Exam 1 Flashcards
Ch. 1-2, 4, 6-9
Characteristics of microbes
microscopic (usually)
single-celled (usually)
most are beneficial (i.e. gut, skin, probiotics such as yogurt & cheese) & essential
5 types of microbes
- bacteria
- viruses (subcellular)
- protozoa
- fungi
- algae (unicellular)
prions
- 6th type of microbe
- Acellular
- no DNA or RNA genome
- infectious protein particles
- submicroscopic
- reproduction: infectious prion physically interacts with normal protein & converts it to infectious form
- examples: mad cow disease, scrapie (can only detect prion disease via autopsy)
“The time has come to close the book on infectious diseases. We have basically wiped out infection in the United States.” - Surgeon General in 1967. Why did he say this? Why was he wrong? what is the challenge?
1940s: Penicillin, other bacterial vaccines, and pesticides
1960s: more chronic diseases started to appear (i.e. obesity, lung cancer)
The challenge: In the past three decades, 40 previously unknown infectious diseases have emerged or reemerged (present day number is higher)
Five leading causes of death
- cardiovascular disease
- INFECTIOUS DISEASE
- cancer
- liver & kidney disease
- diabetes
6 factors responsible for emerging infections
- world population growth
- urbanization
- ecological disturbances
- technological advances
- microbial evolution & adaptation
- human behavior & attitudes
how much of the human population lives in less developed countries? (world population growth)
80%
what will the population be by 2050? (world population growth)
over 9 billion
Thomas Malthus
late 1700s to early 1800s
preacher who warned 200 years ago that unchecked population growth would lead to famine; THE LARGEST PROBLEM WITH POPULATION GROWTH IS INCREASED TRANSMISSION OF INFECTIOUS DISEASES
why does Tokyo, Japan have a reduced level of infectious disease despite high population density? (world population growth)
serious public health control
3 types of transmission (facilitated by overpopulation)
- person-to-person
- biological vector (mosquito, tick, fly to human) by taking in bacteria & releasing it to the next host (mosquitoes) or by feces on food (flies)
- zoonotic (animal to human) - i.e. rabies, consumption, swine flu
effect urbanization has on emerging infections
more of the world’s population is becoming concentrated in cities
poverty => less sanitation & hygiene, safe drinking water, public health infrastructure
what place is home to 68% of the worl’d people living with HIV?
Sub-Saharan Africa
what kind of ecological disturbances are responsible for increase in infectious diseases?
DEFORESTATION (i.e. Limes disease)
CLIMACTIC CHANGE (i.e. malaria, dengue)
NATURAL DISASTERS
- floods in Southern Africa => more mosquitoes carrying malaria & increase in cholera bc lack of safe drinking water
- drought in Eastern Africa => famine & malnutrition weaken immune system)
what kind of technological advances are responsible for increase in infectious diseases?
- travel means arriving at destination before showing symptoms
- NOSOCOMIAL INFECTION (from blood products, organ transplants, invasive medical procedures, immunosuppressive therapy or disease)
how does microbial evolution and adaptation play a role in increasing infectious disease?
- resistance to antibiotics & antimicrobials due to adaptation & selection that is accelerated by misuse:
1) overprescription
2) failure to complete drug regimen
what kind of human behaviors/attitudes contribute to increasing infectious disease?
- COMPLACENCY (false assumption that prevention & control are unnecessary; examples include threatened resurgence of AIDS & decreased immunizations)
- HUMAN MIGRATION (Internally Displaced Persons lack water, shelter, food, & hygiene; Refugees transmit disease in refugee camps)
- SOCIETAL FACTORS (increased day care use, increased population of elderly, globalization & centralization of food supply, increased tattooing & body piercings)
cell first coined by who & when?
Robert Hooke (monk) in 1665
what is the cell theory and who were the three people behind it?
- the cell is the fundamental unit of all organisms
- all organisms are unicellular or multicellular
- all cells are fundamentally alike in structure and metabolism
what makes a microbe?
1) size
2) metabolic diversity - cells obtain energy from metabolism (heterotrophs vs autotrophs)
3) requirement for oxygen
4) prokaryote vs eukaryote
heterotrophs
- metabolize complex ORGANIC molecules (food) as a source of energy & carbon
- depend on autotrophs for organic molecules
autotrophs
- use INORGANIC carbon as an energy source (CO2)
- two types: 1) photosynthetic 2) chemosynthetic
photosynthetic autotrophs
obtain energy directly from sun; produce oxygen
chemosynthetic autotrophs
obtain energy from inorganic compounds
microbes requirement for oxygen - aerobes vs anaerobes vs facultative anaerobes
- AEROBES require O2 for metabolism (breaks down sugars to make energy available)
- ANAEROBES do not use O2. some can tolerate it but others are killed by it
- FACULTATIVE ANAEROBES grow better with O2, but can grow w/o it
what is metabolic diversity important for?
- preventing harmful microorganisms from getting nutrients
- diagnosing
- note: viruses have no metabolism & are neither aerobes nor anaerobes
prokaryote vs eukaryote
- prokaryotes have no internal components (bound by membranes) & no nucleus
- eukaryotes have membrane-bound compartments
viruses
- examples: HIV/AIDS, measles, rabies
- Acellular
- genome RNA or DNA
- obligate intracellular parasite (need living cell to replicate)
- submicroscopic
bacteria
- unicellular
- prokaryotic
- microscopic
- DNA genome, replicate by binary fission (asexual)
- cell wall (except mycoplasmas)
- motile by flagella
- metabolism: heterotrophs & autotrophs
- important human pathogens, most beneficial or harmless
protozoans
- examples: malaria, leishmaniasis
- unicellular
- eukaryotic
- microscopic
- DNA genome, asexual or sexual replication
- No cell wall
- motile by flagella, cilia, or pseudopods
- important human pathogens, most harmless
- Not an intracellular parasite
algae
- examples: dinoflagellates, diatoms
- unicellular or multicellular
- eukaryotic
- microscopic (unicellular only)
- DNA genome, asexual replication
- cell wall
- metabolism: photoautotrophs
- not infectious; some produce neurotoxin harmful to marine life or humans eating toxin-containing fish or shellfish
fungi
- examples: yeast or molds
- unicellular (yeast) or multicellular (molds)
- eukaryotic
- microscopic (yeast only)
- DNA genome, asexual or sexual replication
- cell wall
- non-motile
- metabolism: heterotrophs
- usually harmless or even beneficial; few are pathogenic for humans
symbiosis & types of symbiosis
- “living together”; association between two or more species
- types:
1) mutualism
2) commensalism
3) parasitism
mutualism
both species benefit (i.e. lichens)
commensalism
one species benefits
the other neither benefits nor is harmed (i.e. normal flora)
parasitism
parasite lives at expense of the host (i.e. all microbial pathogens)
Koch’s postulates
1) ASSOCIATION - causative agent must be present in every case of specific disease
2) ISOLATION - causative agent must be isolated in every case of disease & grown in pure culture
3) CAUSATION - causative agent in pure culture must cause disease when inoculated into a healthy & susceptible animal
4) REISOLATION- the causative agent must be reisolated from the lab animal & be identical to the original causative agent
issues with Koch’s postulates?
- trying to isolate only one microbe
- ethical issues (polio only infects humans but can’t inoculate humans with polio)
what three factors does acquiring an infection depend on?
- (n) dose, the number of microbes encountered
- (v) virulence
- (R) resistance, host immunity
severity of infection formula
D = nV/R
infective dose (ID)
- minimal number of microbes necessary for infection
- more virulent organism usually have smaller IDs
LD50
- lethal dose
- number of microbes necessary to kill 50% of the animals infected
virulence & two types of virulence factors
- severity of the disease
- measured by # symptomatic/# infected
- more virulent usually means low ID and high LD
- virulence factors:
1) DEFENSIVE STRATEGIES - allow microbes to escape destruction by the host immune system
2) OFFENSIVE STRATEGIES - result in damage to the host
infectivity
- capacity of agent to produce infection or disease
- measured by # infected/# exposed
pathogenicity
- the capacity of the agent to cause disease in the infected host
- measured by # symptomatic/# exposed
what is the single most important infectious disease that causes death worldwide?
Tuberculosis
toxigenicity
- the capacity of the agent to produce a toxin or poison
- measured by # affected/# exposed
examples of defensive strategies in virulence
1) ADHESINS - enable adherence of pathogens to cell receptors at portal of entry
2) M PROTEIN - capsules prevent phagocytosis
3) WAXY COAT
4) ANTIGENIC VARIATION - trypanosomes can change surface antigens (coat) to avoid antibodies (don’t fit)
- Helicobacter pylori (causes peptic ulcers) secretes enzyme urease to survive in highly acidic stomach
examples of virulence offensive strategies
1) EXOENZYMES - enzymes are proteins that allow invading bacteria to spread throughout tissues & cause damage)
2) TOXINS (endotoxins, exotoxins, toxoids)
endotoxin
- part of Lipopolysaccharide in outer membrane of gram-negative cells; released when cell disintegrates
- causes shock, chills, fever, weakness, small blood clots, & possibly death
- general activity
- minimal toxicity
- heat stable
exotoxin
- proteins synthesized by the microbe & secreted into host’s tissues
- examples include cytotoxin, neurotoxin, enterotoxins
- activity specific for each toxin
- high toxicity
- heat unstable
toxoid
detoxified toxin that retains antigenicity
botulinum toxin vs tetanus toxin
- botulinum toxin causes flaccid muscle paralysis by blocking contraction pathways
- tetanus toxin causes stiffness by blocking relaxation pathways
- both are exotoxins
virulence mechanisms of viruses (defensive & offensive)
- defensive: antigenic variation (i.e. new vaccine every year for influenza)
- offensive: death (lysis) of host cell from:
large numbers of replicating viruses
inhibit host protein synthesis
damage plasma membrane
inhibit host cell metabolism
virulence mechanisms for eukaryotic microbes
combination of offensive & defensive strategies for bacteria (adhesins, toxins, antigenic variation)
5 stages of microbial disease
1) INCUBATION - period between initial infection & symptoms
2) PRODROMAL - period of early symptoms
3) ILLNESS - disease is most acute
4) DECLINE - symptoms subsiding
5) COVALESCENCE - symptoms disappear & recovery
epidemiology
branch of medicine that deals with the source, cause, & control of infectious disease & other public health problems
epidemiologists
- determine why disease outbreaks occur at a particular time and/or place
- population-based disease control
leading causes of mortality in 1900 vs 2015 (epidemiology & quantification)
1900: respiratory infectious diseases heart diseases diarrhea & enteritis 2015: #1 is chronic diseases infectious diseases at the bottom
zika virus
- spread through mosquitos
- affects pregnant women & leads to lack of cranial development in baby
- considered an STD as well bc it can be passed to a pregnant woman by her infected husband
Hippocrates
460 - 377 B.C.
- linked malaria, yellow fever, & swamps
- Father of Medicine
- movement away from supernatural with no knowledge of the germ theory
Edward Jenner
- late 1700s
- observations regarding cowpox lead to smallpox vaccine (1st vaccine)
Ignaz Semmelweis
- mid 1800s
- “savior of mothers”
- early pioneer of antiseptic procedures (lemon-lime handwashing)
- idea: wash hands to prevent childbed fever
- ideas were disregarded until Louis Pasteur & germ theory
John Snow
- 1849
- Broad Street Pump –> cholera outbreaks in London from water supply
4 classifications of disease
1) SPORADIC- occasionally & unpredictable (i.e. tetanus)
2) ENDEMIC - regularly at steady level in particular location (i.e. common cold)
3) EPIDEMIC - sudden increase in morbidity & mortality above norm (i.e. plague)
4) PANDEMIC - epidemics that spread across continents (i.e. 1918 influenza, HIV/AIDS)
2 types of epidemic
1) COMMON-SOURCE - contact w a single contamination source
2) PROPAGATED - person-to-person contact
herd immunity (group immunity)
- proportion of immunized individuals in population
- smaller number of susceptible individuals = less opportunity for contact between them & infected individuals
reproduction rate (R-nought)
- measure of potential for transmission
- mean number of secondary cases, occurring in nonimmunized population in wake of infection
- R-nought must be greater than 1 to spread; if less, it will die out
how do epidemiologists predict time for spread of disease?
by looking at southern vs northern hemispheres
synthetic opioid
fentanyl
why must the vaccine for influenza be adjusted each year?
influenza is an RNA virus which means that more mutations occur = constantly changing
cycle of microbial disease
pathogen –> reservoir (source) of pathogen –> transmission to susceptible host –> portal of entry –> portal of exit
reservoir of infection
- site in which microbes survive & multiply & from which they are transmitted
- all pathogens must have one or more reservoirs to survive
- targets to prevent or stop epidemics
- humans are the only known reservoir for smallpox, gonorrhea, measles, polio, etc.
active carriers
individuals who have a microbial disease
healthy carriers
- have no symptoms & transmit disease
- harbor microbe after recovery indefinitely
- example: Typhoid Mary (Mary Mallon) carrier of pathogen that causes typhoid fever (fecal oral transmission); west nile virus
chronic carriers
- harbor pathogen after recovery, but don’t become ill again
- nontransmittable
zoonoses
- diseases of animals that can affect humans; animals serve as reservoirs & carriers of pathogen
- i.e. west nile virus - active transmission between birds & mosquitos but occasionally travels to dead end host such as horses (high mortality rate) in which the virus cannot get at a high enough amount to be transmittable
nonliving reservoirs
- some organisms can survive & multiply in nonliving environments, such as water & soil
- example: spore formers like Clostridium bacteria can survive in soil
transmission
mechanism for spreading infectious agent to susceptible person
horizontal transmission (direct)
- person-to-person
- touch & sex
- droplets (don’t remain airborne)
- animal bites
vertical transmission (direct)
- transplacental
- mother to child (breast milk, birth canal)
indirect transmission & types
- microbes pass from reservoir to intermediate agent then to host
- types:
~ VEHICLEBORNE - via food, water, biological products, & fomites (inanimate objects)
~ AIRBORNE - aerosols of water or dust particles smaller than droplets; remain airborne for long time
~ VECTORBORNE - arthropods or insects
mechanical passive transmission (vectorborne indirect transmission)
microbes do not invade, multiply, or develop in vector; transmission on feet, etc.
what is happening with vector borne diseases?
- lack of resources for vector control
1980s & 90s DDT (insecticide) became illegal (can bioaccumulate & become resistant) –> emergence of almost eradicated diseases - lack of political will
nosocomial infection distribution
1) urinary tract infections
2) surgical site infections
3) lower respiratory infections
4) other
5) cutaneous
6) IV catheterizations
naming bacteria
- names using Linnaeus’s binomial classification system
- genus name capitalized (usually named after someone)
- species name not capitalized (indicated habitat)
broad spectrum antibiotics vs narrow spectrum antibiotics
- broad spectrum antibiotics work against gram + AND gram - (i.e. Amoxicillin, Tetracycline)
- narrow spectrum antibiotics work against gram + OR gram - (i.e. Z-pak - Azithromycin)
nucleoid
- region of cytoplasm containing chromosomal dsDNA (one or more circular &/or linear chromosomes)
plasmids
- small, circular, independently replicating, dsDNA
- encode limited number of genes
- expand genetic capability of host cell (may encode virulence genes; R FACTORS => plasmids encoding antibiotic resistance genes)
- infectious nature
spores
- viable for long periods (centuries or longer)
- resistant to heat, boiling, drying, radiation & chemical compounds
- important pathogens include ‘Bacillus anthracis’ & ‘Clostridium’
DNA structure
- Deoxyribonucleic Acid => polymer of repeated nucleotides
- nucleotide => a nitrogenous base, deoxyribose, & 1-3 phosphates
- nitrogenous bases: purines (A & G), pyrimidines (C & T)
DNA replication
- “parental” dsDNA separates into single strands
- single strand is template for new “daughter” strand following Chargaff’s rule (A-T; G-C)
- bidirectional
transcription: DNA to mRNA
- RNA polymerase uses one strand of DNA as template for transcribing mRNA copy (complementary)
- begins with promoter. ends with terminator
translation: mRNA to protein
- mRNA is translated by ribosomes into 20 amino acid language of proteins
amino acid structure
- central carbon w one of 20 side chains
- amino group
- carboxyl group
characteristics of genetic code (codons)
- mRNA reads in blocks of three letter codons
- each codon hydrogen bonds with complementary anticodon of tRNA
- 64 possible codons in genetic code:
~ only one start codon
~ 3 stop codons (no tRNA)
~ redundant (most amino acids encoded by two or more codons)
~ 3rd nucleotide may not be significant to specify amino acid identity (“wobble”)
constitutive gene
always expressed (turned on)
regulated genes
- INDUCIBLE GENE expressed only when an inducer is present
- REPRESSED GENE is “turned off” when repressor is present
operons
group of functionally related genes that are controlled by same regulatory sequences (promoter)
mutations
- cause change in nucleotide sequence of DNA
- consequences:
1) harmful
2) beneficial (rare)
3) silent - cause:
~ unrepaired error in DNA replication
~ mutagens (chemical agents or physical agents)
~ transposons “jumping genes”
types of recombination
- VERTICAL: sexual reproduction passes on genetic change from parents to offspring
- HORIZONTAL (lateral): recombination occurs between donor cell & recipient (not reproduction)
~ three examples: transduction, conjugation, & transformation
bacterial conjugation
- requires cell-to-cell contact (transfer of ssDNA)
- donor requires F factor
- donors are F+ (have F plasmid and produce sex pilus)
- recipient is F-
- transfer of ssDNA makes recipient F+
abiotic bacterial growth
temperature, oxygen, water
biotic bacterial growth
disease, competition, predation
bacterial growth - four major growth phases
1) LAG - adaptation to new conditions
2) EXPONENTIAL/LOGARITHMIC - the cell population doubles with each generation
3) STATIONARY - rate of cell division=rate of death (nutrients depleted & toxins accumulate)
4) DEATH - cells dying>rate of cell division
culturing bacteria: diagnostics
- CLINICAL SPECIMEN obtained to grow in culture to identify cause of infection (throat swab, urine or blood culture –> growth medium –> streak across agar plate)
- METABOLIC TESTS
- RAPID STREP ANTIGEN TESTS (identify ‘Streptococcus pyogenes’)
~ type of diagnostic test depends on source
~ can also detect anti-bacterial antibodies in blood or amplify pathogen’s DNA
determining which antibiotic a bacterial isolate is sensitive to
done by:
- spread isolate onto agar plate
- apply antibiotic-containing disks to plate surface
- “ZONES OF INHIBITION” (no growth) form around any disks that inhibit the bacterium’s growth
API-20E test
- multitest procedure
- 20 tests to differentiate bacteria belonging to Enterobacteriaceae family (cause UTIs or diarrhea)
Atypical bacteria
- MYCOPLASMAS ~ no cell wall, no shape ~ very small; special media for growth ~ disease: walking pneumonia - CHLAMYDIAE ~ obligate intracellular parasites ~ disease: urethritis, trachoma, lymphogranuloma venereum - RICKETTSIAE ~ obligate intracellular parasites ~ transmitted by arthropods (except for Q fever)
antibiotics
produced by microbes
sulfonamide (sulfa) drugs
- first “wonder” drugs
- antimicrobials bc they are synthetic
- inhibitor of enzyme involved in folate synthesis (inhibit growth of bacteria but doesn’t kill)
- saved millions in WWII
penicillin
- first antibiotic used in 1941
- discovered by Alexander Fleming (staphylococci in petri dish contaminated with penicillium mold after 2 wk vacation)
- semisynthetic penicillin derivatives include methicillin, ampicillin, & penicillin V
broad-spectrum antibiotics
- inhibit gram + and gram -
- used when bacterium is unknown
- may kill normal flora, allowing non-susceptiable organisms to flourish and antibiotic resistance
- examples: amoxicillin, carbapenems, streptomycin, tetracycline, chloramphenicol
- treats bacteremia, sepsis, pneumonia
narrow-spectrum antibiotics
- treats specific families of bacteria and causes less disruption
- does not kill many normal flora and less resistance
- examples: azithromycin, erythromycin, vancomycin
- treats ear infections, throat infections, UTI, typhoid, pneumonia
bactericidial
directly kills cell
bacteriostatic
inhibits growth of cells, immune system eliminates cells
mechanisms of antibiotics
- INTERFERENCE W CELL WALL SYNTHESIS (beta-lactam antibiotics interfere with peptidoglycan synthesis)
- INTERFERENCE WITH PROTEIN SYNTHESIS (70S ribosomes for bacteria vs 80S for eukaryotes)
- INTERFERENCE WITH CELL MEMBRANE FUNCTION (Polymyxin B is used topically because of toxicity)
- INTERFERENCE WITH NUCLEIC ACID SYNTHESIS (block DNA replication & RNA polymerase)
- INTERFERENCE WITH METABOLIC ACTIVITY (antimetabolites bind with enzymes [molecular mimicry] and makes them inactive; sulfa drugs mimic a precursor to folic acid)
acquisition of antibiotic resistance
results from genetic change such as:
- CHROMOSOMAL MUTATION (confers resistance to only a single antibiotic)
- acquisition of R (RESISTANCE) PLASMID from resistant strains (resistance to several antibiotics; 1st report in Japan in 1959 with Shigella)
- TRANSPOSONS “JUMPING GENES” (carry antibiotic resistance genes)
natural selection favors survival of resistant cells
mechanisms of antibiotic resistance
- ENZYMATIC INACTIVATION (beta-lactamase cleaves penicillins; break down antibiotics)
- ALTER ANTIBIOTIC UPTAKE (membrane pump to expel antibiotics; decrease membrane permeability)
- MODIFY TARGET OF ANTIBIOTIC (antibiotic receptor site)
- DEVELOP ALTERNATE METABOLIC PATHWAY (i.e. resistance to sulfonamides)
*bacteria share antibiotic resistance genes by HORIZONTAL GENE TRANSFER
consequences of antibiotic misuse
- gonorrhea resistance to quinolones in Hawaii
- more than 90% of Staphylococcus aureus strains are resistant to penicillin and other antibiotics
- vancomycin resistance appearing in staphylococci and enterococci
- drug-resistant TB strains increasing
food intoxication (food poisoning)
- ingestion of bacterial toxins (with or without the microbe present)
- N/V and diarrhea (some can result in numbness and tingling around lips and cause damage to nerves and organs)
- symptoms appear quickly
foodborne infection
- bacteria multiply in intestinal tract, secrete an enterotoxin, and may invade cells of intestinal tract
- N/V, diarrhea, and possibly bloody stools
- symptoms can start 1 hour after eating to 10 days later (some parasite infections take months to develop symptoms)
- symptoms can last from one day to months
Botulism
- caused by neurotoxin of Clostridium botulinum (gram + spore-forming bacillus) found in soil
~ anerobic symptoms: paralysis, lethargic
~ therapy: antitoxin and mechanical ventilation (until body can metabolize toxin out)
~ botox - Clostridium perfringens food poisoning
staphylococcal food poisoning
- caused by staphylococcus aureus (g+ coccus)
- most common food poisoning (under reported bc its not a notifiable disease)
- found in nasal passages
- heat stable enterotoxin
- symptoms: n/v, abdominal cramps, diarrhea
- severe symptoms appear within a few hours; quick recovery
- treatment: rest, fluids, meds to calm stomach (antibiotics not useful)
salmonellosis
- caused by several species of Salmonella (g- bacilli)
- symptoms: (gastroenteritis) n/v, abdominal cramps, diarrhea, possibly fever
- symptoms develop 12-72 hours after infection; last 5-7 days
- treatment: manage symptoms, hydrate, antibiotics not necessary unless it spreads from intestines
salmonella enteritidis
- in intestinal tracts
- prevention: no vaccine; don’t eat raw or undercooked eggs, poultry, or meat; wash hands and surfaces
salmonella typhi
- causes typhoid fever
- organism invades cells lining of small intestines; causes ulcers, bloody stools, fever, and possibly delirium
- treatment: antibiotics and wash hands
- prevention: two vaccines available that require repeated immunization, wash hands, avoid eating raw foods, don’t drink untreated water
shigellosis
- caused by several species of Shigella (g- bacillus)
- symptoms: gastroenteritis and possible dysentery
- symptoms occur 1-2 days after infection and last 5-7 days
- treatment: oral or IV rehydration and possibly antibiotics
- prevention: no vaccine, wash hands
- threat of antibiotic resistance
cholera intoxication
- caused by exotoxin secreted by vibrio cholerae (g- curved rod)
- symptoms: rice-water diarrhead
- treatment: oral rehydration therapy, no antibiotics
enterotoxigenic E. coli
- lives in intestines; commensal bacteria usually
- most common cause of traveler’s diarrhea
- prevention: coliform test
E. Coli O157:H7
- symptoms: severe stomach cramps, diarrhea (often bloody), vomiting
- incubation period 3-4 days; most recover in 5-7 days
- most cases are mild; Hemolytic uremic syndrome (significant blood loss) may result in death in children under 5
- treatment: non-specific supportive therapy, hydration, no antibiotics
- prevention: consumption of contaminated food, water, and feces
campylobacteriosis
- caused by campylobacter jejuni (g- bacillus)
- symptoms: bloody diarrhea, cramping, abdominal pain, fever, n/v 2-5 days after exposure
- treatment: hydration and occasionally antibiotics
- prevention: food handling
listeriosis
- caused by listeria monocytogenes (g+ bacillus)
- grows under refrigeration
- symptoms: fever, muscle aches or stiff neck (similiar to meningitis)
- prevention: food safety
- treatment: antibiotics
pseudomembranous colitis
- caused by clostridium difficile (g+ spore-forming bacillus)
- depletion of normal flora by use of antibiotics may allow C. diff to grow out & cause diarrhea
4 steps to prevent foodborne illness
1) clean
2) separate
3) cook
4) chill (keep fridge below 40F)
diphtheria
- airborne bacterial disease
- caused by exotoxin produced by Corynebacterium diphtheria (g+ bacillus)
- kills epithelial cells –> forms leathery pseudomembrane
- symptoms: weakness, sore throat, fever, swollen glands; 2-3 days for thick coating to build in nose and throat (suffocation in children); toxin diffuses into bloodstream and may cause damage to heart
- treatment: diptheria antitoxin and antibiotics
- prevention: isolation and vaccination (TDAP)
pertussis - whooping cough
- caused by Bordetella pertussis (g- coccobacillus)
- humans are the only reservoir
- exotoxin damaged ciliated cells that clear mucous from air passages => “whoop”
- reemerging disease
- symptoms develop 5-10 days after being exposed
- early symptoms: runny nose, low-grade fever, mild cough, apnea
- later symptoms: 1-2 weeks of progression include paroxysms (fits) of rapid coughs followed by whoop, vomiting, exhaustion (coughing can last for 100 days)
- treatment: antibiotics, hydrate
- prevention: VACCINATION (DTaP) [booster q 10 years], good hygiene
