PATH Exam

virulence plasmids

virulence plasmids

possessed by pathogenic species

saprophytic

most members of Bacillus genus; organisms prevalent in soil, water, air, and on vegetation

Bacillus insect pathogen

B. thuringiensis

Bacillus

large aerobic, gram + rods that occur in chains

B. cereus

can grow in foods; cause food poisoning; may produce disease in immunocompromised humans

food poisoning produces

enterotoxins (diarrhea); emetic toxins (vomiting)

principle pathogen of Bacillus genus

B. anthracis

B. anthracis

causes anthrax

typical bacillus organisms

long chains; form spores at the center

B. anthracis colonies

round; “cut glass” appearance in transmitted light; hemolysis is uncommon

bacillus species where hemolysis is common

B. cereus, saprophytic bacilli

bacillus growth characteristics

spores are resistant to environmental changes; may persist for years on dry earth

sterilizing anthrax spores

autoclaving or irradiation

anthrax

primarily a disease of herbivores; farm animals

how humans get anthrax

contact with infected animals or their feces

anthrax portal of entry in animals

mouth and GI tract

cutaneous anthrax

entry of spores through injured skin

GI anthrax

spores in mucous membranes

inhalation anthrax (woolsorters’ disease)

inhalation of spores into the lungs

injection anthrax

outbreaks among those injecting heroin that has been contaminated with anthrax spores

what happens when anthrax is in the body

spores germinate at entry site, growth of vegetative organisms causes gelatinous edema and congestion

how bacilli spreads

lymphatics to the bloodstream, then multiply in the blood and tissues

anthrax virulence factors

capsule; anthrax toxins

B. anthracis capsule

gene is present on plasmid, pXO2

polyγD glutamic acid capsule (B. anthracis)

antiphagocytic

three proteins in anthrax toxins

protective antigen (PA), lethal factor (LF), edema factor (EF)

protective antigen (PA)

binds to specific cell receptors; forms a membrane channel allowing EF and LF entry

edema factor (EF)

adenylate cyclase; forms edema toxin with PA; responsible for cell and tissue edema

lethal factor (LF)

forms lethal toxin with PA; major virulence factor and causes death of infected animals and humans; impairs innate and adaptive immunity

where anthrax toxin genes are encoded

pXO1

anthrax clinical findings

95% of cases are cutaneous, 5% are inhalation; GI is very rare (usually when people eat infected animal meat)

injection anthrax characterizations

extensive, painless, subcutaneous edema

GI anthrax characterizations

animals aquire through ingestion of spores; rare in humans; abdominal pain, vomiting, bloody diarrhea

inhalation anthrax characteristics

hemorrhagic necrosis and edema of mediastinum; possibly hemorrhagic pleural effusions, cough, sepsis, bowel ulceration

cutaneous anthrax characteristics

usually on exposed surfaces (arms, hands, face, neck)

as many as 20% of cutaneous anthrax patients

may experience sepsis; consequences of systemic infection (including meningitis) and death

examined specimen of cutaneous anthrax

fluid or pus from a local lesion

examined specimen of inhalation anthrax

blood, pleural fluid, and cerebrospinal fluid

examined specimen of GI anthrax

stool or other intestinal contents

animals that should be annually vaxxed against anthrax

animals that graze in known anthrax districts

types of b. cereus

emetic type, diarrheal form

emetic B. cereus

food poisoning from fried rice, milk, pasta; produces toxins that cause disease; manifested by nausea, vomiting, abdominal cramps, diarrhea; recovery within 24 hours

B. cereus commonly contaminates

rice

diarrheal B. cereus

food poisoning from meat dishes/sauces; incubation period of 1-24 hours; profuse diarrhea, abdominal pain, cramps; spores secrete one of three enterotoxins that induce fluid accumulation

B. cereus causing eye infections

introduced to the eye by foreign bodies associated with trauma; ex. endophthalmitis, severe keratitis

B. cereus causing localized infections

wound and systemic infections; ex. endocarditis, catheter-associated bacteremia, central nervous system infections, osteomyelitis, and pneumonia

clostridium species

large, gram positive spore forming anaerobic motile bacilli

clostridia spores

usually wider than diameter of the rods; placed centrally, sub-terminally, terminally

clostridia hemolysis

most produce a zone of beta-hemolysis

clostridium botulinum

causes botulism; found in soil, animal feces; seven varieties of toxins (A-G)

Types A, B, E, F (c. botulinum)

principle causes of human illness

Types A and B (c. botulinum)

associated with variety of food

Type E (c. botulinum)

fish products

Type C (c. botulinum)

limberneck in birds (Leg weakness that progresses to flaccid paralysis of the legs, wings, neck, and eyelids)

Type D (c. botulinum)

botulism in mammals

Type G (c. botulinum)

not associated with disease

botulinum toxin

absorbed from gut, enters blood stream, binds to motor neuron receptors; causes lack of muscle contraction, paralysis; usually ingested by contaminated food

foodborne botulism

most cases; intoxication resulting from
the ingestion of food in which C. botulinum has grown and produced toxin

wound botulism

tissue contamination with spores; primarily
in injection drug users

infant botulism

usually from honey

inhalation botulism

very rare; toxin enters respiratory tract

clostridium tetani

tetanus; found in soil, feces of horses and other animals; several types (distinguished by flagellar antigens); remains strictly localized in an area; causes rigidity, convulsive spasms of skeletal muscle

tetanus

incubation period of 3-21 days; 30% fatality rate; toxin spreads via lymphatic and vascular system affecting motor neurons; lock jaw is usually first symptom; muscle rigidity with reflex spasms can cause fractures, tendon ruptures, respiratory failure; death due to respiratory failure, cardiovascular instability

c. tetani toxins

tetanolysin, tetanospasmin produced by spore germination

tetanolysin

hemolysin; no pathogenic consequence

tetanospasmin

peptide responsible for tetanus

most common invasive disease causing clostridia

C. perfringens (90%)

how spores reach tissue in invasive clostridial infections

contamination of traumatized areas (soil, feces), from intestinal tract

C. perfringens and food poisoning

caused by an enterotoxin of C. perfringens; usually grown in meat dishes; intense diarrhea in 7-30 hrs

gas gangrene (myonecrosis)

lethal infection of soft tissue; rapid progressive gangrene of injured tissue, produces foul-smelling gas

number of infection causing Clostridium species

30

gangrene cause

blood flow to a large area of tissue being cut off.; affected skin turns greenish/blackish

severe diarrheal disease caused by C. difficil

pseudomembranous colitis

toxins C. difficil produces

toxins A and B

pseudomembranous colitis

severe diarrheal disease (watery or bloody); caused by toxins A and B; abdonimal cramps, leukocytosis, fever

corynebacteria

gram positive, aerobic, nonmotile, catalase positive, clubbed/irregularly shaped rods

corynebacteria species

more than 88; 53 have been recovered from human clinical infections

C. diptheriae

principal human pathogen of corynebacteria; causative agent of respiratory or cutaneous diptheria

C. diptheriae spreading

droplets or skin contact to susceptible individuals

C. diptheriae growth

bacilli grow on mucous membranes, skin abrasions; toxigenic bacteria begin producing toxin

wound/skin diphtheria

membrane forms on infected wound that fails to heal

c. diphtheriae pathogenicity

invasion or toxogenesis

invasion (c. diphtheriae)

colonization and bacterial proliferation of local tissues of the throat

toxigenesis (c. diphtheriae)

inhibition of protein synthesis in cells; destruction of epithelium of mucous membranes, grayish pseudo-membrane formed in tonsils, pharynx, larynx

toxigenesis (c. diphtheriae) distinct toxic damage

arenchymatous degeneration, fatty infiltration, and necrosis in heart muscle (myocarditis), liver, kidneys (tubular necrosis), and adrenal glands; may produce nerve damage

c. diphtheriae inflammation

if beginning in respiratory tract, sore-throat and low-level fever form

staphylococcus characteristics

gram-positive spherical cells (1 μm diameter); grapelike irregular clusters; nonmotile and non-sporeforming

S. aureus colonies

gray to deep yellow colonies with beta hemolysis

staphylococcus in normal microbiota

found on skin, respiratory and GI tracts

pathogenic staphylococcus

may cause abscesses, pyogenic infections, fatal septicemia; often hemolyze blood, coagulate plasma, produce variety of enzymes/toxins

pathogenic staphylococcus species

S. aureus, S. epidermis, S. lugdunensis, S. saprophyticus

staphylococcus species that account for 75% of infections

S. epidermis, S. lugdunensis, S. warneri, S. hominis

S. aureus

only coagulase + species; invasive properties; has Protein A; causes skin infection in form of boils, blisters, redness

streptococci

gram positive, spherical bacteria; forms pairs or chains; in normal flora or pathogenic

S. pyogenesis

beta-hemolytic human pathogen; associated with local or systemic invasion; produces capsule that resists phagocytosis

S. pyogenesis capsule

binds to hyaluronic-acid-binding protein present on human epithelial cells then
disrupts intercellular junctions

streptokinase

produced by many strains of group A beta hemolytic streptococci

hyaluronidase

splits hyaluronic acid

Deoxyribonucleases A, B, C, and D

degrade DNA facilitating the spread of
streptococci in tissue by liquefying pus

Streptolysin O

forms pores in host cell membranes, including neutrophils,
macrophages and epithelial cells leading to host cell death