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Triple I > Bacterial Pathogens > Flashcards

Bacterial Pathogens Flashcards

To learn Forgie's bugs.

1
Q

Haemophilus influenzae

A
  • Small gram negative bacilli.
  • LOS endotoxin.
  • Outer membrane protein (OMP) and fimbriae for adhesion.
  • IgA protease.
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2
Q

What is the difference between typable H. influenzae and non-typeable (ntHi) H. influenzae?

A

Typeable forms have a capsule which make them capable of bloodstream invasion. The capsule makes them resistant to phagocytosis. The ntHi lack this capsule and cannot cause bloodstream infection.

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3
Q

Which is the most dangerous type of H. influenza?

A

Haemophilus influenzae type B (HiB).

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4
Q

What are some of the clinical symptoms of typeable H. influenzae?

A
  • Usually result from HiB.
  • Bacteremia
  • Meningitis
  • Pneumonia (cough, fever, purulent sputum)
  • Cellulitis
  • Epiglottitis
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5
Q

What are some of the clinical symptoms of non-typeabe H. influenzae?

A

Nonencapsulated H. influenzae.

  • Sinusitis & otitis media
  • Pneumonia
  • Purulent conjunctivitis (pink eye)
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6
Q

How is H. influenzae diagnosed?

A

Bacterial cultures from blood, sputum, and CSF. H, influenzae requires factor V and X from RBC for growth. Must be cultured on chocolate agar.

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7
Q

What drugs would be given to treat H. influenzae?

A

Amoxicillin - Clavulanate
or
Cefotaxime / Ceftriaxone

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8
Q

Staphylococcus aureus

A
  • Gram positive cocci in clumps (grapes).
  • Aerobic
  • Protein A (prevent opsonization), coagulase, and catalase.
  • Hyaluronidase, staphylokinase, lipase, and protease.
  • Hemolysins, exfoliatin, enterotoxin, toxic shock (TSST-1).
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9
Q

What is the function of staphylokinase?

A

It breaks down blood clots allowing staphylococcus aureus to escape and spread from clots.

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10
Q

What does exfoliatin do?

A

It results in blistering on the skin known as “scalded skin syndrome”.

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11
Q

What does TSST-1 stand for? What bacteria causes it?

A

Toxic Shock Syndrome Toxin 1. It is released by staphylococcus aureus.

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12
Q

How is staphylococcus aureus infection diagnosed?

A

Swabs are taken from affected sites for gram stain and culture growth (Gram +ve cocci in bunches).

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13
Q

How is staphylococcus aureus treated?

A
  • Drain any abscesses.
  • Cloxacillin, first generation cephalosporins, clindamycin.
  • MRSA is typically treated with vancomycin.
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14
Q

Describe the possible clinical presentations of S. aureus.

A
  • 25% of people are asymptomatic carriers.
  • Direct infections (folliculitis, impetigo, cellulitis, furuncles, carbuncles, abscesses).
  • Bloodstream infections with abscesses forming due to seeding of distant sites.
  • Several toxin mediated syndromes (food poisoning, scalded skin syndrome, toxic shock syndrome).
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15
Q

How is S. aureus spread?

A

Through droplet or direct contact.

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16
Q

How is H. influenzae spread?

A

Through direct contact.

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17
Q

Streptococcus pneumoniae

A
  • Gram positive diplococci.
  • Aerobic
  • > 95 different polysaccharide capsules.
  • IgA protease & Adhesins
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18
Q

What are some of the clinical presentations of Strep. pneumoniae?

A
  • Pneumonia (fever, cough, purulent rusty sputum).
  • Meningitis
  • Otitis media (bulging gray or yellow tympanic membrane)
  • Sinusitis
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19
Q

How is Strep. pneumoniae diagnosed?

A

Clinically, X-Ray, sputum, CSF and blood for gram stain and culture.

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20
Q

How is Strep. pneumoniae treated?

A
  • High dose ampicillin or second generation cephalosporin.

- For meningitis vancomycin and cefotaxime should be given until CSF culture and sensitivity are returned.

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21
Q

Where is asymptomatic Strep. pneumoniae carried in humans?

A

The nasopharynx. Upto 50% of people are asymptomatic carriers of Strep. pneumonia.

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22
Q

Streptococcus pyogenes

A
  • Gram positive cocci in chains.
  • Aerobic
  • Hyaluronic capsule.
  • M protein, Protein F, DNase, hyaluronidase, SPE.
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23
Q

What are protein F, M protein, and SPE in the context of strep pyogenes?

A

Protein F: functions in adhesion.
M Protein: functions in adhesion and inhibits complement activation {MAJOR virulence factor}.
SPE: Strep pyrogenic exotoxin.

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24
Q

How is Strep. pyogenes spread?

A

Through direct contact or droplets.

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25
Q

Describe the clinical presentation of strep. pyogenes.

A
  • Superficial: Impetigo, erysipelas, pharyngitis.
  • Deep: Necrotizing fasciitis, bacteremia.
  • Post streptococcal syndromes: acute rheumatic fever, glomerulonephritis, scarlet fever.
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26
Q

What are two symptoms of scarlet fever?

A

Sandpaper rash and strawberry tongue.

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27
Q

What is a symptom of post strep glomerulonephritis?

A

Tea coloured urine.

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28
Q

How is strep. pyogenes treated?

A

Penicillin, amoxicillin, erythromycin, first generation cephalosporin, TMP/SMX, and clindamycin are all effective.

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29
Q

How is strep. pyogenes diagnosed?

A

Swabs for gram stain or culture. The primary reason for treating strep throat is to prevent rheumatic fever.

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30
Q

What are some symptoms of rheumatic fever?

A

Arthritis, carditis, subcutaneous nodules, erythema marginatum, and chorea (neurological disorder resulting in quick jerky movements of the face and shoulders).

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31
Q

Bordetella pertussis {Whooping cough}

A
  • Small gram negative bacillus.
  • Aerobic
  • Polysaccharide capsule.
  • Filamentous hemagglutinin, fimbriae and pertactin for adhesion.
  • PERTUSSIS TOXIN, adenylate cyclase toxin, tracheal toxin, dermonecrotic toxin, hemolysin.
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32
Q

What three stages present during most bordetella pertussis infections?

A

Catarrhal stage: Runny nose, low fever, cough.
Paroxysmal stage: coughing, mucous pooling in airways, fits of coughing {WHOOPING COUGH in children}.
Convalescent stage: Intermittent fits of coughing and possible secondary bacterial infections.

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33
Q

How does bordetella pertussis spread?

A

Droplet transmission between humans.

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34
Q

How is bordetella pertussis diagnosed?

A

Nasopharyngeal aspirate for DFA, PCR, and culture.

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35
Q

How would you treat bordetella pertussis?

A
  • Macrolides will reduce the duration of symptoms and infectivity of the host.
  • TMP/SMX
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36
Q

Clostridium botulinum

A
  • Gram positive bacillus.
  • Anaerobic.
  • Botulinum toxin and spore formation.
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37
Q

How is Clostridium botulinum spread?

A

Spores are found in soil and water and subsequently contaminate meats, vegetables, and fish.

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38
Q

How is C. botulinum diagnosed?

A
  • NO fever with descending symmetrical paralysis.
  • Normal sensation and consciousness.
  • Anaerobic cultures and toxin assay of serum, stool, and food.
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39
Q

How is C. botulinum treated?

A
  • Supportive care with artificial ventilation.
  • Trivalent antitoxin (against toxin types A,B,E).
  • Penicillin antibiotics are effective against wound and infant botulism.
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40
Q

How does C. botulinum present clinically?

A

1) Generalized botulism (intoxication).
- Muscle weakness, diplopia, difficulty swallowing, speech problems, symmetrically descending paralysis. No fever, no sensory issues, and normal LOC.
2) Wound botulism.
- Wound directly contaminated with spores causes paralysis of limb. May result in generalized botulism.
3) Infant botulism.
- Ingestion of spores followed by poor feeding and then paralysis.

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41
Q

Clostridium difficile

A
  • Gram positive bacillus.
  • Anaerobic
  • Exotoxins A & B.
  • Spore formation.
  • Flagella (H antigen)
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42
Q

How is C. difficile spread?

A

Through spores and fecal-oral transmission.

5% - 10% carry C. difficile asymptomatically.

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43
Q

How does C. difficile present clinically?

A

Pseudomembranous colitis may occur up to 10 weeks after an antibiotic course. Symptoms include (possibly bloody) diarrhea, fever, abdominal pain & cramping. Toxic megacolon may occur.

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44
Q

How is C. difficile diagnosed?

A

Diarrheal stool toxin assay & endoscopy for possible pseudomembranes.

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45
Q

How is C. difficile treated?

A

Stop offending treatments (antibiotics) and start oral metronidazole. Oral vancomycin is the secondary line of therapy.

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46
Q

Clostridium tetani

A
  • Gram positive bacilli.
  • Anaerobic
  • Tetanus toxin, spore formation, flagella (H antigen), and hemolysin.
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47
Q

How is Clostridium tetani spread?

A
  • Spores are found in soil and water. It may also be found in the GIT of both humans and animals.
  • Wounds or bites may inoculate the spores into damaged tissue.
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48
Q

How does Clostridium tetani present clinically?

A
  • Muscle spasm near the wound, 1-2 weeks later lockjaw or trismus occurs. Gradual involvement of other facial, and later body, muscles.
  • Neonatal tetanus has very high mortality and presents with fever, rigidity, and weakness.
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49
Q

How is Clostridium tetani diagnosed?

A

Strychnine poisoning is in the differential. Many patients will not remember the dirty wound. Dental infections may cause trismus but the dental infection can be found and other symptoms will not be present.

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50
Q

What is trismus?

A

Reduced opening of the muscles of the jaw - lockjaw.

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51
Q

How is Clostridium tetani treated?

A
  • Secure airway (cABC).
  • Strychnine blood level.
  • Wound history and possible debridement.
  • Immunization status.
  • Start TIG (tetanus immune globulin).
  • Tetanus toxoid vaccine.
  • Metronidazole
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52
Q

Corynebacterium diphtheriae

A
  • Gram positive club shaped bacillus.
  • Aerobic
  • Does not have a capsule.
  • Diptheria toxin (if infected with lysogenic phage).
  • Storage granules (containing phosphate for energy).
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53
Q

How is Corynebacterium diphtheriae spread?

A

Respiratory droplets of direct contact with skin discharge from an infected patient or carrier.

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54
Q

How does Corynebacterium diphtheriae present clinically?

A
  • Fever, malaise and a sore throat 2-4 days after exposure. If toxin is produced in susceptible host a gray membrane forms over the tonsils.Local inflammation and risk of asphyxiation.
  • 1-2 weeks after infection myocarditis, arrhythmia and demyelination of nerves causing paralysis and neuropathy may occur.
  • Skin infection and gray membrane over ulcers in those with poor hygiene.
55
Q

How is Corynebacterium diphtheriae diagnosed?

A
  • Throat swab for gram stain and culture.

- Toxin detection via PCR.

56
Q

How is C. diphtheriae treated?

A
  • Penicillin and erythromycin.
  • Antitoxin
  • Supportive care.
  • If diphtheria is suspected do not wait for culture results before beginning treatment.
57
Q

Which disease may present with gray membranes over the tonsils?

A

Diphtheria caused by Corynebacterium diphtheriae.

58
Q

Escherichia Coli

A
  • Gram negative bacillus with endotoxin.
  • Aerobic
  • Sometimes has a polysaccharide capsule.
  • Flagella (H antigen), pili, capsule (K antigen), exotoxin, acid resistant phenotypes.
59
Q

What antigen is typically associated with flagella?

A

The H antigen.

60
Q

How is E. coli transmitted?

A

Transmission is fecal oral.

61
Q

How does E. coli manifest clinically?

A
  • Hemorrhagic colitis: nausea, watery (bloody) diarrhea. A fever is rare.
  • Hemolytic uremic syndrome (HUS): 10% of those with EHEC develop HUS.
62
Q

What is hemolytic uremic syndrome (HUS)?

A
  • Further development of E. coli infection.
  • Caused by the action of shigatoxin on blood vessels.
  • Thrombocytopenia due to clots forming as a result of small vessel damage.
  • Anemia through hemolysis of RBC.
  • Blood vessel damage in the kidneys cause renal failure and uremia.
63
Q

What is uremia?

A

A raised level of urea and other nitrogenous waste in the blood.

64
Q

How is E. coli infection diagnosed?

A

Stool is cultured for EHEC (Enterohaemorrhagic Escherichia Coli). Assays may also be done for shiga-like toxin.

65
Q

How is E. coli infection treated?

A

Supportive care only. Antibiotic increase toxin production and should be avoided.

66
Q

What is an interesting fact about the treatment of E. coli?

A

Antibiotics should be avoided. They enhance toxin production. Treatment should involve supportive methods only.

67
Q

Helicobacter pylori

A
  • Gram negative bacillus.
  • Microaerophilic (low levels of oxygen).
  • Does not have a capsule.
  • Urease, VacA (vacuole formation), CagA (injects genes into host cells), flagella, and adhesin.
68
Q

How is H. pylori spread?

A

It is transmitted through a fecal - oral route.

69
Q

What are some of the symptoms of H. pylori?

A

Gastritis, gastric and duodenun ulcers, and gastric carcinoma.

70
Q

How is H. pylori diagnosed?

A
  • Stains and cultures from endoscopic biopsy.
  • Serology
  • Growth on urea containing agar, or breath test.
71
Q

How do we treat H. pylori?

A

Proton pump inhibitors + amoxicillin + clarithromycin.
or
Proton pump inhibitors + clarithromycin + metronidazole.
or
Bismuth, tetracycline, metronidazole, and omeprazole.

72
Q

Listeria monocytogenes

A
  • Gram positive bacillus.
  • Aerobic
  • Intracellular
  • No capsule.
  • Listeriolysin O (escape from the phagosome so it can multiply in the host cell), endotoxin-like substance, tumbling motility, grows at cool temperatures.
73
Q

What does Listeriolysin O do in the context of Listeria monocytogenes?

A

It helps Listeria monocytogenes escape from the phagosome so it can multiple within the host cell that phagocytized it.

74
Q

How is Listeria monocytogenes transmitted?

A

Contact with contaminated soil or animals, or ingestion of contaminated food.

75
Q

What is the clinical presentation of Listeria monocytogenes?

A

Gastroenteritis, meningitis in the elderly, neonatal, or immunocompromised, and granulomatosis infantiseptica (neonatal granulomas and abscesses on skins, eyes, organs, and brain).

76
Q

How is Listeria monocytogenes diagnosed?

A

Blood culture and lumbar puncture in the neonates and elderly. Gram stain and bacterial culture.

77
Q

How is Listeria monocytogenes treated?

A
  • Ampicillin is the treatment of choice. Aminoglycosides may offer a synergistic effect with ampicillin.
  • Vancomycin may be used if the patient has an allergy to ampicillin.
78
Q

Mycoplasmae pneumonia

A
  • Mycoplasma have no cell wall.
  • Aerobic
  • Cell membrane contains sterols, adhesin proteins, hydrogen peroxide production.
79
Q

What disease is caused by mycoplasma pneumoniae?

A

Bronchopneumonia

80
Q

How is Mycoplasma pneumoniae transmitted?

A

Transmission is through respiratory droplets from other humans. No known reservoirs exist.

81
Q

How does Mycoplasma pneumoniae infection present?

A
  • Bronchopneumonia (called walking pneumonia because the patient often looks better than the X-Ray would suggest).
  • A variety of extrapulmonary manifestations.
82
Q

How is Mycoplasma pneumonia diagnosed?

A

Clinical recognition, chest X-Ray, PCR for bacterial DNA, serology.
- Culture to slow to be clinically useful.

83
Q

How is Mycoplasma pneumonia treated?

A

Macrolides shorten the duration of the illness. Tetracycline and levofloxacin may occasionally be used.

84
Q

Pseudomonas aeruginosa

A
  • Gram negative bacilli.
  • Aerobic
  • Slime layer
  • Toxin A, protease, phospholipase, flagellum, pilus.
85
Q

How is Pseudomonas aeruginosa transmitted?

A

Ingestion or skin/eye contact with the organism in soil or water.

86
Q

How does Pseudomonas aeruginosa present clinically in immunocompetent patients?

A
  • Hot tub folliculitis
  • Otitis externa
  • Contact lens related corneal infections
87
Q

How does Pseudomonas aeruginosa present clinically in immunocompromised patients?

A
  • Skin infections
  • Pneumonia*
  • UTI
  • Bacteremia
  • Endocarditis
  • Meningitis
  • Cystic fibrosis patients will often develop chronic pneumonia.
88
Q

How is Pseudomonas aeruginosa diagnosed?

A
  • Grape like odour and fluorescence.

- Gram stain and culture.

89
Q

How is Pseudomonas aeruginosa treated?

A
  • Piperacillin
  • Aminoglycans
  • Carbapenems
  • Ciprofloxacin
  • Ceftazidime or Cefepime
90
Q

Vibrio cholerae

A
  • Gram negative bacilli.
  • Anaerobic
  • Flagella, Pili, CHOLERA TOXIN, adhesins, neuraminidase.
91
Q

How is Vibrio cholerae transmitted?

A

Ingestion of contaminated food or water.

92
Q

What are some clinical symptoms of Vibrio cholerae infection?

A
  • Massive amounts of diarrhea with flecks of mucous (rice water stools).
  • Dehydration, cardiac arrhythmias.
  • In extreme forms rapidly fatal infection. Fatal within hours.
93
Q

How is Vibrio cholerae diagnosed?

A
  • Rice water stools in conjunction with an outbreak, travel, or consumption of raw shellfish.
  • Stool samples.
94
Q

How is Vibrio cholerae treated?

A
  • Intravenous and oral fluids {primary treatment}
  • Antibiotics to decrease symptom duration.
  • Ciprofloxacin, TMP/SMX, Azithromycin.
95
Q

Salmonella enterica (serovar enteritidis)

A
  • Gram negative bacilli.
  • Aerobic
  • Intracellular
  • Polysaccharide capsule.
  • Non-pili appendages for adhesion, flagella, can survive within macrophages.
96
Q

How is Salmonella enterica (serovar enteritidis) transmitted?

A

A high inoculum is needed and is typically transmitted from an animal source.

97
Q

What is the clinical presentation of Salmonella enterica (serovar enteritidis)?

A
  • Enteritis (fever, vomiting, diarrhea (or constipation), abdominal pain).
  • Bacteremia
98
Q

How is Salmonella enterica (serovar enteritidis) diagnosed?

A
  • Culture blood, stool, and other affected areas (such as bone).
99
Q

How is Salmonella enterica (serovar enteritidis) treated?

A

The enteritis cannot be treated by anything other than fluid replacement. Bacteremia will be treated with ceftriaxone or ciprofloxacin.

100
Q

Salmonella enterica (serovar typhi)

A
  • Gram negative bacilli.
  • Aerobic
  • Intracellular
  • Polysaccharide capsule.
  • Non-pili appendages for adhesion, flagella, can survive within macrophages.
101
Q

How is Salmonella enterica (serovar typhi) transmitted?

A

Fecal oral transmission from another human.

102
Q

What is the clinical presentation of Salmonella enterica (serovar typhi)?

A
  • Typhoid fever (fever, diarrhea, (or constipation), abdominal pain).
  • Spread via macrophages in the bloodstream to the liver and spleen.
  • Spleen causes flu like symptoms and a rash (rose spots).
103
Q

How is Salmonella enterica (serovar typhi) diagnosed?

A

Culture of the stool, blood, and other affected areas.

104
Q

How is Salmonella enterica (serovar typhi) treated?

A

Ceftriaxone or ciprofloxacin.

105
Q

What is the main symptomatic difference between Salmonella enterica (serovar typhi) and Salmonella enterica (serovar enteritidis)?

A

The former causes typhoid fever while the later causes enteritis.

106
Q

Shigella dysenteriae

A
  • Gram negative bacillus.
  • Aerobic
  • Intracellular
  • Does not have a capsule.
  • Enterotoxin against intestine cells (kills them and causes blood stools), stomach acid survival, intracellular spread protein (IcsA), low infectious dose.
107
Q

How is Shigella dysenteriae transmitted?

A

Fecal oral route from infected human feces.

108
Q

What is the clinical presentation of Shigella dysenteriae?

A
  • Fever, nausea , and abdominal cramping.
  • Abdominal pain intensifies within days, accompanied by bloody diarrhea with pus.
  • Post infection complications include hemolytic uremic syndrome (HUS) and Reiter-syndrome arthritis.
109
Q

How is Shigella dysenteriae diagnosed?

A

Stools are sent to the lab for white blood cell stain and culture.

110
Q

What is the treatment for Shigella dysenteriae infection?

A

Rehydration, quinolones, azithromycin, and TMP/SMX.

111
Q

Treponema pallidum (syphilis)

A
  • Spirochaete bacterium with outer and inner membrane.

- Endoflagella

112
Q

How is Treponema pallidum transmitted?

A
  • Close human contact.
  • Vertical transmission.
  • Blood transfusions.
113
Q

What are some clinical symptoms of Treponema pallidum infection?

A
  • Chancre is a painless crater at the site of inoculation.
  • This is followed by a red macular rash over the entire body.
  • Multiple symptoms can manifest years later (cardiovascular syphilis).
  • Congenital syphilis causes growth retardation, hepatosplenomegaly, skin lesions, brain and bone abnormalities…
114
Q

How is Treponema pallidum diagnosed?

A
  • Microscopy (fluorescent stains).
  • Screening tests.
  • Confirmatory lab tests.
115
Q

How is Treponema pallidum treated?

A

Penicillin (desensitize to allergy if needed).

116
Q

What bacteria causes syphilis?

A

Treponema pallidum

117
Q

Bacteroids fragilis

A
  • Non toxic LPS.
  • Gram negative bacilli.
  • Anaerobic
  • Capsule
  • Neuraminidases, proteases, lipases.
  • Fimbriae
  • Endogenous
118
Q

How is Bacteroides fragilis transmitted?

A

It is found in the typical human gut flora. It is endogenous. Disease occurs when it gets somewhere that it should not be.

119
Q

What are some clinical symptoms of Bacteroides fragilis?

A

Infections may occur anywhere in the body:

  • Brain abscesses.
  • Chronic sinusitis.
  • Dental infections.
  • Bite wound infections.
  • Abdominal abscesses.
  • Gynecological abscesses.
120
Q

How is Bacteroides fragilis infection diagnosed?

A

Gram stain and culture. The location of the infection and foul odour of drainage is also indicative.

121
Q

How is Bacteroides fragilis treated?

A
  • Surgical intervention is often needed to repair the defect and to drain abscesses.
  • Antibiotics that cover gram negative bacilli.
  • Imipenem, pipercillin-tazobactam, ampicillin/gentamicin/metronidazole.
122
Q

Campylobacter jejuni

A
  • Gram negative rod.
  • May or may not have a capsule {controversial}.
  • Flagella, extracellular toxins (cytotoxin, enterotoxin).
  • Most common cause of enteritis in the developed world.
123
Q

How is Campylobacter jejuni transmitted?

A

Ingestion of fecally contaminated food or fecal - oral transmission from humans OR animals.

124
Q

What is the clinical presentation of Campylobacter jejuni infection?

A
  • Enteritis
  • Bacteremia may be seen in the immunocompromised.
  • Post infectious entities: (Guillain barre Syndrome {ascending paralysis}, post infection arthritis, hemolytic uremic syndrome (HUS) {rare}).
125
Q

How is Campylobacter jejuni diagnosed?

A
  • Direct examination of stool for WBC, gram stain.
  • Stool culture.
  • Blood culture.
126
Q

How is Campylobacter jejuni treated?

A
  • Fluid and electrolyte replacement.

- If severe macrolides may be given.

127
Q

What is often the first treatment for GIT affecting infections?

A

Fluid replacement and maintenance. Many GIT bugs result in diarrhea and dehydration is a major concern.

128
Q

Chlamydophila

A
  • Does not gram stain (arranged like gram negative but does not have peptidoglycan).
  • Aerobic
  • Intracellular
  • Masquerades as nutrients to be taken into host cells.
  • Alters the pH of the phagosome, prevents phago-lysosmal fusion, “slurps” cellular nutrients.
129
Q

What is typically needed by intracellular bacterial pathogens?

A

A method to avoid being digested within the cell. Many enter the cell through phagocytosis but must either escape before being digested by a lysosome or be resistant to lysosomal digestion.

130
Q

How is Chlamydophila spread?

A

Enters through the epithelial cells of the eyes, RT, GIT, or GU tract.

131
Q

How does Chlamydophila present clinically?

A

STI:
- Trachoma (chronic eye inflammation).
- Urethritis, cervicitis, pelvic inflammatory disease (PID).
- Lymphogranuloma venereum (painful genital ulcers with lymph node enlargement).
RTI:
- Mild pneumonia.

132
Q

How is Chlamydophila infection diagnosed?

A

Often coexists with other STI. PCR or DNA probes from genital or eye specimens.

133
Q

How is Chlamydophila treated?

A

Must attain a high intracellular concentration. Macrolides are the treatment of choice with doxycycline also being effective.

134
Q

What two clinical syndromes are associated with C. perfringens?

A

Food poisoning and gas gangrene.

Triple I (7 decks)

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