Nucleic acid
(2) Gene expression and protein synthesis
b. Regulation
(1) Control of enzyme activity (feedback regulation)
(2) Control of enzyme synthesis
D. Genetics
1. Variation in populations of cells and viruses - terminology
a. Genotype and phenotype
b. Haploidy and diploidy
c. Asexual and sexual
2. Mutations
a. Spontaneous; induced (radiation, chemical mutagens)
b. Selection of mutants
c. Types of mutations ( nutritional, antibiotic resistance, lethal, etc.)
3. Recombination
a. Transformation
b. Transduction (generalized; specialized)
c. Conjugation
4. Gene manipulation
a. Plasmids
b. Genetic elements
c. Genetic engineering - recombinant DNA techniques
d. Application of genetic engineering
E. Viruses
1. Structure
a. Type of nucleic acid
b. Capsid, envelope, specialized structures
2. Multiplication of viruses
a. Lytic acid
b. Lysogenic cycle
c. Retroviruses
3. Effects of viruses on cells
a. Isolation and detection of viruses
b. Cytopathologic effects
c. Transformation and oncogenesis
d. Control of viral replication
III. Control of Microorganisms (15%)
A. Principles of microbial control
1. Factors influencing success of control methods
a. Number and nature of microorganisms
b. Strength of control agent
c. Time, temperature, and pH
2. General methods of control
a. Bactericidal vs. bacteriostatic
b. Sterilization
c. Asepsis
d. Disinfection and antisepsis
e. Sanitation
f. Antibiosis and chemotherapy
B. Physical methods of control
1. Incineration
2. Dry heat
3. Moist heat
a. Boiling water
b. Pressurized steam - autoclave
c. Pasteurization
4. Radiation
a. Ultraviolet
b. Ionizing
C. Chemical methods of control
1. Chemical agents
a. Halogens
b. Alcohols
c. Phenols
d. Heavy metals
e. Aldehydes
f. Gases
g. Detergents
h. Peroxides
i. Dyes
D. Chemotherapeutic agents and antibiotics
1. Modes of action
2. Chemotherapeutic agents (nucleic acid analogs and others)
a. Antiviral agents
b. Antifungal agents
c. Antiparasitic agents
3. Antibiotics (penicillin and others)
a. The problem of antibiotic resistance
b. Antibiotic sensitivity assays
IV. Disease, Resistance, and the Immune System (20%)
A. The disease process
1. Host - parasite relationships
a. The concepts of infection and disease
b. The normal flora
The fetus is normally gearm free while in utero. Following birth, E. coli and other bacteria containded in foods begin to colinize the large intestines and remain there throughout life, forming the normal flora.
c. Commensalism
d. Mutualism
e. Antibiosis
f. Opportunists
g. Virulence
2. Progress of disease
a. Periods of disease
b. Clinical and subclinical disease
3. Types of diseases
a. Communicable and noncommunicable disease
b. Endemic, epidemic, and pandemic diseases
c. Acute and chronic diseases
d. Primary and secondary diseases
e. Local and systemic diseases
f. Nosocomial disease
4. Establishment of disease
a. Transmission
b. Portal of entry
c. Dose
d. Virulence factors
B. Nonspecific resistance to disease
1. Mechanical and chemical factors
a. Skin
Subum, an oily substande produced by sebaceous (oil) glands, forms a protective coating over the skin, with one of the substances in sebum, the unsaturated faty acids, inhibits bacterial growth. Perspiration contains lysozyme, an enzyme can break down gram-positive bacterial cell walls.
b. Mucous membranes
c. pH (cell, tissue, organ)
d. Lysozyme
Lysozyme, an enzyme can break down gram-positive bacterial cell walls. It is found in, perspiration, tears, sliva, and nasal secretion.
2. Phagocytosis
a. Types of phagocytes
polymorphonuclear leukocytes (granulocytes)
phagocytic monocytes (macrophages)
Reticuloendothelial system (mononuclear phagocytic system) (below)
b. Mechanism of phagocytosis
Opsonisation is the process by which a micro-organisms is coated with proteins to make them more easily phagocytosable. The body produces these proteins and they circulate in the plasma,
Outcome - the phagocytosis of microorganisms may result in three intercellular outcomes
- the ingested microorganism may be killed,
- the microorganism may continue to survive, or
- the microorganism may even multiply within the phagocytic cell. The specific natures of the microorganism and the phagocytic cell influence the potential outcome.
c. Reticuloendothelial system (mononuclear phagocytic system)
3. Inflammation
Inflammation is a tissue response to injury from localise area of infection or physical tissue injury by release of substances from the infecting organisms or from the chemicals (chemical mediators) released from cells in the injured tissues, especially histamine from the mast cells.
The inflammation process includes:
a)the dialation of the arterioles and venules, increasing blood flow which results in the charicteristic redness and warmth,
b) the opening of the endothelial cell junctions in the post-capillary venule which will allow plasma proteins to flow into the tissue, and
c) first, the adhesion of leukocytes to endothelial cells of the post-capillary venule, and second by the migration of phagocytes, polymorphonuclear leukocytes (neutrophils) and mononuclear phagocytes (monocytes, macrophages), into the tissue.
4. Individual, species, and racial immunities
C. Principles of immunology
1. Antigens
a. Definition, composition, and type of antigens
b. Haptens
c. Immunologic tolerance
d. Self vs. nonself
2. The immune system
a. B lymphocytes
b. T lymphocytes
c. Location and operation of the immune system
d. Cell - mediated immunity -- process, stimulation, lymphokines
e. Antibody - mediated (humoral) immunity -- antibody structure and origin, five types of antibodies, primary and secondary antibody responses, opsonization, antigen - antibody reactions, neutralization, precipitation, agglutination
f. The complement system
g. The alternative pathway
3. Types of immunity
a. Naturally acquired, active immunity
b. Artificially acquired, active immunity
c. Naturally acquired, passive immunity
d. Artificially acquired, passive immunity
4. Serological and diagnostic reactions
a. Radioimmunoassays
b. Neutralization reactions
c. Precipitation and agglutination
d. Complement
e. Monoclonal antibody
f. Fluorescent antibody tests
g. Enzyme - linked immunosorbent assay (ELISA)
h. Western - blot analysis
i. Polymerase chain reaction (PCR)
j. Gene probe
D. Disorders of the immune system
1. Type I anaphylactic hypersensitivity
a. Allergens and IgE
b. Basophils and mast cells
c. Degranulation and mediator release
d. Atopic disease
2. Type II cytotoxic hypersensitivity
a. Transfusion reactions
b. Hemolytic disease of the newborn
c. Autoimmune reactions
3. Type III immune complex hypersensitivity
a. Immune complex formation
b. Serum sickness
c. Systemic lupus erythematosus (SLE)
Goodpasture's disease, rheumatoid arthritis, Arthus reaction
4. Type IV cellular hypersensitivity
a. Infection allergy
b. Contact dermatitis
c. Tuberculin skin test
5. Immune - deficiency disease
V. Biology of Infectious Diseases (25%)
Infectious diseases can be studies according to the causitive agent, as in bacterial, either gram positive or gram negative, viral, fungi, algae, protozonns, or multicellular parasites.
In this outline, they are studied according to the primary human system effected by the disease, as in respiratory tract diseases, gastroenteric tract, and urinary tract, skin and blood diseases.
Parameters for the study of infectious disease:
- Recognition of the disease syndrome (symptoms)
- Etiology of the disease
- unique morphological characteristics of the agent(s)
- unique physiological characteristics of the agent(s)
- unique cultural characteristics of the agent(s)
- Mode of transmission and portal of entry
- Methods of immunization
- Methods of prevention, control, and/or treatment
A. Respiratory tract disease
1. Bacterial diseases
a. Tuberculosis
b. Diphtheria
c. Pertussis
d. Streptococcal diseases
e. Bacterial pneumonia
f. Primary atypical pneumonia
g. Legionnaires' disease
h. Bacterial meningitis
i. Chlamydial diseases
2. Viral disease
a. Common cold
b. Influenza
c. Measles
d. Mumps
e. Chickenpox
f. Rubella
g. Viral pneumonia
3. Fungal disease
a. Cryptococcosis
b. Histoplasmosis
c. Aspergillosis
4. Protozoal diseases - Pneumocystis carinii pneumonia
B. Gastrointestinal tract disease and intoxications
1. Bacterial infections and intoxications
a. Typhoid fever
Typhoid used to be a notifiable disease -WHO
b. Cholera
Cholera is a notifiable disease -WHO
c. Salmonellosis
d. E. coli disease
Escherichia coli are one of the large group of heterogeneous enteric gram negative rods, enterobacteriaceae. It is part of the normal flora of the intestines. Normally do not cause disease, but become pathogenic in other areas, such as the urinary tract, where it is the leading cause of UTI.
E coli of different groups are responsible for a number of diarrheal diseases. For example:
Enteropathic E coli (EPEC) has been previously associated with nursery diarrhea outbreaks in developed countries, and is an important cause of infant diarrhea in developing countries. Self limited watery diarrhea is the usual result of EPEC infection. Antibiotics shorten the diarrhea course and cure EPEC infection.
Enterotoxigenic E coli (ETEC) probably cause 50 to 65% of traveler's diarrhea., as well as being an important cause of infant diarrhea in developing countries. ETEC produce a heat labile exotoxin (LT) which results in hypersecretion of water and chlorides as well as inhibiting reabsorption, resulting in diarrhea. LT stimmulates antibodies, with the people who reside in the areas where ETEC is prevelent in the water supply, as in developing countries, having antibodies lessening their risk for diarrhea on reexposure.
With some ETEC strains, a heat stable enterotoxin (STa) as well as LT, with a sever diarrhea resulting.
Enterohemorrhagic E coli (EHEC) strains have become an Emerging Infectious Disease (EID), in particular the serotype E coli O157:H7. Producing an afebrile hemorrhagic diarrhea, and as a serious complication, hemolytic uremic syndrome (HUS) characterized by blood in the urine and kidney failure, E coli O157:H7 is an occasional non pathogenic resident of animal intestines but with poor slaughtering techniques the beef is contaminated, and with human ingestion disease results. Disease may also result from water supplies contaminated by cattle feces. Children and the elderly are especially prone. Termed hamburger disease, because the contaminated ground meat is mixed into the center and may survive in an under cooked meet paddy, proper through cooking reduces risk.
e. Campylobacter disease
f. H. pyloric disease
Helicobacter pylori, a gram negative spiral shaped rod, is found associated with peptic, gastric and duodenal, ulcers. Since the rate of infection is greater than incidence of related ulcers, other factors are involved such as susceptibility with type O blood.
Prevalence increases with age with 30% under 30 and 40 to 60% over 60. Developing countries have a adult rate of over 80%. Rates are higher in lower socioeconomic groups. Intrafamilal clustering occurs. Acute epidemics of gastritis are associated with H pylori, and suggest a common source, and fecal oral transmission route. Infection may persist for years or life.
H pylori produces urease, neutralizing acid. Damage to the mucus layer occurs.
Triple therapy of metronidazole, and either bismuth subsalicylate or bismuth subcitrate (Pepto-Bismol�) with either amoxicillin or tetracycline for 14 days results in 70 to 95% effective eradication. With Eradication of H pylori results in ulcer disappearance. Recurrence is low. Early treatment decreases antibody response and those individuals are thought to be at risk for subsequent reinfection.
Rapid tests are available. Breath test has the individual swallow radioactivity labeled urea, with 30 minutes later, radioactivity labeled CO2 can be detected in the breath.
g. Shingellosis
h. Botulism
i. Staphylococcal food poisoning
A short incubation period of 1 to 8 hours before the onset of symptoms characterizes Staphylococcus aureus food poisoning. S aureus produces a toxic that is heat stable and can survive boiling for 30 minutes; however, foods prepared in advance and not properly stored chilled before serving are the usual source. Large masses left to cool slowly, and room temperature cooling are other sources. Competing organisms are killed through the cooking process, allowing food then contaminated by S aureus allows bacterial proliferation with the cooling and improper storage at room temperature. Reheating does not destroy the toxin The toxin directly stimulates the vomiting reflex center, producing the usual first symptom, followed by abdominal cramps and diarrhea. Recovery is usual within 24 hours. The process is afebrile.
j. Clostridium perfringens food poisoning
Contamination of meat with the animal abdominal contents during the slaughtering process sets the process for Clostridium perfringens food poisoning. With the cooking process, oxygen levels are lowered and the spores germinate. With a generation time of 20 minutes, meat dishes such as pies and stews allowed to remain warm provide ideal growing medium. With ingestion, the organism sporulate in the intestines, producing a toxin which results in marked hypersecretion in the jejunum and ileum producing diarrhea. Onset of diarrhea is usually within 6 to 12 hours, and symptoms do not usually include vomiting or fever.
k. Brucellosis
2. Viral diseases
a. Hepatitis A
Spread by the fecal oral route, including contaminated water, the hepatitis A virus (HAV) is a picornavirus of the genus Hepatovirus, with only the one serotype known. HAV can be destroyed by boiling water for five minutes, and by cooking meat to greater then 85 oC (> 185 oF). Surfaces need to be cleaned by 10% (1:10 dilution) of chlorine bleach. HAV is resistant to the normal concentrations of chlorine used for water disinfectant.
HAV, like other hepatitis viruses, starts with gastrointestinal symptoms of nausea, vomiting and anorexia with mild fever; however, onset is abrupt with HAV but insidious with other hepatitis viruses. Jaundice may occur. Disease is mild for children and may not be noticed, but adults experience a more sever process. Relapse may occur 1 to 4 months later. Recovery confers life long immunity. A persistent carrier state has not been detected, and seams unlikely. Protective immune globulin is available for HAV, and provides protection for several months. An inactivated vaccine is available.
Hepatitis type E (HEV), originally classified as an NANB, is transmitted enterically by the fecal oral route, and resembles HAV infection but is not serologically related. Similar to HAV, cronic liver disease does not result; however, in the pregnant female a 20% mortality rate exists.
b. Enteroviral infections
(Not to be confused with: Enteroviruses are a group of viruses that enter through the alimentary tract. These include poliomyelitis virus, Coxsackie viruses and echo viruses.)
Norwalk Virus
Food borne, or oral fecal route, the Norwalk virus is worldwide in distribution, with most in developing countries having antibodies by age 4, yet in developed countries antibodies are not acquired until later in life. it is noted for outbreaks on cruse ships, military units, and in other close quarter locations.
After an incubation period of 10 to 48 hours, average of 24 hours, the symptoms of abdominal cramps, diarrhea, nausea and vomiting, low grade fever, headache, and general malaise that lasts from 24 to 48 hours. although large numbers are rapidly infected, hospitalization and sequelae is rare.
3. Protozoal diseases
a. Amoebiasis
b. Giardiasis
Cryptosporidium parvum is an important cause of diarrhea disease especially in infants and small children. Unknown before 1976, the number of cases has been increasing. Transition is primarily the fecal-oral route between humans, with recreational water sources, pools, as an important source because Cryptosporidiosis is chlorine resistant and can last in a pool or other recreational water areas for weeks.
There is no reliable treatment, with the disease course lasting about two weeks. Diarrhea, loose or watery stool, with stomach cramps and a slight fever are common symptoms. The diarrhea my cycle between mild improvement followed by return of watery diarrhea. Symptoms appear between 2 to 10 days after being infected
Those at risk for dehydration, young children and infants, the elderly, and pregnant females are at risk for sequel; as well, immunocompromised individuals may experience serious sequela.
C. Urogenital tract diseases
1. Bacterial diseases
a. Gonorrhea
b. Syphilis
c. Chlamydia
2. Viral disease
a. Genital herpes
b. Genital warts
3. Fungal infections -- candidiasis
4. Protozoal infections -- trichomoniasis
D. Skin and wound disease
1. Bacterial infections
a. Tetanus
b. Staphylococcal infections
c. Anthrax
d. Leprosy
e. Gas gangrene
2. Viral diseases
a. Smallpox
b. Rabies
c. Warts
d. Herpes simplex infections
3. Fungal diseases
a. Ringworm (tinea)
b. Candidiasis
E. Blood diseases
1. Bacterial diseases
a. Plague
Plague is a notifiable disease -WHO
b. Tularemia
c. Spotted fevers
d. Typhus fevers
e. Q fever
f. Lyme disease
g. Toxic shock syndrome
2. Viral disease
a. Yellow fever
An arbovirus, arthropod-borne or mosquito-borne viral disease of the flavivirus group.
Yellow fever is a notifiable disease -WHO
Symptoms can vary from mild flu-like illness to a severe hepatitis and hemorrhagic fever.
Following injection of the virus into the body, an incubation period of three to six days occures. There are then two disease stages.
Although some mayhave no symptoms at all, the early, "acute", stage is exibited by fever, muscle pain especially backache, headache, shivers, loss of appetite, nausea and vomiting. Noted is that the high fever is paradoxically associated with an uncaracteristically slow pulse. Most patients improve after three to four days and symptoms disappear.
Up tp 15%, however, enter the second, "toxic", stage and present within 24 hours with reoccurance of fever and thereafter multiple body systems are affected.
Jaundice rapidly develops and the patient complains of abdominal pain with nausea and vomiting. Bleeding, simmilar to hemorragic fevers, can occur from the mouth, nose, eyes as well as the stomach and digestive tract.
The second or "toxic" state has a fatality rate of 50% and these patients usually die within 10 to 14 days. The others recover without significant organ damage
Occuring only in both sub-Saharan Africa and tropical South America, it is in Africa that it is endemic and the majority of the cases are reported. A variety of vectors are responsible for disease transmission in Africa.
In Africa, infants and children are at greatest risk for infection with a fatality rate approximately 23%.
In South America, young men with an occupational exposure to forested or transitional areas are the most likely presenting individuals with a fatality rate approximately 65%.
A safe, effective vaccine, with few side effects, is available for prevention. Side effects include a mild headaches, myalgia, low-grade fevers, or other minor symptoms . Hypersensitivity reaction occurs especially with a history of egg allergies.
Travelers are advised to be vaccinated. Taking precautions against exposure to mosquitoes is also strongly recommended.
Vector is the Aedles aegypti mosquito, and monkeys are a natural reservoir. The virus can replicate in both the arthropod and humans.
Dengue
An arbovirus, arthropod-borne or mosquito-borne viral disease of the genus Flavivirus.
Dengue has become the major public health arthropod borne viral disease supplanting yellow fever.
b. Viral encephalitis
Arboviruses, Arthropod-borne viruses, that may result in encephalitis for humans are of three virus families: the Togaviridae (genus Alphavirus), Flaviviridae, and Bunyaviridae.
West Nile
An arbovirus, arthropod-borne or mosquito-borne viral disease of the genus Flavivrus.
Most who become infected, do not develop symptoms. It is estimated that 20% develop mild symptoms which include fever, headache, and body aches, with occasionally a skin rash on the trunk of the body as well as swollen lymph glands, giving rise to the common name of West Nile Fever. There is about a 1 in 150 occurrence of the development of severe infection, West Nile encephalitis or meningitis, include headache, high fever, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, and paralysis. Advancing age over 50 years places the individual at a greater risk of sever infection and neurological symptoms as well as fatal encephalitis. Currently it is postulated that the North American form appears to have greater affinity to produce encephalitis.
Incubation is 3 to 14 days, with mild disease symptoms generally lasting a few days. Symptoms of the severe disease state, encephalitis and meningitis, may last up to several weeks; however, neurological effects or damage may be permanent, as with all encephalitis and meningitis diseases.
Treastment is supportive. Ribavirin in high doses and interferon-2b have been used, but no controlled studies have been undertaken. And, again, no controlled studies have been undertaken for the use of steroids, antiseizure medications, or osmotic agents.
Unexplained encephalitis or meningitis developing in late summer or early fall, especially in older adults, should be considered as having a viral origin.
Vaccines are under development. Prevention, window screesn and bearier clothing with the use of repellent, DEET (N,N-diethyl-3-methylbenzamide) is recommended.
Four main virus agents of encephalitis in the United States.
Eastern Equine Encephalitis (EEE)
Western Equine Encephalitis (WEE)
St. Louis Encephalitis (SLE)
La Crosse (LAC) encephalitis
Japanese
An arbovirus, arthropod-borne or mosquito-borne viral disease of the genus Flavivrus, and is related to SLE.
Japanese enceplalitis is the most important worldwide cause of arboviral encephalitis
Following the incubation period of 5 to 14 days, symptoms onset is usually sudden, including fever, headache and vomiting, resolving in 5 to 7 days if there is no CNS involvement. Mortality is less than 10%, but in children this can exceed 30%. Neurologic sequelae occures in up to 30% of cases.
A vaccine is currently available.
e. Hemorrhagic fevers
Hantaan virus - Hantavirus
Lassa fever
South American Hemorrhagic Fevers (Junin & Machupo)
African Hemorrhagic Fevers (Marburg & Ebola)
c. Hepatitis B and hepatitis C
Hepatitis B and hepatitis C are transmitted through blood or body fluids.
Hepatitis B virus (HBV) is a hepadnavirus which can result in cronic infection, especially in infants. 90 to 95% of adult patients recover completely; however, 80 to 95% of infants and young children develop a cronic carrier state, and are at high risk for developing hepatocellular carcinoma.
Rapid developing fulminant hepatitis is associated with 70 to 90% mortality, with survival of those over 40 year of age uncommon. Fulminant HBV is also associated with superinfection with other agents, including HDV.
Clinically, HBV is frequently subclinical with an insidious onset, following a varying incubation period from 50 to 180 days, averaging 60 to 90 days, which makes for the infections origin difficult. In the adult, infection is not apparent at rate of 65 to 80 per cent.
Transmission is via blood primarily and body secretions secondary. Incubation time is related to the exposure dose of HBV.
A vaccine is available. Hepatitis B immune globulin (HBIG) is effective on exposure but effectiveness is decreased if delayed greater than three days. It provides no preexposure prophylaxis value due to the effective and available vaccine.
In the infant borne to a mother who is infected during pregnancy, or is a carrier of HBV, both HBIG and HBV vaccine is given at different sites within a few hours of birth to reduce mother to infant transmission. A second dose at one month and a third at six months of age are given.
Hepatitis type D (Delta Hepatitis) (HDV) is found in conjunction with HBV infection. It is associated with a higher rate of liver damage and mortality in HBV infection group. Resolution of HBV infection results in resolution of HDV as well. Because of the need for coinfection with HBV, this vaccine is effective.
Hepatitis C
A flavivrus, hepatitis C virus (HCV) is transmitted through blood products and to a lesser extent, body substances. Mother to infant transmission is less than for HBV. HCV infection is usually subclinical but more than half HCV infections progress to chronic hepatitis. No vaccine is available.
d. Infectious mononucleosis
Epstein-Barr (EB) virus - also refered to as "mono"
Transmission is via saliva transfer in sharring of drinks or kissing.
Following an incubation period of four to seven weeks, symptoms include sore throat, fever, headach, swollen lympth nodes, and generalized weakness and fatique. Hepatitis or a rash may also develop. Recover occures usually within a few weeks, but low grade fever and weakness or fatique may persist for weeks to months in some individuals. Immunity therafter is permanant.
In the developing world, EB virus is a childhood disease, with 90% having antibiodies by age four, and the disease often asymptomatic. In the developed world, disease is usually delayed untill late childhood or early adulthood, in the age range of 15 to 25 years.
A potential complication is rupture of the spleen which is enlarged during the disease process.
EB virus is related to the development of Burkitt's lymphoma in malaria areas of Africa.
EB virus is one of the causes of the chronic fatigue syndrome (CFS).
3. Protozoal disease
a. Malaria
b. Sleeping sickness
c. Toxoplasmosis
Helminthic
Schistosomiasis
Swimmer's Itch
F. Nosocomial and opportunistic disease
G. Acquired immunodeficiency syndrome (AIDS)
1. Human immunodeficiency virus (HIV)
2. Transmission and epidemiology
3. Pathology (including opportunistic infections)
4. Diagnosis
5. Treatment
VI. Environmental, Food, and Industrial microbiology (10%)
A. Environmental (ecological) microbiology
1. Terrestrial environment (soils)
a. Flora of soil
b. Biogeochemical cycles (carbon, nitrogen, sulfur, phosphorus)
c. Biodegradation and recycling
2. Aquatic environment
a. Fresh water and marine environment
b. Aquatic pollution (eutrophy, human waste, food waste, industrial waste)
c. Pollution abatement
(1) Waste water treatment (specific treatment, community systems)
(2) Preparation of drinking water
B. Food microbiology
1. Foods produced using microorganisms
2. Spoilage of food by microorganisms
3. Preservation methods
C. Industrial microbiology
1. Alcoholic beverages (beer, wine, distilled spirits)
2. Production of organic compounds (organic acids, amino acids, vitamins, enzymes, steroids, antibiotics, other pharmaceuticals)
3. Biological insecticides
4. Genetically engineered or recombinant DNA products
