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81 Cards in this Set

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staphylcocccal
Common inhabitant of the skin and mucous membranes
Spherical cells arranged in irregular clusters
Gram-positive
Lack spores and flagella
May have capsules
31 species
Staphlococcus aureus
Grows in large, round, opaque colonies
Optimum temperature of 37oC
Facultative anaerobe
Withstands high salt, extremes in pH, and high temperatures
Produces many virulence factors
Virulence factors of S. aureus
Enzymes:
Coagulase – coagulates plasma and blood; produced by 97% of human isolates; diagnostic
Hyaluronidase – digests connective tissue
Staphylokinase – digests blood clots
DNase – digests DNA
Lipases – digest oils; enhances colonization on skin
Penicillinase – inactivates penicillin
toxins: Virulence factors of S. aureus
Toxins:
Hemolysins (α, β, γ, δ) – lyse red blood cells
Leukocidin – lyses neutrophils and macrophages
Enterotoxin – induce gastrointestinal distress
Exfoliative toxin – separates the epidermis from the dermis
Toxic shock syndrome toxin (TSST) – induces fever, vomiting, shock, systemic organ damage
Folliculitis (s.aureus)
superficial inflammation of hair follicle; usually resolved with no complications but can progress
Furuncle (s.aureus)
boil; inflammation of hair follicle or sebaceous gland progresses into abscess or pustule
Carbuncle (s.aureus)
– larger and deeper lesion created by aggregation and interconnection of a cluster of furuncles
Impetigo (S.aureus)
bubble-like swellings that can break and peel away; most common in newborns
Osteomyelitis (systemic)(S.aureus)
infection is established in the metaphysis; abscess forms
Toxigenic disease
(S.aureus)
Food intoxication – ingestion of heat stable enterotoxins; gastrointestinal distress
Staphylococcal scalded skin syndrome – toxin induces bright red flush, blisters, then desquamation of the epidermis
Toxic shock syndrome – toxemia leading to shock and organ failure
Identification of Staphylococcus
Frequently isolated from pus, tissue exudates, sputum, urine, and blood
Cultivation, catalase, biochemical testing, coagulase
positive bubbles (S.aureus)
MRSA – methicillin-resistant S. aureus
95% have penicillinase and are resistant to penicillin and ampicillin
MRSA – methicillin-resistant S. aureus – carry multiple resistance
Some strains have resistance to all major drug groups except vancomycin
HA-MRSA (hospital-acquired MRSA) account for 80% of Staph. infections
Treatment and Prevention of Staphylococcal Infections
Treatments:
Abscesses have to be surgically perforated
Systemic infections require intensive lengthy
Preventions:
Universal precautions by healthcare providers to prevent nosocomial infections
Hygiene and cleansing
Streptococcal
Gram-positive spherical/ovoid cocci arranged in long chains; commonly in pairs
Non-spore-forming, nonmotile
Can form capsules and slime layers
Facultative anaerobes
Do not form catalase, but have a peroxidase system
Most parasitic forms are fastidious and require enriched media
Small, nonpigmented colonies
Sensitive to drying, heat, and disinfectants
b-hemolytic Streptococci
Streptococcus pyogenes
Most serious streptococcal pathogen
Strict parasite
Inhabits throat, nasopharynx, occasionally skin
Virulence Factors: Hyaluronic acid capsule, Streptolysins, Erythrogenic toxin (pyrogenic – cause fever and rash
Streptococcus pyogenes
transmission
Transmission – contact, droplets, food, fomites
Necrotizing Fasciitis
In rare cases, skin infections can lead to necrotizing fasciitis (flesh-eating disease)
Infecting Streptococci release exotoxins that poison epidermal and dermal tissues
Flesh dies and sloughs off, allowing the Streptococci to invade deeper tissues
More dangerous infections are mixed with anaerobic bacteria or involve septicemia
Streptococcal pharyngitis
S. Pyogenes Diseases
strep throat infection
Scarlet fever
S. Pyogenes Diseases
strain of S. pyogenes carrying a prophage that codes for erythrogenic toxin; can lead to sequelae
(systemic infection)
Rheumatic fever
Long-Term Complications of S. Pyogenes
follows overt or subclinical pharyngitis in children or scarlet fever; can lead to carditis with extensive valve damage possible, arthritis, chorea, fever
Can last 3-6 months; effects not apparent until adulthood
Treatment and Prevention
S. Pyogenes Diseases
Treated with penicillin or penicillin derivatives
Long-term penicillin prophylaxis for people with a history of rheumatic fever or recurrent strep throat
No treatment for rheumatic fever and acute glomerulonephritis once developed, must treat preceding infections to avoid these conditions
α-Hemolytic Streptococci: Viridans Group
Once invaded these types can cause
Bacteremia,
meningitis,
abdominal infection,
tooth abscesses
Persons with preexisting heart disease are at high risk; S. mutans produce slime layers that adhere to teeth, basis for plaque
Persons with preexisting heart conditions should receive prophylactic antibiotics before surgery or dental procedures
Colonization of heart by forming biofilms
subacute endocarditis
Streptococci: Viridans Group
Blood-borne bacteria settle and grow on heart lining or valves
People with heart disease at higher risk.
Colonization of heart by forming thick biofilms called vegetations
Diagnosis: Blood cultures
Treatment: Long term administration of penicillin-G treatments
Streptococcus pneumoniae
Causes 60-70% of all bacterial pneumonias
Culture requires blood or chocolate agar & growth improved by 5-10% CO2
All pathogenic strains form large capsules – major virulence factor
Causes pneumonia and otitis media (ear infections)
Pneumonia:
Streptococcus pneumoniae
Occurs when cells are aspirated into lungs of susceptible individuals
Pneumococci multiply and induce an overwhelming inflammatory response
Otitis media:
Streptococcus pneumoniae
Occurs when cells gain access to middle ear by way of eustachian tube
Results in meningitis in some cases (most common cause of adult meningitis and a common cause of meningitis in children)
Meninigitis: Severe Inflammation of the lining of the Brain and spinal cord.
diagnosis, treatment, and prevention of Streptococcus pneumoniae
Gram stain of specimen – presumptive identification
Quellung test or capsular swelling reaction
Traditionally treated with penicillin G or V
Increased drug resistance
Two vaccines available for high risk individuals:
Capsular antigen vaccine for older adults and other high risk individuals – effective 5 years
Conjugate vaccine for children 2 to 23 months
Conjugate vaccine: vaccine made of pneumococcal Ags associated with diptheria Ags
Neisserial Diseases
genus neisseria
Gram-negative, bean-shaped, diplococci
None develop flagella or spores
Capsules on pathogens
Pili
Strict parasites, do not survive long outside of the host
Aerobic or microaerophilic
Produce catalase and cytochrome oxidase
Pathogenic species require enriched complex media
Neisseria gonorrhoeae: Gonorrhea
Males – urethritis, yellowish discharge, scarring, and infertility
10% of males are asymptomatic
Females – vaginitis, urethritis, salpingitis (PID) mixed anaerobic abdominal infection, common cause of sterility and ectopic tubal pregnancies
50% of females are asymptomatic
Diagnosis and Treatment of gonorrhea
Gram stain – Gram-negative intracellular (neutrophils) diplococci from urethral, vaginal, cervical, or eye exudate – presumptive identification
20-30% of new cases are penicillinase-producing PPNG or tetracycline resistant TRNG
Combined therapies indicated
Recurrent infections can occur
Reportable infectious disease
Neisseria meningitidis: The Meningococcus
Virulence factors:
Capsule
Adhesive fimbriae
IgA protease
Endotoxin: 12 strains
Prevalent cause of meningitis; sporadic or epidemic
Human reservoir – nasopharynx; 3-30% of adult population; higher in institutional settings
High risk individuals are those living in close quarters, children 6 months-3 years, children and young adults 10-20 years
Disease begins when bacteria enter bloodstream, cross the blood-brain barrier, permeate the meninges, and grow in the cerebrospinal fluid
Very rapid onset; neurological symptoms; endotoxin causes hemorrhage and shock; can be fatal
diagnosis, treatment, and prevention, meningococcus meningitis
Diagnosis:
Gram stain CSF, blood, or nasopharyngeal sample
Culture for differentiation
Treatment and Prevention:
Treated with IV penicillin G, cephalosporin
Prophylactic treatment of family members, medical personnel, or children in close contact with patient
Primary vaccine contains specific purified capsular antigens
Tetanus:Clostridium tetani
Common resident of soil and GI tracts of animals
Causes tetanus or lockjaw, a neuromuscular disease
Most commonly among geriatric patients and IV drug abusers; neonates in developing countries
Spores usually enter through accidental puncture wounds, burns, umbilical stumps, frostbite, and crushed body parts
Anaerobic environment is required for vegetative cells to grow and release toxin
Tetanospasmin – neurotoxin causes paralysis by binding to motor nerve endings; blocking the release of neurotransmitter for muscular contraction inhibition; muscles contract uncontrollably
Death most often due to paralysis of respiratory muscles
treatment and prevention:
Tetanus:Clostridium tetani
Treatment aimed at deterring degree of toxemia and infection and maintaining homeostasis
Antitoxin therapy with human tetanus immune globulin; inactivates circulating toxin but does not counteract that which is already bound
Control infection with penicillin or tetracycline; and muscle relaxants
Vaccine available; booster needed every 10 years
Botulism; Food Poisoning
intoxication associated with inadequate food preservation
botulism: Clostridium botulinum
spore-forming anaerobe; commonly inhabits soil and water
Botulin toxin is carried to neuromuscular junctions and blocks the release of acetylcholine, necessary for muscle contraction to occur

Double or blurred vision, difficulty swallowing, neuromuscular symptoms
treatment and prevention of
botulism: Clostridium botulinum
Determine presence of toxin in food, intestinal contents or feces

Administer antitoxin; cardiac and respiratory support

Infectious botulism treated with penicillin

Practice proper methods of preserving and handling canned foods; addition of preservatives
Tuberculosis (TB): Mycobacterium tuberculosis
Virulence factors – contain complex waxes and cord factor that prevent destruction by lysosomes or macrophages
Gram-positive irregular bacilli
Acid-fast staining
Strict aerobes
Produce catalase
Possess mycolic acids and a unique type of peptidoglycan
Do not form capsules, flagella, or spores
Grow slowly
epidemiology: TB
Predisposing factors include: inadequate nutrition, debilitation of the immune system, poor access to medical care, lung damage, and genetics

Estimate 1/3rd of world population and 15 million in U.S. carry tubercle bacillus; highest rate in U.S. occurring in recent immigrants

Bacillus very resistant; transmitted by airborne respiratory droplets
primary TB
Infectious dose 10 cells
Phagocytosed by alveolar macrophages and multiply intracellularly
After 3-4 weeks; Tubercle formed -- immune system attacks, forming tubercles, granulomas consisting of a central core containing bacilli surrounded by WBCs
If center of tubercle breaks down into necrotic caseous lesions, they gradually heal by calcification
Secondary and Extrapulmonary TB
Secondary:
If patient doesn’t recover from primary tuberculosis, reactivation of bacilli can occur
Tubercles expand and drain into the bronchial tubes and upper respiratory tract
Gradually the patient experiences more severe symptoms
Violent coughing, greenish or bloody sputum, fever, anorexia, weight loss, fatigue
Untreated, 60% mortality rate
Extrapulmonary:
During secondary TB, bacilli disseminate to regional lymph nodes, kidneys, long bones, genital tract, brain, and meninges
These complications are grave
diagnosis TB
Mantoux test – local intradermal injection of purified protein derivative (PPD); look for red wheal to form in 48-72 hours – induration; established guidelines to indicate interpretation of result based on size of wheal and specific population factorsX-rays
X-rays
Direct identification of acid-fast bacilli in specimen
Cultural isolation and biochemical testin
treatment and prevention of TB
6-24 months of at least 2 drugs from a list of 11

One pill regimen called Rifater (isoniazid, rifampin, pyrazinamide)
Vaccine based on attenuated bacilli Calmet-Guerin strain of M. bovis used in other countries
In the US it is reccommended:
the vaccine should be considered for infants and children who do not test positive for TB but who are:Continually exposed to a patient with infectious TB of the lungs (and the child cannot be removed from this person)Exposed to a person with TB that is resistant to antituberculosis drugs
Pseudomonas:
Small gram-negative rods with a single polar flagellum

Free living
Primarily in soil, sea water, and fresh water; also colonize plants and animals

Important decomposers and bioremediators

Frequent contaminants in homes and clinical settings

Use aerobic respiration; do not ferment carbohydrates

Produce oxidase and catalase

Many produce water soluble pigments
Pseudomonas aeruginosa
Common inhabitant of soil and water
Intestinal resident in 10% normal people
Resistant to soaps, dyes, quaternary ammonium disinfectants, drugs, drying
Frequent contaminant of ventilators, IV solutions, anesthesia equipment
Opportunistic pathogen
Pseudomonas aeruginosa: nosocomial infection,UTI, abscesses
Common cause of nosocomial infections in hosts with burns, neoplastic disease, cystic fibrosis
Complications include pneumonia, UTI, abscesses, otitis, and corneal disease
Endocarditis, meningitis, bronchopneumonia
Grapelike odor and greenish-blue pigment (pyocyanin)
Multidrug resistant
Treated with third generation antibiotics
Vaccine trials underway
Tularemia: Francisella tularensis
Gram negative Rod
Causes tularemia, a zoonotic disease of mammals
endemic to the northern hemisphere, particularly rabbits – AKA “Rabbit Fever”
Transmitted by contact with infected animals, water and dust or bites by vectors
Tularemia:Francisella tularensis
signs and symptoms:
ID: 10 – 50 bacteria; incubation period of 3 – 21 days
Infection usually occurs through inoculation of skin abrasion or eyes
Signs and symptoms:
Headache, backache, chills, malaise, and weakness
Fever, ulcerative skin lesions, swollen lymph glands, conjunctivitis, sore throat, intestinal disruption, pulmonary involvement (severe)
10% death rate in systemic and pulmonic forms

Intracellular persistence can lead to relapse
Tularemia: Treatments and Preventions
Treated with Gentamicin or tetracycline

Attenuated vaccine being made

Potential bioterrorism agent
Because of such low ID and considered to be one of the most infectious bacteria
Pertussis: Bordetella pertussis
Minute, encapsulated coccobacillus
Causes pertussis or whooping cough, a communicable childhood affliction
Acute respiratory syndrome
Often severe, life-threatening complications in babies
Reservoir – apparently healthy carriers
Transmission by direct contact or inhalation of aerosols
Virulence factors
Receptors that recognize and bind to ciliated respiratory epithelial cells
Toxins that destroy and dislodge ciliated cells
Loss of ciliary mechanism leads to buildup of mucus and blockage of the airways
Vaccine – DTaP – acellular vaccine contains toxoid and other Ags
Enterobacteriaceae Family
Large family of small, non-spore-forming gram-negative rods

Many members inhabit soil, water, decaying matter, and are common occupants of large bowel of animals including humans
Facultative anaerobes, grow best in air
All ferment glucose, reduce nitrates to nitrites, oxidase negative, and catalase positive
Divided into coliforms (lactose fermenters) and non-coliforms (non-lactose fermenters)
Enrichment, selective and differential media utilized for screening samples for pathogens
Escherichia coli:
coliforms (lactose fermenters)
The Most Prevalent Enteric Bacillus
Most common aerobic and non-fastidious bacterium in gut
150 strains
Some have developed virulence through plasmid transfer, others are opportunists
Enterotoxigenic E. coli
causes severe diarrhea due to heat-labile toxin and heat-stable toxin – stimulate secretion and fluid loss; also has fimbriae
Enteroinvasive E. coli
causes inflammatory disease of the large intestine
Enteropathogenic E. coli
linked to wasting form infantile diarrhea
Enterohemorrhagic E. coli,
O157:H7 strain, causes hemorrhagic syndrome and kidney damage
Escherichia coli
Pathogenic strains frequent agents of infantile diarrhea – greatest cause of mortality among babies
Causes ~70% of traveler’s diarrhea
Causes 50-80% UTI
Coliform count – indicator of fecal contamination in water
Often complicate surgery, endoscopy, tracheostomy, catheterization, dialysis and immunosuppressant therapy

Usually effectively treated with antimicrobics (man-made antibiotics) and enterotoxin inactivation and rehydration in some instances
E. coli O157:H7
ID = 100 cells
Infection can lead to intestinal hemorrhage
Virulence associated with a cell wall receptor that allows cell to fuse to host cell, providing direct contact for toxin delivery
Contains gene for shiga toxin from Shigella
Heat-labile exotoxin that can injure nerve cells, nerves and the intestine
Reservoir in intestine of cattle, allowing it to rather easily contaminate food chain
Rapidly identified using Rainbow Agar:
O157:H7 colonies appear black
Salmonella typhi: non-coliforms (non-lactose fermenters)
Gram negative; true pathogens
Flagellated; survive outside the host
Resistant to chemicals – bile and dyes
Salmonella typhi – most serious pathogen of the genus; cause of typhoid fever; human host
Typhoid Fever
(salmonella typhi)
Bacillus enters with ingestion of fecally contaminated food or water; occasionally spread by close personal contact
Asymptomatic carriers; some chronic carriers shed bacilli from gallbladder
Bacilli adhere to small intestine, cause invasive diarrhea that leads to septicemia
Treat with chloramphenicol or sulfatrimethoprim
2 vaccines for temporary protection
Plague: Yersinia pestis
nonenteric
Tiny, gram-negative rod, unusual bipolar staining and capsules
Virulence factors – capsular and envelope proteins protect against phagocytosis and foster intracellular growth
Coagulase
Endotoxin
Murine toxin
Yersinia pestis
(plague how do u get)
Humans develop plague through contact with wild animals (sylvatic plague) or domestic or semidomestic animals (urban plague) or infected humans

Found in 200 species of mammals – rodents, without causing disease

Flea vectors – bacteria replicates in gut, coagulase causes blood clotting that blocks the esophagus; flea becomes ravenous
ID 3-50 bacilli
Bubonic
bacillus multiplies in flea bite, enters lymph, causes necrosis and swelling called a bubo in groin or axilla
Septicemic
progression to massive bacterial growth; virulence factors cause intravascular coagulation subcutaneous hemorrhage and purpura – black plague
Pneumonic
– infection localized to lungs, highly contagious; fatal without treatment
Diagnosis, Treatment and Prevention of Plague
Diagnosis depends on history, symptoms, and lab findings from aspiration of buboes

Treatment: streptomycin, tetracycline, or chloramphenicol

Killed or attenuated vaccine available

Prevention by quarantine and control of rodent population in human habitats
Haemophilus meningitis:
Haemophils influenza
Tiny gram-negative pleomorphic rods

Fastidious, sensitive to drying, temperature extremes, and disinfectants
None can grow on blood agar without special techniques – chocolate agar
Require hemin, NAD, or NAD
Can only grow within human cells
agent of acute bacterial meningitis
Also may cause; epiglottitis, otitis media, sinusitis, pneumonia, and bronchitis
Haemophilus meningitis: transmitted, prevention, treatment, signs and symptoms
Transmitted through discharges from nasopharynx
Similar to meningococcal meningitis
Symptoms and signs:
Fever, vomiting, stiff neck, neurological impairment
Treatment:
Combination of chloramphenicol and ampicillin is usually effective
Untreated cases have 90% fatality rate, but even with prompt diagnosis and treatment, 33% of children sustain residual disability
Prevention:
Outbreaks in families and day cares may necessitate rifampin prophylaxis of contacts
Subunit vaccine available, often delivered with DTaP
Syphilis: Treponema Pallidum
Causes Syphilis
Human is the natural host
Extremely fastidious and sensitive; cannot survive long outside of the host
sexually transmitted and transplacental
Genus Treponema
Thin, regular, coiled cells

Live in the oral cavity, intestinal tract, and perigenital regions of humans and animals

Pathogens are strict parasites with complex growth requirements

Require live cells for cultivation
Stages of Syphilis
Primary:
Spirochete binds to the epithelium, multiplies, and forms a chancre
Fluid from the chancre is highly contagious
Chancre spontaneously heals as the spirochete moves into the blood
Secondary
Spirochete is multiplying in the bloodstream
Rash forms on the skin, palms and soles with fever, headache and sore throat
The rash disappears spontaneously
Latency/Tertiary
If left untreated, tertiary syphilis forms
Damage to multiple tissues and organs
Cardiovascular and Neuromuscular
Syphilis Diagnosis and Testing
Stages of syphilis can mimic other diseases

Consider symptoms, history, microscopic, and serological testing
RPR, VDRL, FTA-ABS

Treatment: penicillin G
Lyme Disease:Borrelia burgdorferi
Complex lifecycle involving mice and deer and transmission by ticks
Acquired by tick bites
Nonfatal, slowly progressive syndrome that mimics neuromuscular and rheumatoid conditions
50-70% get bull’s eye rash
Fever, headache, stiff neck, and dizziness
If untreated can progress to cardiac and neurological symptoms, polyarthritis
Treated with tetracycline or amoxicillin
Campylobacteriosis: Campylobacter sp.
Slender, curved, or spiral bacilli, often S-shaped or gull-winged pairs

Polar flagella

Common residents of the intestinal tract, genitourinary tract, the oral cavity of birds and mammals

Most important:
Campylobacter jejuni
Campylobacter fetus
Campylobacter jejuni: Bacterial
Gastroenteritis
Important cause of bacterial gastroenteritis
Transmitted by beverages and food
Reach mucosa at the last segment of small intestine near colon; adhere, burrow through mucus and multiply
Heat-labile enterotoxin CJT stimulates a secretory diarrhea like that of cholera
Symptoms of headache, fever, abdominal pain, bloody or watery diarrhea
Treatment with rehydration and electrolyte balance therapy
Rickettsia Genus
Small obligate intracellular parasites
Gram-negative cell wall
Nonmotile pleomorphic rods or coccobacilli
Ticks, fleas, and lice are involved in their life cycle
Bacteria enter endothelial cells and cause necrosis of the vascular lining – vasculitis, vascular leakage, and thrombosis
Rocky Mountain Spotted Fever: Rickettsia rickettsi
transmitted
Rickettsia rickettsii is transmitted to humans through a tick bite and is the most common rickettsial infection in North America
Rocky Mountain Spotted Fever: signs, treatment, and prevention
First symptoms are fever, chills, headache and a spotted rash appears in days
If untreated central nervous system can become involved and fatality rates are 20% if untreated
Requires immediate treatment, even in suspected cases
Diagnosed by analyzing for rickettsias in tissue biopsy or blood
Treated with tetracycline or chloramphenicol
Prevention:
Protective clothing, insect repellant
New vaccine has shown some success in protecting at-risk individuals
Chlamydial urethritis: Chlamydia trachomatis
Human reservoir and 2 strains can infect humans:

Trachoma – attacks the mucous membranes of the eyes, genitourinary tract, and lungs
Ocular trachoma – severe infection, deforms eyelid and cornea, may cause blindness
Inclusion conjunctivitis – occurs as baby passes through birth canal; prevented by prophylaxis
STD – second most prevalent STD; urethritis, cervicitis, salpingitis (PID), infertility, scarring
Lymphogranuloma venereum – disfiguring disease of the external genitalia and pelvic lymphatics
Chlamydial urethritis: symptoms,diagnosis, treatment, and prevention
Symptoms: urethritis, cervicitis, salpingitis (PID), infertility, scarring
Diagnosis: often requires examination of host cells, culturing analyses, or molecular analyses
Treatment: intracellularly acting antibiotics (tetracyclines and azithromycin)
Prevention: condom use; pro-phylactic treatment of partners of infected individuals
The Chlamydiaceae Family
Small, gram-negative, obligate intracellular parasites
Alternates between:
Elementary body – small metabolically inactive, extracellular, infectious form released by the infected host
Reticulate body – noninfectious, actively dividing form, grows within host cell vacuoles