Lecture 20 Flashcards
genus bacillus
Gram +, endosperm forming, motile, rods, aerobic or facultative, catalase positive, soil and saprophytes
Bacillus anthracis 2 virulence
Block rods, central endospores, immunogenic and antiphagocytic polypepticle capsule
Makes anthrax exotoxin
Anthrax exotoxin
Bacillus anthracis
Edema, cell death, tissue destruction
Bacillus anthracis life cycle
Animals become infected via spores then spores germinate into vegetative cans inside the host
Bacillus anthracis made of infection
Animals and humans come into contact with shores and they germinate inside the host to form vegetative cells which release the anthrax exotoxin
3 types of anthrax
Cutaneous, gastrointestinal, inhalation anthrax
Cutaneous anthrax
Most common least dangerous, spores enter through cuts in the skin, inoculation site forms raised lesion called papule, papule erupts to form painless black lesion called eschar
Gastrointestinal anthrax
Rare but deadly, ingest spores via contaminated meat, causing acute inflammation of GI tract, nausea, fever, vomiting, blood, severe diarrhea
GI anthrax survival rate
50% if untreated, 60% if treated
Inhalation anthrax
Deadliest form, 99% mortality if untreated, spores inhaled into lungs, engulfed by macrophages and transported to lymph modes, causes pulmonary edema, internal hemorrhaging, shock, rapid death
Anthrax treatment
Antibiotics
Anthrax vaccine
Subunit vaccine for high risk groups
Bacillus cereus
Air and dust-borne, multiplies readily in cooked foods, can survive short heating, spores germinate and release enterotoxins at room temperature
Which cooked foods does bacillus cereus multiply on
Rice, potatoes, and meat dishes
Entorotoxins
Released by B. cereus cause food intoxication which leads to acute vomiting, nausea, abdominal cramps, and diarrhea
Symptoms disappear after 24 hours
Genus clostridium
Gram +, endospore forming rods, anaerobic, catalase negative
Genus clostridium found
As saprobes in the environment and some are commensals with humans and animals
Clostridium morphology
Terminal ovoid or round spores
Clostridium genus makes some of the
Most potent exotoxins that are some of the most poisonous substances on earth
Clostridium species cause
Wound and tissue infections, food intoxication
Clostridium perfringens
Large rectangular, spore forming, found in soil/dust/human animal feces
Clostridium perfringens endospores not
Usually seen in clinical specimens
Clostridium perfringens entrance and causes
Contaminated meat especially reheated stews and gravies
Causes food intoxication
Clostridium perfringens symptoms
Sub-acute watery diarrhea, severe abdominal cramping, no vomiting
Other form Clostridium perfringens
Spores introduced through anaerobic wounds germinate and release gas and alpha toxin
Alpha toxin
Released by clostridium perfringens, causes RBCs to rupture, edema, and tissue destruction
C. Perfringens and muscles
Does Myonecrosis (muscle death), during this process muscle carbohydrates are fermented and gas is released into the tissue causing gas gangrene
Gas gangrene symptoms
Edema, large bullae, crepitus (skin makes noises), tissue necrosis, fever, and shock
Rapidly fatal if untreated
Gas gangrene treatment
Debridement (surgical removal of tissue), amputation, large doses of antibiotics, and hyperbaric oxygen therapy
Clostridium difficile found
Normal resident of colon usually present in 4-15% of population
Clostridium difficile is a common
Nosocomial infection
C. Diff overgrowth associated with
Antibiotic use
C. Diff overgrowth causes
Antibiotic-associated/pseudomembrane colitis
First and second most common GI diseases in industrialized countries
- Salmonellosis
- Clostridium difficile
Half a million infections in the US each year
C. diff superinfection releases and causes
Exotoxins released causing diarrhea, inflammation, and intestinal damage giving rise to pseudomembranous colitis
Severe cases C. Diff
Death from intestinal perforation
C. Diff highest risk group
Nursing homes
C. Diff treatment
Removal of antibiotics in uncomplicated cases, stranger antibiotics in severe cases, and fecal transplantation
Clostridium tetani found
Resident of soil and GI tract of some animals
C. tetani resembles
Tennis racket or drumstick, terminal endosperm
C. tetani enterance
Spores enter through wound, deep implantation to germinate in anaerobic tissue
Usually deep muscles
C. tetani vegetative cells release
Teranospasmin the tetanus toxin which blocks muscle relaxation
Spastic paralysis
Tetanospasmin is released into tissue and absorbed by peripheral nerves and carried to target neurons in spinal column, inhibits muscle relaxation causing muscles to contract uncontrollably
Trismus
Spastic paralysis begins in jaw, trismus is jaw muscle spasms causing lock jaw
Risus sardonicus
Facial muscle spasms producing wry, mask-like grin
If spastic paralysis untreated
Paralysis descends, rigid back, death from paralysis of respiratory muscles
Clostridium tetani treatment
TIG tetanus immune globulin the antitoxin immunotherapy
Respirator and tracheostomy may be needed
Tetanus vaccine
DTap vaccine containing teanus toxoid
Booster recommended every 10 years
Clostridium botulinum found
Soil, water, intestinal tract of animals
Clostridium botulinum under anaerobic conditions
Vegetative cell releases the most potent microbial toxin, botulinum toxin
Botulism
Intoxication associated with eating canned or preserved foods
3 types of botulism
Botulinum food poisoning, infant botulism, wound botulism
Botulism infection process
Ingested or secreted botulism toxin travels to the neuromuscular junctions of skeletal muscles, blocks release of acetylcholine and keeps the muscle from contracting leading to flaccid paralysis
Botulinum food poisoning results from
The improper canning of food especially homemade canned vegetables, smoked meats, cheese spreads
Spores germinate in can producing botulinum toxin
Botulinum food poisoning incubation
1-2 days
Botulinum food poisoning affects
Muscles supplied by the cranial nerves first causing eyelid drooping, double vision, loss of facial expression, dry mouth, difficulty chewing and swallowing, followed by flaccid paralysis
Flaccid paralysis
Floppy, relaxed
Infant botulism occurs in
Infants less than one year old, most common form in US
Infant botulism entrance
Infant ingested spores in dust or honey
Infant botulism infection process
Immature GI tract allows spore germination and growth of vegetative cells
Infant botulism symptoms
Constipation, generalized weakness, weak crying, poor feeding, lethargy, loss of head control (floppy baby syndrome) and possible respiratory arrest
Wound botulism
Spores enter a wound or puncture
Wound botulism symptoms
Similar to food botulinum muscles of face supplied by cranial nerves
Botox
Injects super-diluted botulinum toxin into wrinkled areas to create controlled muscle weakening
Wears Off, repeat every 4-6 months
Clostridium botulinum treatment
Antitoxin must be administered early for greatest effectiveness, patients managed with respiratory and cardiac support systems
Botulism prevention
Proper canning techniques, adequate pressure cooking achieves sterilization, throw away bulging cans, botulinum toxin inactivated at 100°C
Listeria monocytogenes
Gram +, rod, facultative anaerobe
Listeria monocytogenes can grow in
Acidic conditions, high salt, wide temp range including cold growth
Listeria monocytogenes found
Soil and water mainly
Animals, plants, and food are secondary sources of infection
Listeriosis
Infection from listeria causing gastroenteritis leading to food poisoning from refrigerated foods usually unpasteurized milk or cheeses, deli meats, or unwashed produce
Listeria can
Cross the placenta or infect babies during delivery causing neonatal septicemia and meningitis
Corynebacterium diphtheriae
Gram positive bacilli, irregular shaped and pleimorophic
Club-shaped
Non-motile, grows best with oxygen
Corynebacterium found
Plants and animals and colonize the skin and mucous membranes of humans
C. Diphtheriae reservoir
Humans only through respiratory spread
C. Diphtheriae etiologic agent
Diphtheria
Diphtheria most common
Children from 1-10 yrs old non-immunized
1st stage corynebacterium dip
Local, primary infection in the upper respiratory tract
2nd stage corynebacterium dip
Toxin production and toxemia
Virulence of corynebacterium dip due to
Diphtheria exotoxin only produced by lysogenic strains
Diphtheria exotoxin causes
Exudative pharyngitis which evolves into a thick pseudomembrahl
Pseudomembrane components
Dead cells, fibrin, bacteria, lymphocytes, gray pigment
Pseudomembrane can cause
Suffocation by obstructing the air way
Diphtheria toxin can diffuse
Into neck tissue causing edema so the patient appears bull-necked
Diphtheria spread
Toxin doesn’t invade deeper than epithelial but disseminated
Then damages heart causing myocarditis
Diphtheria treatment
Antibiotics and diphtheria antitoxin
Mycobacteria genus
Gram +, irregular shaped bacilli, long filamenteus
Acid-fast bacilli (afb)
Strict aerobe
Mycobacteria grow
Well on simple nutrients/media but slower compared to other bacteria
2 mycobacteria species of medical importance
Mycobacterium tuberculosis
Mycobacterium leprae
Mycobacterium TB virulence
No exctoxins/enzymes, cord factor (waxes) prevent destruction by phagocyte lysosomes
Cord factor contributes
To serpentine cord formation
Mycobacterium TB transmission
Fine respiratory droplets
TB stats
1/4 world population infected, 1-2 million deaths a year, leading killer of HIV infected worldwide
Primary tubereulosis
10 cells, bacilli phagocytized by alveolar macrophages multiply intracellularly
Weeks later cell-mediated immune response form tubercles
Secondary tuberculosis
Tubercles with masses of bacilli expand and drain into the bronchial tubes and upper respiratory tract
Symptoms worsen violent cough, green or bloody sputum, low fever, night sweats, weight loss, fatigue, chest pain
Extrapulmonary tuberculosis
Deactivation of bacilli allows them to disseminate rapidly to extrapulmonary sites like kidneys, bones, brain genital tract
High mortality
Treatment for all TB stages
Multidrug therapy lasting from 6-24 months
TB vaccine
Only outside the US, live attenuated BCG vaccine
Mycobacterium leprae
Causes leprosy, HanSen’s bacillus, strict parasite, can’t culture
Slowest growing of all species
Mycobacterium leprae infection
Direct contact transmission, not very contagious, multiplies in macrophages of skin and spreads to nerves
2 forms of leprosy
Tuberculoid leprosy
Lepromatous leprosy
Tuberculoid leprosy
Superficial infection with shallow skin lesions containing few bacilli
Damage to nerves causes loss of pain perception
Easily treated
Lepromatous leprosy
Deeply modular infection causing severe disfigurement to face and extremities
