Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/22

Click to flip

22 Cards in this Set

  • Front
  • Back
Diagnosis assisted by CXR with widened mediastinum, bloody pleural tap and cultures of blood, pleural fluid or CSF for GPRs
Anthrax
Bacillus anthracis
GASTROINTESTINAL ANTHRAX
Presents in which 2 ways?
Oropharnyngeal Anthrax (hard palate, post pharynx)
Cervical edema, necrosis
Often fatal, death from bacteremic spread

Abdominal Anthrax (large bowel, cecal lesions)
Fever, nausea and vomiting
2-5 days stools become bloody, tissue invasion leads to bacteremic spread and death
Diagnosis of Anthrax
Be able to recognize clinical syndromes
High clinical suspicion in right setting is crucial to diagnosis/therapy due to high mortality
Cultures + GPR (skin/vesicles, sputum, pleura, CSF, blood)
Toxin assays (ELISA)
Bacillus cereus
causes what diseases in which people?
FOOD POISONING
TRAUMATIC OCULAR INFECTIONS

Normal flora, potential culture contaminant
Contaminant of drug paraphernalia/heroin
Immunocompromised (HIV, corticosteroids, Sickle Cell Disease) host or IVDU, risk of serious infection (bacteremia, meningitis)
Immunocompetent hosts, usually contaminant (wounds, cultures) but can see associated
Bacillus cereus
Extracellular products contribute to the manifestations of clinical disease:
Enzymes (collagenase, hemolysin, protease, phospholipase) contribute to tissue destruction
Toxins (enterotoxins) lead to diarrhea/emesis
Antimicrobial agents produced by bacteria (examples: polymyxin, bacitracin) help bacteria to compete
Two types of Food Poisoning from B. Cereus:
EMETIC form (vomiting predominate feature)
Incubation <6 H
Similar to S. aureus food poisoning
FRIED RICE
DIARRHEAL form (cramps, nausea, watery stools)
Incubation 10-12 H, improved in 24 H
Similar to C. perfringens food poisoning
Contaminated meats (turkey) or vegetables
Where will you find the toxin of B. Cereus?
Due to enterotoxin production

Culture the food!

Self-limited, no antibiotic therapy needed.
Prevention – avoid cooling foods at RT (keep <10°C) and must be properly reheated to destroy spores (>60°C)
Bacilus Ocular Infections
B. cereus predominates, other Bacillus sp.

Trauma (soil exposure) or foreign body (particles of dust, soil or metal shrapnel)
Intravenous drug abuse (IVDA)

Manifests: panophthalmitis, ocular abscess

Extracellular enzymes destroy eye tissues

Rapid 12-48 H (pain, redness, visual )

Early diagnosis, surgical therapy and antibiotics (IV, intra-vitreal); IV Clindamycin, Vancomycin
Aerobic, club shaped, “diptheroids”
C. diptheriae – cause of diptheria

C. jeikeium (Group JK) – cause of bacteremia in immunocompromised patients /neutropenia, hospital acquired infections (IV catheters)
Resistant to antibiotics, sens. VANCOMYCIN
C. diptheriae
Non spore forming GPR
Club shaped on gram stain
EXOTOXIN
Virulence factor
Inhibits protein synthesis
Extremely potent
Responsible for tonsilar/pharyngeal exudate production of DIPTHERIA
Antibodies to toxin are protective
DIPTHERIA
Epidemiology
Humans are reservoir
Asymptomatic carrier state (< 5%) on skin and in pharynx
Immunization reduces carrier state
Infected patient/carrier contacts susceptible host
Transmission through bacteria in airborne droplets or contact with secretions/exudate
COLDER months, temperate climates, crowded conditions
Diptheria: Those at risk today
Those at risk today:
Children < 15 yo if unvaccinated

Unimmunized or unboosted adolescents/adults (urban poor, those with no access to health care, IVDU)
Diptheria
Clinical Manifestations
Respiratory tract (local disease) incubates 2-3d

Toxin produces inflammation, dense necrotic exudate in pharynx/trachea
necrotic collection of cells, fibrin, dead respiratory epithelial cells, RBCs, WBCs and bacteria
removal promotes bleeding of submucosa

Exudate is tough and leathery, grey

Extends and can occlude airway obstruction

Soft tissues of the neck can swell, “bull neck”

Death can be caused by aspiration of the membrane

Fever, sore throat and membrane development (tonsils, posterior pharynx)
Cervical lymph nodes common
Once toxin is absorbed, can see systemic effects on tissues at distant sites (risk increases with severity of disease)
CARDIAC TOXICITY (MYOCARDITIS)
1-2 wks after illness; up to 10-15% infected
Lead to arrhythmia, heart block, heart failure if progresses
NEUROLOGIC TOXICITY
Up to several months later
Cranial neuropathies to wide range of presentations
Diptheria
Clinical Manifestations
Fever, sore throat and membrane development (tonsils, posterior pharynx)
Cervical lymph nodes common
Once toxin is absorbed, can see systemic effects on tissues at distant sites (risk increases with severity of disease)
CARDIAC TOXICITY (MYOCARDITIS)
1-2 wks after illness; up to 10-15% infected
Lead to arrhythmia, heart block, heart failure if progresses
NEUROLOGIC TOXICITY
Up to several months later
Cranial neuropathies to wide range of presentations
Diagnose Diptheria
Use clinical clues to prompt early therapy
Tonsillitis/pharyngitis with associated membrane with febrile/toxic appearance
Cervical adenopathy, cervical swelling (“bull neck”)
Paralysis of palate, hoarseness or stridor
Listeria monocytogenes
Small gram positive rod
Cocci, diplococci
25°C TUMBLING MOTILITY
Intracellular pathogenesis
Rare cause of disease but risk to select population
Risk for food borne disease
Listeria monocytogenes
Epidemiology
Zoonosis, ubiquitous in nature (soil, decaying vegetable matter, feces)
Vertical transmission, no other human-human
Up to 70% raw vegetables; raw milk, fish, meats (including processed meats), poultry
FOODS: coleslaw, unpasturized soft cheeses, ready-to-eat products/meats, smoked fish
Those at Risk for Listeria:
Neonates and elderly (extremes of age)
Pregnant women
Impaired cell mediated immunity, immunosuppression (steroids, transplant recipients)
HIV + (100 x more likely than HIV-), low incidence due to prophylactic antibiotics
Incubation for Listeria Food Poisoning
Incubation ranges 11-70 days

Infection most likely begins with contaminated food ingestion (possible maternal-fetal)

Gastric surgery or H2 blockers promote infection (stomach pH increased)
Binds epithelial cells, able to escape INTRACELLULAR killing
Survives intracellularly
Filopods (bacteria push against membrane) to allow passage to adjacent cells, avoiding exposure to immune system and escaping immunosurveillance
Pathogenesis of Listeria?
Clinical Manifestations of Listeria
Meningitits
Bacteremia
Gastroenteritis
Neonatal infection
Listeriosis during pregnancy
Listeria: Neonatal infection
Infection in-utero (placenta) GRANULOMATOSIS INFANTISEPTICA – immediate spontaneous abortion/neonatal death
Infection at parturition - meningitis 2wk post-birth or immediate sepsis after delivery