Gram Positive Rods

Question 1

Corynebacterium diptheriae

1. Mech of pathogenesis
2. Key clinical features of disease
3. Method of lab isolation
4. Treatment and prevention

Answer 1

Note: Aerobe
Note: “Necrotic white membrane on soft palate and tonsils + upper airway and larynx obstruction (heavy snoring)” + bull neck
1. Epidemiology: Only passed hume to human through respiratory droplets or contact. Only present in regions lacking vaccination
2. Mech of pathogenesis: Has AB setup TOXIN (b stays at membrane, A is the actual toxin that enters cell. A specifically attacks Elongation Factor 2 (EF-2)…you need this to work in order for peptide in ribosome to move along and generate an open space for the next peptide. A toxin stops this movement, ending peptide synth. A toxin enters cell by binding to CD-9/Heparin-binding/EGF. Binds to EF-2, and stops it. Stupid potent. Those low in Iron are more susceptible (STEP1).)
3. Key clinical features of disease: No spores. Sore throat, inflammation. The necrotic tissue (gray debris…forms pseudomembrane) is at the back of the throat since this is where the bacteria resides and kills cells. Heart, liver, kidneys are susceptible to damage if A toxin gets to blood stream. Also note enlarged neck due to lymph nodes swelling. Airway can narrow as a result of inflammation, and this can lead to asphyxiation (dying due to lack of O2.). When the A toxin reachs the heart, you will note rheart rhythms (due to diptheria myocarditis)…can kill you due to heart failure.
4. Method of lab isolation: Tinsdale’s agar (has potessium tellurite). Makes distinct black colonies with halo around it. ON gram stain, bigger at one end (club shaped hence “coryneform”), several microns long. Note: No toxin = safe bacteria
5. Treatment and prevention: Neutralize toxin (diphtheria anti-toxin) and remove the bacteria (Erythromycin pr penicillin). Prevent overall with vaccination.

Question 2

Bacillus anthracis

1. Mech of pathogenesis
2. Key clinical features of disease
3. Method of lab isolation
4. Treatment and prevention

Answer 2

Note: Bacillus cereus is similar bacteria. Also from food borne illness, in which case the issue is person ate the toxin, usually found in rice…cooking rice activates the spores, allowing them to make the toxin.
1. Epidemiology: Acquired from livestock (sheep, goat, etc). Few cases not since animals are vaccinated. The spores can be weaponized and then spread through inhalation. This is then eaten by macrophages, triggers inflammation, and can be rapidly fatal
2. Mech of pathogenesis: A binding partner binds to (Edema factor (works by increasing cAMP) and Lethal Factor (Causes cell death, leads to necrosis) (A). Without the binding partner (B), neither of these can work. Edema portion screws up heart.
3. Key clinical features of disease: Spores. Crap tone of fluid buildup around lung and mediastinum + nodules. 95% of cases are cutaneous (skin eschar if person does not handle animals). Only expect pustule formation under skin is transported via contact. If the spores are breathed in, expect hemorrhagic lymphadenitis (tissue necrossis and edema, both caused by the toxin). Death within 1 to 2 days
4. Method of lab isolation: Blunt-ended bacilli in long chains (Bamboo). Spores in the centers of these bamboo. Comma shape on blood agar (taile present), Not motile either
5. Treatment and prevention:
(If infection by skin) doxycycline, ciproflaxin, erythromycin
(If inhalation) Ciprofloxacin + cllindamycin

Question 3

Listeria monocytogenes

1. Mech of pathogenesis
2. Key clinical features of disease
3. Method of lab isolation
4. Treatment and prevention

Answer 3

Note: Aerobe
Note: “Gram stain showed pleomorphic short gram positive rods and coccobacilli, which exhibited a characteristic tumbling motility in hanging drop preparation”
Note: monocytogenes is the only Listeria that affects humans
Note: Second common on this list (FOOD BORNE ILLNESS)
Note: Surives in a tone of condition types, including hot vs cold
1. Epidemiology: More susceptible to immunocompromise, infants, neonates. Weak against adults.
2. Mech of pathogenesis: Enters GI after ingested. Attached to epithelial cells. stays there and spreads cell to cell. Specifically enters macrophage, incorporates into phagolysosome, produces listeriolysin O (creates pore into phagolysosome to allow for escape into cytoplasm of epithelial cell). Once in cytoplasm, assembles actin to create filament tail for meovement.to macrophage surface. Now is able to go from cell to cell without exiting the cell into the lumen. Overall: cell -mediated immunity
3. Key clinical features of disease: No spores. In adults, expect gastroenteritis with low-grade fever. Immunocompromised/kiddies/pregnant women patients suffer meningitis or bacteremia. Pregnant woman get flu-like symptoms and/or preterm delivery. Baby born, if still live, has rave rash. Common cause of neonatal meningitis
4. Method of lab isolation: Tumbling motility in agar + catalase positive + “umbrella motility” in semi-solid sutrient agar. Looks like strep, but the catalase pos helps knock that option out.
5. Treatment and prevention: Ampicillin in conunction with gentamicin

Question 4

Clostridium perfringens

1. Mech of pathogenesis
2. Key clinical features of disease
3. Method of lab isolation
4. Treatment and prevention

Answer 4

“Gas ganggrene”

1. Epidemiology: Found in vagina and large intesting and skin. Spores = ubiquitous.
2. Mech of pathogenesis: Makes alpha Toxin (phospholipase C within it, which separates glycerol backbone from polar head, damaging cell membranes of all cell types. Also has sphingomyelinase activity which breaks down sphingomyelin), which lysis wbcs, rbcs, epithelial cells, and platelets, blocking th ecapillaries and cutting off blood flow. Ultimately leads to tissue necrosis. C. perfringens also makes DNase and hyaluronidase (breaks down tissue). But she really want you to know alpha toxin.
3. Key clinical features of disease: Spores. spore forming, anaerobes, gram pos rods, ubiquitous, found in animal intestinal tract. these guys make the notable toxins (gas gangrrene, tetanus, botulism.). They are all grown on blood agar in like a sealed jar. can have single or double zone of hemolysis (c, perfrinens has double zone.). can ferment sugar or digest proteins. This is how they destroy human tissue. Generally, expect Crepitus (air in soft tissue) and progressive necrosis to soft tissue. For this particular one, usually caused by spores entering a traumatic injury, placing the spore into anaerobic environment. if ingested, leads to food poisoning without fever. In case of Enteritis necroticans toxin, will literally necrotize the bowel. A special case is clostridial endometritis (complication which can screw up baby and lead to abortion). Incubation period: less than 24 hours.
4. Method of lab isolation: Rod shaped, non motile, gram pos. HAS DOUBLE ZONE HEMOLYSIS on blood agar
5. Treatment and prevention: Aggressive surgical debreidment in high O2 environment. Hyperbaric O2 therapy. Antibiotics is after. you really need surgery tho.

Question 5

Clostridium botulinum

1. Mech of pathogenesis
2. Key clinical features of disease
3. Method of lab isolation
4. Treatment and prevention

Answer 5

Note: The most toxic toxin. period. More than Cyanide. 1 gram can kill 1.5 million people. Issue is specifically the toxin.

1. Epidemiology: Spores foun world wide in anaerobbic environment. highly resistant to heat, acid, high salt.
2. Mech of pathogenesis: No fever. Presents as cranial nerve dysfunction. SYMMETRIC neurologic effects. You’ll see double or blurred vision. Symmetric descending weakness. Ultimately leads to respiratory arrest. Responsiveness is preserved. HR is normal/slow and BP is normal. In infants, it presents as hypotonia. They were given honey with botulism spores. Leads tot he baby’s hypotonia (floppy baby)
3. Key clinical features of disease: Spores. Neuromuscular paralysis. Has a toxin, containing domains A, B, and E. Parts B and E are used for entry, A is the toxin. Toxin is ingesgted, then absorbed through the gut, binds to postynaptic PARAsympathetic nerves. Does not cross bbb. Most of activity is at Motor Neuron End Plates. Botulism toxins works by reaching snare proteins to gain access to the Ach vessicles in postynaptic cleft. It legit clips off the snare protein, preventing the Ach vesciles form docking and ending ability for Ach to be released in neuro conduction. No Ach = no muscle contraction. Snare cutting is permanent. Only way to overcome it is to grow a whole new postsynaptic terminal and synaps (6 months.). DOes not affect adrenergic or sympathetic nerves. Degree of illness of patient = how much toxin did they ingest. Vaccuum packed/canned and alkaline foods are more susceptible. Foods being eaten without being cooked is also susceptible. HONEY is PRIME susceptibilitys.
4. Method of lab isolation: anaeroibic identification,. Use mouse bioassay
5. Treatment and prevention: Treat with immediate antitoxin (Heptavalent (A-G) horse botulism immune serum…binds the toxin and prevents whatever is available from getting into the nerve terminals. Use penicillin to prevent additional muscle nerve loss.

Question 6

Clostridium tetani

1. Mech of pathogenesis
2. Key clinical features of disease
3. Method of lab isolation
4. Treatment and prevention

Answer 6

1. Puncture wound + soil exposure. Toxin is taken up by motor neurons, where problem occurs.
2. Mech of pathogenesis: Toxin at the wound site. Sinlge gene product. Toxin = tetanospasmin (neurotoxin). Toxin gets to CNS and makes way to cell body of motor neuron. Blocks release of GABA from inhibitory intraneuron. End result: the motor neuron is continuously firing, not disabled like that of botulism.
3. Key clinical features of disease: Spores. Muscle spasm and contractions. “Spasmic paralysis”. Early stage = LOCK JAW (jaw muscles a stopped). Patients also can get restlessness or sweating or increased heart rate. Spasm contractions are painful. Opisthotonos position.
4. Method of lab isolation: Clinical presentation. Endospores located at one end (racquet)
5. Treatment and prevention: Human tetanus hyperimmune globulin in order to prevent the remaining toxin from binding to the intraneuron…upon binding it’s too late. Infection of the bacteria tetani DOES NOT CONFER IMMUNITY. Get new vaccine booster for the TOXIN (confers immunity) every 10 years.

Question 7

Clostridium difficile

1. Mech of pathogenesis
2. Key clinical features of disease
3. Method of lab isolation
4. Treatment and prevention

Answer 7

Note: Hospital acquired infection associated with antibiotic use. Most common on this list.

1. Epidemiology: Nosocomial pathogen (originates in hospital). Spore acquired fecally/orally.
2. Mech of pathogenesis: Damages epithelial cells in colon. More toxin = more colon damage.
3. Key clinical features of disease: Spores. Has AB toxin setup…from inactivated Rho family protein. expect pseudomembrane presentation in the colon just like disphtheria in the pharynx. expect watery diarrhea. Can also cause fuliment colitis, which makes patients very ill.
4. Method of lab isolation: Hard to culture. Hates O2. Use blood agar. Nagative in catalase, indole, and urease. Leaves body in spore form.
5. Treatment and prevention: Prevention. Treat with probiotics and antibiotics vancomycin or fidaxomicin. USE CLINDAMYCIN!!!!!!!

Question 8

Propionibacterium acnes

1. Mech of pathogenesis
2. Key clinical features of disease
3. Method of lab isolation
4. Treatment and prevention

Answer 8

1. Mech of pathogenesis
2. Key clinical features of disease: acne
3. Method of lab isolation
4. Treatment and prevention