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84 Cards in this Set

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Common characteristics for anaerobes
-Mixed infections
- Energy by fermentation only
- Do not use oxygen as final electron acceptor
-Difficult to isolate
-Poor sampling techniques
Anaerobic culture methods
- Gas pack
- Oxyplates
- Anaerobic glove box
Name anaerobes
Actinomyces
Bactereides
Clostridium
Characteristics of actinomyces
- Gram positive rods
- Resemble fungi
- Non spore forming
- Can be facultative or strict anaerobes
- NF of GI, skin, mucosal surfaces
- Opportunnistic pathogen
- Grows slowly in culture
- Chronic, slowly developing infections
Pathogenesis and immunity of actinomyces
- Only causes disease when normal mucosal surfaces are disrupted by surgery, trauma or infection
- Characterized by multiple abscesses connected to sinus tracts
- Macroscopic colonies resembling grains of sand - called SULFUR GRANULES - look yellow or orange, some present in pus
Most common actinomyces infection
Cervicofacial
-Lumpy jaw, poor oral hygiene, invasive dental work
- Acute pyogenic , slowly evolving painless process
- Tissue swelling with fibrosis and scarring with open draining sinus tracts
Dx for actinomyces
-Organisms are inside of sulfur granules
-Thin gram + branching bacilli
- After 1 week irregulat appearance of molar tooth
Treatment for actinomyces
-Debridement and prolonged antibiotic therapy (4-6 weeks)
- Penicillin G
-Prevention - difficult, good oral hygiene
Bacteroides fragilis
- Gram negative pleomorphic rods
- LPS is not toxic
- Not killed by short exposure to oxygen but wont grow in presence of oxygen
Clinical syndromes Bacteroides fragilis
- Respiratory tract infections
- Brain abscesses
- Intraabdominal infections- B. fragiles most common anaerobe recovered in those, blunt trauma, penetrating wounds, ruptured bowel or post surgery, can cause absesses and bacteremia, caused mainly by appendicitis and diverticulitis
- Contaminated small bowel syndrome
- Gynecological infections
- Skin and soft tissue infections - bites
- Oral cavity
How do you diagnose Bacteroides fragilis
- Bad smell
- Gas in specimen
All anaerobes are susceptible to penicillin except _
Bacteroides fragilis
Clostridium characteristics
- Gram +
- Spore forming
- Motile or non motile rods
- Strict anaerobe
Name 4 pathogenic species of Clostridium
- Clostridium tetani
- Clostridium botulinum
- Clostridium difficile
- Clostridium prefringens
Most significant characteristic of Clostridium tetani
-Production of potent exotoxins - submicrogram amount can kill a person
Clostridium tetani is found where
All soils - found in feces in both animals and humans
How do you get C. tetani
- PENETRATING WOUND
- This allows introduction of endospores to the wound
- Bacteria germinate and release toxin - TETANOSPASMIN - causes tetanus
- Tissue damage lowers O2 concentration and allows organisms to grow (strict anaerobes)
- It is not very invasive and toxin is released due to bacteria death and autolysis
Describe C. tetani pathogenesis
- TOXIN!! - tetanospasmin
- A/B toxin - B binds to gangliosides and A gets in
- Travels to CNS via retrograde axonal transport
- ACTS ON SPINAL CORD to prevent release of inhibitory transmitters like GABA or glycine
- Promotes muscle over activity - any stmulus will not be down graded by inhibitory response - paralyzing muscle spasms
- CLASSIC SPASTIC PARALYSIS
Primary target organ for C. tetani
SPINAL CORD
Describe tetanus
- Clinical symptoms will start from 3-21 days after Clostridium gets into the wound
- Muscle rigidity follows descending pattern - starts with lock jaw and goes down
- OPISTHOTONOS - long violent asphyxial paroxysmal spasms caused by minor stimuli - light, touch, etc
- Risus sardonius - terrible smile like expression on face
Death in tetanus comes from _
Respiratory failure
Mortality - 60%
Treatment and prevention in tetanus
- Supportive care - respirator, reduced light, benzodiazepines
- TIG - tetanus immuno globulin - neutralizes circulating toxin, once its bound its uneffective
- After TIG can treat with antibiotics (not before - antibiotics kill bacteria and release additional toxin)
Prevention - DTP vaccine and boosters every 10 years
3 types of botulism
- Classic - INTOXICATION, NOT INFECTION - ingestion of toxin with the food (canned food)
- Wound botulism- rare
- Infant botulism - HONEY with botulinum spores
Describe botulinum toxin
- AB toxin
- A subunit gets into the cell and blocks release of Ach
- Results in FLACCID PARALYSIS
- Cranial nerves affected first followed by descending paralysis of motor nerves
Which toxin does NOT affect CNS
Botulinum toxin
Death in botulism
- Toxin induced failure of respiratory muscles
Describe classic botulism
- Ingestion of improperly canned food
- Usually begins 12-48 hours after ingestion but can be as early as 6 hours
- Earlier onset - worst disease
- Begins with nausea and vomitting followed by acute symmetrical impairment of CN's - blurred vision, double vision, ptosis, difficulty speaking and swallowing
- Descending weakness or paralysis in all muscles
Treatment of botulism
- Immediate administration of antitoxin
- Supportive care - respirator, medication
- Mortality - 25%
- Stomach emptying
- NO ANTIBIOTICS because intoxication not an infection
- REPORTABLE DISEASE
FLoppy baby syndrome
- INFECTION
- Infants ingest endospores from honey
- Similar to adult botulism but not as severe
- Infants present with constipation, progressive weakness, cranial nerve dysfunction and failure to thrive
- Can also cause respiratory distress
- Mortality - 2%
Clostridium difficile characteristics
- Slender gram + sporulating anaerobe, found in small numbers in GI
-Presents in patients with broad spectrum antibiotic use which kills off normal flora causing disease
Clostridium difficile causes what disease
Pseudomembranous colitis - associated with clindamycin and lincomycin antibiotic treatment
- 4-8 days after beginning of treatment
- Presents with profuse mucoid GREEN watery foul smelling DIARRHEA - can also see high fever, leukocytosis and severe abdominal pain
- Pseudomembrane - mucosa covered with gray and yellow patches that contain fibrin, mucus and leukocytes
- If unchecked patient is at risk to develop intractable colitis, intestinal perforation and toxic megacolon
Treatment and prevention of C. difficile
- Stop broad spectrum antibiotic disease
- Treat with vancomycin or metronidazole
- Prevention difficult - resistant to disinfectants
- Nosocomial spread usually
3 diseases caused by Clostridium prefringens
- Gas gangrene
- Food poisoning
- Enteritis
Dx of Clostridium Perfrinigens
- Double zone of hemolysis on blood agar
- Growth in milk causes STORMY FERMENTATION
Gas gangrene
- 1-4 days after a wound
- Local pain
- Hypovolemia because of circulating toxin
- Toxic delirium becoming incoherent and disoriented
- Patient can also present with tachycardia, tachypnea, hypotension and moderate fever
General characteristics of mycobacterium
- Facultative intracellular parasites (MACROPHAGE - principal host cell)
- Immunocompromised people
Why doesnt mycobacterium stain well
High content of lipid in cell wall - need to do acid fast stain
Mycobacterium tuberculosis characteristics
Facultative intracellular aerobic gram positive bacillus
ACID FAST BACILLUS
Most important virulence factor for mycobacterium
Ability to survive inside the cell (macrophage) - doesnt get digested or destroyed by macrophage
Cord factor
- Causes M. tuberculosis grow in long rope-like aggregates
- Inhibits fusion of macrophage's lysosome with phagosome which allows it to survive in the macrophage
- Stimulates granuloma formation
- Blocks PMN migration
Sulfatides
Long chain fatty acids on the outer membrane of M. tuberculosis - block or reverse priming of monocytes
- Virulence factor - produces M. tuberculosis from intracellular killing
- Blocks LPS of INF gamma activation
Epidemiology of M. tuberculosis
- Native Americans, Eskimos, Asians, Hispanics and Blacks are most susceptible
- 1/2 of worlds population is infected
- in USA 20000-30000 cases each year (mostly in immunocompromised people, also homeless and IV drug users)
Pathologic hallmark of TB
Formation of granulomas around foci of infection
Host immune response to M. tuberculosis depends on what?
Cell mediated immunity - T cells - activates macrophages to cause respiratory burst
Transmission of M.tuberculosis
-Droplet aerosol discharged in air (coughing, talking)
Primary TB
- Occurs in persons with no previous experience with M. Tuberculosis
- Pneumonic - occurs with inhalation 1-10 organisms, lodge in alveolus where macrophages phagocytize bacteria
- Symptoms are FLU LIKE (mild), low grade fever
-Dissemination from initial site of infection to other sites through lymphatics (causes hilar lymphadenopathy in children)
- After several weeks become tuberculin positive (skin test)
Primary lesions in TB are called and they can form complex called _
Granulomas or tubercles
Ghon complex - calcification of tubercles causing a scar - can be picked up by X ray as spot on the lung
2ndary TB
-Occurs in presense of positive tuberculin test (skin test) and in spite of acquired cellular immunity
- Usually occurs from REACTIVATION of old infection
- Initial lesions undergo NECROSIS (caseous necrosis)
- Coughing blood, night sweats, weight loss, fever
Disseminated form of TB is called
Miliary TB - bones, spleen, meninges, kidney, etc
Tuberculin testing
Delayed type hypersensitivity specific for M. tuberculosis
- + begins after 3-4 weeks of infection and can last for years
- Positive result DOES NOT mean person has active disease - could be previous infection or vaccine, need to do follow up chest X ray
Mycobacterium leprae characteristics
Hansens bacillus
- CAN NOT grow on lab media - grow in mouse foot pads and armadillos
- Long generation time
- Grows inside macrophages, endothelial cells, epithelial cells and Schwann test
Name major forms of leprosy
Tuberculoid leprosy
Lepromatous leprosy
Border line leprosy
Tuberculoid leprosy
- Least severe - in people with good cell mediated immune response
- Characterized by granulomas, few bacilli in body fluids and extensive nerve damage
- Patient develops red cutaneous nodules that resemble tubercles and contain granulomas - no sensation in lesions
Tuberculoid vs Lepromatous leprosy in terms of lesions
Tuberculoid - macular lesions
Lepromatous - nodular lesions
Border line leprosy
- Patients present with claw hand, foot drop or facial palsy
- Lesions present as flat red or white
- Nerve damage and anesthesia
- Few granulomas
Lepromatous leprosy
- Most severe form of leprosy
- Very poor cell mediated immunity response
- ABSENSE OF GRANULOMAS
- Huge number of bacilli in body fluids
- Progressive disfiguring lesions
Mitsuda skin test
- Analogous to PPD but for leprosy
- Not valuable clinically
- Helps to differentiate between forms of disease
Dx of M. leprae
- Acid fast bacilli in skin biopsy
-Anesthetic lesions
- Enlarged peripheral nerves
Treatment for leprosy
Dapsone + rifampin
Atypical mycobacterium
MAC - Mycobacterium avium-intracellulare
- OPPORTUNISTIC ONLY
- Through GI in immunocompromised (98% in AIDS patients)
- Causes TB like respiratory infection and intestinal erosion causes diarrhea
3 forms of MAC disease
- Pulmonary - white males 45-65 years old with preexisting condition (COPD, emphysema, TB) - chronic productive cough, dyspnea, fever, night sweats, fatigue, granulomas with or w/out caseation
- Subacute lymphadenitis- swollen but not painful, in children under 5
- Disseminated disease - AIDS patients - diarrhea, vomitting, abd. pain, weight loss
Mycobacterium marina
Tropical fish + cut - causes cutaneous granulomas
Spirochetes general characteristics
Spiral shaped gram negative bacteria with periplasmic flagella
- Motile
- DO NOT HAVE LPS
3 types of spirochetes
Treponema
Borrelia
Leptospira
Treponema pallidum causes_
SYPHILLIS
What protects spirochetes against phagocytosis
Covered with human fibronectin
Transmission of syphillis
- STD - most common
- Blood
- Congenital
Name 3 phases of syphillis
- Primary - chancre at site of infection
- Secondary - rash over entire body
- Tertiary - destruction of some tissue - can be neural, cardiac
Primary syphillis
- Chancre develops where infection is inoculated (genitals usually)
- Begins as papule and erodes to PAINLESS ulcer with raised borders
- Painless regional lymphadenopathy after 1-2 weeks
- Ulcer heals on its own after 1-2 months
- Ulcer is highly contagious
Secondary syphillis
- Begins as flu like syndrome - 4-10 weeks after chancre - sore throat, fever, headache, myalgia
- All over rash - can be variable - macular, papular, pustular
- Can cover entire skin surface - including palms and soles - resolves after several months, highly contagious
Characteristics of secondary syphillis rash
- Characteristic "nickel and dime" rash on palms and soles
- Flat, shiny areas on tongue and mucous patches
Granulomatous lesions in tertiary syphillis
- Gummas - bone, skin, tissues
Congenital syphillis
- Serious fetal disease
- Latent infection, multiorgan malformations or fetal death
- Rhinitis, desquamating rash, teeth/bone malformations
- Blindness, deafness, cardiovascular syphillis
How do you diagnose syphilis
- DOES NOT GROW IN CULTURE
- Dark field microscopy or fluorescent labeled
- Serology
Treatment and prevention of syphilis
Prevention - no vaccine, safe sex practices, find and treat partners
Treatment - penicillin
Borrelia burgdorferi causes_
Lyme disease
Vector for Lyme disease
Tick
Borrelia recurrentis causes
Relapsing fever - outer envelope surrounds periplasmic flagella
3 stages of Lyme disease
Stage 1 - erythema migrans (Bulls eye ) and flu like symptoms - at site of tick bite, not painful, appears 3-30 days after bite and can persist for 2-3 weeks
Stage 2- arthritis, CN palsies, AV nodal block, severe malaise and fatigue
Stage 3 - prolonged arthritis, encephalitis, blue pigmentation of skin
How do you diagnose Lyme disease
- History of tick bite
- CDC recommends Ab titer followed by immunoblot
To diagnose Lyme disease need to meet one of criteria
- Erythema migrans (rash)
- One of the late manifestations (arthritis) + lab ID
Lab criteria for dx of Lyme disease
- Isolation of B. burgdorferi
- Diagnostic level of IgM and IgG Ab's
- Significant increase between convalescent and acute Ab titers
Treatment Lyme disease
- Doxycycline or amoxicillin
- Penicillin in late stages
Relapsing fever
- Borrelia recurrents