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84 Cards in this Set
- Front
- Back
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Common characteristics for anaerobes
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-Mixed infections
- Energy by fermentation only - Do not use oxygen as final electron acceptor -Difficult to isolate -Poor sampling techniques |
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Anaerobic culture methods
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- Gas pack
- Oxyplates - Anaerobic glove box |
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Name anaerobes
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Actinomyces
Bactereides Clostridium |
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Characteristics of actinomyces
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- 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 |
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Pathogenesis and immunity of actinomyces
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- 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 |
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Most common actinomyces infection
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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 |
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Dx for actinomyces
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-Organisms are inside of sulfur granules
-Thin gram + branching bacilli - After 1 week irregulat appearance of molar tooth |
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Treatment for actinomyces
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-Debridement and prolonged antibiotic therapy (4-6 weeks)
- Penicillin G -Prevention - difficult, good oral hygiene |
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Bacteroides fragilis
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- Gram negative pleomorphic rods
- LPS is not toxic - Not killed by short exposure to oxygen but wont grow in presence of oxygen |
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Clinical syndromes Bacteroides fragilis
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- 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 |
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How do you diagnose Bacteroides fragilis
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- Bad smell
- Gas in specimen |
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All anaerobes are susceptible to penicillin except _
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Bacteroides fragilis
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Clostridium characteristics
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- Gram +
- Spore forming - Motile or non motile rods - Strict anaerobe |
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Name 4 pathogenic species of Clostridium
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- Clostridium tetani
- Clostridium botulinum - Clostridium difficile - Clostridium prefringens |
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Most significant characteristic of Clostridium tetani
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-Production of potent exotoxins - submicrogram amount can kill a person
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Clostridium tetani is found where
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All soils - found in feces in both animals and humans
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How do you get C. tetani
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- 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 |
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Describe C. tetani pathogenesis
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- 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 |
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Primary target organ for C. tetani
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SPINAL CORD
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Describe tetanus
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- 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 |
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Death in tetanus comes from _
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Respiratory failure
Mortality - 60% |
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Treatment and prevention in tetanus
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- 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 |
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3 types of botulism
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- Classic - INTOXICATION, NOT INFECTION - ingestion of toxin with the food (canned food)
- Wound botulism- rare - Infant botulism - HONEY with botulinum spores |
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Describe botulinum toxin
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- 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 |
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Which toxin does NOT affect CNS
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Botulinum toxin
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Death in botulism
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- Toxin induced failure of respiratory muscles
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Describe classic botulism
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- 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 |
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Treatment of botulism
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- Immediate administration of antitoxin
- Supportive care - respirator, medication - Mortality - 25% - Stomach emptying - NO ANTIBIOTICS because intoxication not an infection - REPORTABLE DISEASE |
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FLoppy baby syndrome
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- 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% |
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Clostridium difficile characteristics
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- 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 |
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Clostridium difficile causes what disease
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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 |
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Treatment and prevention of C. difficile
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- Stop broad spectrum antibiotic disease
- Treat with vancomycin or metronidazole - Prevention difficult - resistant to disinfectants - Nosocomial spread usually |
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3 diseases caused by Clostridium prefringens
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- Gas gangrene
- Food poisoning - Enteritis |
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Dx of Clostridium Perfrinigens
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- Double zone of hemolysis on blood agar
- Growth in milk causes STORMY FERMENTATION |
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Gas gangrene
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- 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 |
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General characteristics of mycobacterium
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- Facultative intracellular parasites (MACROPHAGE - principal host cell)
- Immunocompromised people |
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Why doesnt mycobacterium stain well
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High content of lipid in cell wall - need to do acid fast stain
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Mycobacterium tuberculosis characteristics
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Facultative intracellular aerobic gram positive bacillus
ACID FAST BACILLUS |
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Most important virulence factor for mycobacterium
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Ability to survive inside the cell (macrophage) - doesnt get digested or destroyed by macrophage
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Cord factor
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- 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 |
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Sulfatides
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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 |
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Epidemiology of M. tuberculosis
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- 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) |
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Pathologic hallmark of TB
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Formation of granulomas around foci of infection
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Host immune response to M. tuberculosis depends on what?
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Cell mediated immunity - T cells - activates macrophages to cause respiratory burst
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Transmission of M.tuberculosis
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-Droplet aerosol discharged in air (coughing, talking)
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Primary TB
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- 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) |
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Primary lesions in TB are called and they can form complex called _
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Granulomas or tubercles
Ghon complex - calcification of tubercles causing a scar - can be picked up by X ray as spot on the lung |
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2ndary TB
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-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 |
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Disseminated form of TB is called
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Miliary TB - bones, spleen, meninges, kidney, etc
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Tuberculin testing
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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 |
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Mycobacterium leprae characteristics
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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 |
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Name major forms of leprosy
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Tuberculoid leprosy
Lepromatous leprosy Border line leprosy |
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Tuberculoid leprosy
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- 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 |
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Tuberculoid vs Lepromatous leprosy in terms of lesions
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Tuberculoid - macular lesions
Lepromatous - nodular lesions |
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Border line leprosy
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- Patients present with claw hand, foot drop or facial palsy
- Lesions present as flat red or white - Nerve damage and anesthesia - Few granulomas |
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Lepromatous leprosy
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- Most severe form of leprosy
- Very poor cell mediated immunity response - ABSENSE OF GRANULOMAS - Huge number of bacilli in body fluids - Progressive disfiguring lesions |
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Mitsuda skin test
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- Analogous to PPD but for leprosy
- Not valuable clinically - Helps to differentiate between forms of disease |
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Dx of M. leprae
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- Acid fast bacilli in skin biopsy
-Anesthetic lesions - Enlarged peripheral nerves |
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Treatment for leprosy
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Dapsone + rifampin
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Atypical mycobacterium
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MAC - Mycobacterium avium-intracellulare
- OPPORTUNISTIC ONLY - Through GI in immunocompromised (98% in AIDS patients) - Causes TB like respiratory infection and intestinal erosion causes diarrhea |
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3 forms of MAC disease
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- 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 |
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Mycobacterium marina
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Tropical fish + cut - causes cutaneous granulomas
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Spirochetes general characteristics
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Spiral shaped gram negative bacteria with periplasmic flagella
- Motile - DO NOT HAVE LPS |
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3 types of spirochetes
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Treponema
Borrelia Leptospira |
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Treponema pallidum causes_
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SYPHILLIS
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What protects spirochetes against phagocytosis
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Covered with human fibronectin
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Transmission of syphillis
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- STD - most common
- Blood - Congenital |
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Name 3 phases of syphillis
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- Primary - chancre at site of infection
- Secondary - rash over entire body - Tertiary - destruction of some tissue - can be neural, cardiac |
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Primary syphillis
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- 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 |
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Secondary syphillis
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- 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 |
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Characteristics of secondary syphillis rash
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- Characteristic "nickel and dime" rash on palms and soles
- Flat, shiny areas on tongue and mucous patches |
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Granulomatous lesions in tertiary syphillis
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- Gummas - bone, skin, tissues
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Congenital syphillis
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- Serious fetal disease
- Latent infection, multiorgan malformations or fetal death - Rhinitis, desquamating rash, teeth/bone malformations - Blindness, deafness, cardiovascular syphillis |
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How do you diagnose syphilis
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- DOES NOT GROW IN CULTURE
- Dark field microscopy or fluorescent labeled - Serology |
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Treatment and prevention of syphilis
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Prevention - no vaccine, safe sex practices, find and treat partners
Treatment - penicillin |
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Borrelia burgdorferi causes_
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Lyme disease
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Vector for Lyme disease
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Tick
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Borrelia recurrentis causes
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Relapsing fever - outer envelope surrounds periplasmic flagella
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3 stages of Lyme disease
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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 |
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How do you diagnose Lyme disease
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- History of tick bite
- CDC recommends Ab titer followed by immunoblot |
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To diagnose Lyme disease need to meet one of criteria
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- Erythema migrans (rash)
- One of the late manifestations (arthritis) + lab ID |
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Lab criteria for dx of Lyme disease
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- Isolation of B. burgdorferi
- Diagnostic level of IgM and IgG Ab's - Significant increase between convalescent and acute Ab titers |
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Treatment Lyme disease
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- Doxycycline or amoxicillin
- Penicillin in late stages |
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Relapsing fever
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- Borrelia recurrents
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