Microbiology: Clostridium, Bacillus, Corynebacterium

Front 1

Define the staining characteristics, morphology, unique structures, and unique nutritional or cultural requirements of CLOSTRIDIUM.

Back 1

Clostridium is:
gram + bacilli
Spore forming
Obligate anarobe
Culture on blood or thioglycolate broth

Front 2

What is the molecular mechanism of tetanus toxin? What is the presentation?

Back 2

C. tetani has two virulence factors:
Tetanolysin and tetanospasmin

Tetanospasmin is actively released and bind to the anterior horn cells of the peripheral nerves and blocks inhibitory transmitters.

Causes spastic paralysis, trismus, generalized rigidity and death from respiratory interference.

Front 3

What is the mechanism of botulism toxin? What is the presentation?

Back 3

C. botulinum produces a protein neurotoxin. It blocks cholinergic transmission at the NMJ. 1ug is lethal.

Causes flaccid paralysis. Patient will be weak, dizzy, constipated with urine retention, diplopia, dysphagia. Generally, muscles do not work.

Front 4

Describe the pathogenesis of gas gangrene. What organism causes it?

Back 4

C. perfringens

Gas gangrene is caused initially by tissue anoxia and accumulation of lactic acid and a decrease in oxygen radical potential in the tissue. This allows the organism to grow and release toxin creating a perpetuating anaerobiosis and myonecrosis.

Front 5

What is the etiology of tetanus? What is the source of infection?

Back 5

C. tetani

From soil borne spores

Front 6

What is the etiology of botulism? What is the source of infection?

Back 6

C. botulinum

Soil is the reservoir, but the source of infection is usually food.

Front 7

What is the etiology of gas gangrene? What is the source of infection?

Back 7

C. perfringens

Reservoirs are soil and the GI tract, and transmission is via wound contamination.

Front 8

What is the etiology of PMC and AAD? What is the source of infection?

Back 8

C. difficile

Reservoir is soil and 5% are natural carriers causing autogenous infection

Front 9

Why do we vaccinate for tetanus and not for botulism? What is the antigen in the tetanus vaccine?

Back 9

The tetanus vaccine is a DPT vaccine (diphtheria, pertussis, tetanus). The antigen is the tentanus toxin.

Tetanus is more common.

Front 10

Why do natural infections with tetanus and botulism not confer immunity?

Back 10

Small amounts of the natural toxin are enough to kill the patient, but not enough for an immune response.

Front 11

How is tetanus diagnosed? What is the therapy for tetanus?

Back 11

Diagnosis is done on exudates and direct exam showing gram positive bacilli. Cultured on anaerobic blood agar or thioglycolate broth.

Biochemical identification is possible.

Treat ASAP. Therapy is metronidazole with debridement of the wound. Antitoxin and curare-like drugs are used to release tetanus.

Front 12

How is botulism diagnosed? What is the therapy for botulism?

Back 12

Diagnosis is done with a food or feces specimen. Culture is done on anaerobic blood agar or thioglycolate broth.

Treat ASAP. Therapy is the trivalent antitoxin (ABE)--has to be given before symptoms appear. Must give respiratory support.

Front 13

How is gas gangrene diagnosed? What is the therapy for gas gangrene?

Back 13

Diagnosis can be done on pus, blood, tissue or food specimens. Direct exam shows plump gram positive rods. Can be cultured on anaerobic blood agar or thioglycolate broth. Biochemical identification is possible. NOTE: a positive report must match clinical signs.

Treat ASAP. Treat with debridement of lesions, penicillin and hyperbaric oxygen. Antitoxin is polyvalent.

Front 14

How is PMC diagnosed? What is the therapy for PMC?

Back 14

Diagnosis is done with a stool sample. Direct examination is useful when pseudomembranous exudate is present. Can be cultured on anaerobic blood agar or thioglycolate broth. ELISA will detect ToxA and microtiter cytotoxicity assay to detect ToxB.

Treat by replacement of fluids and vancomycin.

Front 15

Describe the genetics of toxin production for tetanus and botulism.

Back 15

Tetanus toxin is plasmid regulated

Botulism toxin is plasmid, phage, and chromosome coded.

Front 16

What is the pathogenesis of PMC?

Back 16

Following a course of antibiotic use, C. difficile will grow and release ToxA and ToxB, the colon will respond to the toxemia. Patient gets leukixytic infiltration, fibrin and mucus release from the membranes.

Front 17

What are the exotoxins of C. difficile? What are the mechanisms?

Back 17

Toxin A: enterotoxin which activates phospholipase A2. Is a chemotactic for PMN causing cytokine release in the lumen of the ileum. Also disrupts tight junctions, increasing permiability resulting in diarrhea.

Toxin B: cytotoxin which is lethal to tissue. Causes actin to depolymerize, destroying cell cytostructure.

Front 18

Describe the stain reaction, morphology, unique features, and growth requirements of BACILLUS ANTHRACIS.

Back 18

Gram + bacilli
Spore forming
encapsulated
facultative anaerobic

Cell wall have D-glutamic acid polypeptide and polysaccharide somatic antigen.

Front 19

What are the various routes of transmission for B. anthracis?

Back 19

Cutaneous
Inhalation
Ingestion

Front 20

Describe the pathogenesis of B. anthracis.

Back 20

Cutaneous lesion: spores under the dermis, lead to replication and toxin production, forming eschar and necrosis.

Inhalation: spore a phaged, taken to lymph nodes, leads to germination, replication, and toxemia.

Ingestion: Germination, replication, toxemia of submucosa leading to necrosis and ulceration of the gut.

Front 21

What chemotherapy is used to control anthrax?

Back 21

Treat with ciprofloxacin, but also penicillin and tetracycline. Penicillin and tetracycline resistance is not uncommon.

Control of disease with animal vaccinations in endemic areas.

Front 22

Describe the shape, arrangement, stain, sporulation, and unique growth requirements of CORYNEBACTERIUM DIPHTHERIAE.

Back 22

Gram + bacilli
non-spore forming
palisade or chinese letter forms

Non-motile and have metachromatic granules that are detected with Albert stain.

Culture on tellurite which inhibits the growth of gram negatives and normal URT flora.

Front 23

What is diphtheroid? Where are there found naturally?

Back 23

non-pathogenic Corynebacterium. Can be found in soil, water, plants, and food products. Also in the normal flora of the mucus membranes and skin.

Front 24

What is the mechanism of diphtheria toxin?

Back 24

Toxin has two fragments (A and B) and blocks protein synthesis by inactivating EF-2. Because EF-2 is slow the entire EF-2 population can be trapped.

Front 25

What are the biochemical and gene control mechanism for diphtheria toxin production?

Back 25

Toxin synthesis is regulated chromosomally by the diphtheria toxin repressor (DTxR). In the presence of high iron concentration the repressor will bind the operator and shut down toxin production.

Front 26

What is the relationship between the pseudomembrane, diphtheria toxin production, and pathogenesis?

Back 26

After 2-6 days of incubation, microbes will locally release exotoxin (pharynx) causing localized damage. This causes an exudative pharyngitis. Exudate turns into pseudomembrane made of bacteria, lymphocytes, plasma cells, fibrin and dead cells. Pseudomembrane can become a respiratory obstruction.

Front 27

What is necessary for the diagnosis of diphtheria?

Back 27

Toxigenicity testing.

Diagnosis must be made using Elek test for the presence of toxin. PCR can also test for the presence of the tox gene.

Front 28

What is the frequency of diphtheria?

Back 28

<100 cases reported annually

Front 29

What is the host and reservoir for diphtheria? How is it transmitted?

Back 29

Humans are the only known reservoir of diphtheria. It is transmitted via respiratory droplets and skin contact.

Front 30

How is diphtheria prevented? How are epidemics terminated?

Back 30

Infected are treated with antitoxin and the rest are vaccinated.