Dr. Miller Block 4 – Flashcards

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Staphylococci epidermidis
answer
  • Gram positive cocci in pairs, short chains, and grape like clusters
  • Grow best aerobically but can grow anaerobically using fermentative pathways
  • Relatively simple nutritional requirments: Blood agar is used for primary isolation-hemolytic reactions
  • Colony color: white
  • Catalase +
  • Coagulase -
  • Glucose Fermentation +
  • Mannitol Fermentation -
  • Novobiocin sensitive
  • Common as normal skin flora
  • Occassional disease resulting from foreign body colonization (shunts, catheters, joint protheses) which can lead to bacteremia, and endocarditis
  • Frequently methicillin-resistant (MRSE) 
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Staphylococci saprophyticus
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  • Gram positive cocci in pairs, short chains, and grape like clusters
  • Grow best aerobically but can grow anaerobically using fermentative pathways
  • Relatively simple nutritional requirments: Blood agar is used for primary isolation-hemolytic reactions
  • Common as normal skin flora
  • Important cause of UTI in young sexually active females
  • Colony color: white
  • Catalase (+)
  • Coagulase (-)
  • Glucose Fermentation (-)
  • Mannitol Fermentation (V)
  • Novobiocin Sensitivity (resistant)
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Staphylococci aureus
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  • Gram positive cocci in pairs, short chains, and grape like clusters
  • Grow best aerobically but can grow anaerobically using fermentative pathways
  • Relatively simple nutritional requirments: Blood agar is used for primary isolation-hemolytic reactions
  • Colony color: pale yellow, orange, or golden
  • Catalase (+)
  • Coagulase (+)
  • Glucose Fermentation (+)
  • Mannitol Fermentation (+)
  • Novobiocin sensitive
  • May normal flora in anterior nares
  • Transient on the skin surface
  • Some colonization on moist skin areas
  • Cellular Antigens
    • Peptidoglycan-inflammatory
    • Teichoic acid-inflammatory
    • Protein A-major protein component of cell wall covlently linked to peptidoglycan.  Nonspecific interaction with Fc of some immunoglobulin. Anti-phagocytic
    • Capsule-anti-phagocytic
  • Hemolytic/Cytolytic toxins:
    • RBC hemolytic-iron acquisition
    • Kills/inhibits phagocytic cells
    • Tissue necrosis
    • α -toxin: major exotoxin nearly all human strains
      • Channel forming toxin
      • Most important extracellular virulence factor elevated levels in CA-MRSA strains
  • Non-hemolytic/Cytolytic toxins:
    • attack white cells ONLY
    • Kills/inhibits phagocytic cells
    • Tissue necrosis
    • Panton-Valentine Leukocidin (PVL):
      • Kills neutrophils, macrophages
      • Highly associated with CA-MRSA strain
      • No added virulence
    • Leukocidin A/B:
      • Major contribution to MRSA pathogenesis in murine model
      • Kills neutrophils, macrophages
  • Exo-enzymes: coagulase, penicillinase, hyaluronidase, lipases, nucleases, staphylokinases (fibrinolysin)
  • Transmission often from normal flora
    • Self contamination
    • Person-to-person
  • Infections from another skin disease (person to person)
  • Clinical Manifestations
    • Cutaneous infections
    • Scalded Skin Syndrome
    • Toxic Shock Sydrome
    • Food Poisoning
    • Pneumonia
    • Metastatic Infections
    • Arthritis
    • Endocarditis
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Cutaneous Infections of S. aureus
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  • Folliculitis, boils, carbuncles, wound infections
    • Most common bacterial infection in humans
    • Can be superfical or Deep
    • Frequent abscess formation, occasional spread via fascitis (necortizing fascitis)
    • Extreme inflammation, pain, purulent
    • May disseminate to bloodstream-sepsis can occur
    • Eyelid infection-conjunctivitis, sticky eye in neonates
  • Impetigo
    • Encrusted pustuls on superifical layers of skin
    • Frequently seen in younger children 
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Scalded Skin Syndome: S. aureus
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  • Exfoliative Toxin: lysis of attachment between cells of the granular layer of the epidermis 
  • Bacteria is not present in the bloodstream but rather the toxin is present in the bloodstream
    • Local infection, systemic toxemai
  • Most common in neonates and children < 4 yrs
  • Generalized exfoliative dermatitis: generalized painful erythema and dramatic bullous desquamation of large areas of skin.  Focus of infection may be distant.
  • Bollus impetigo-localized version of the syndrome with infection at the site of the lesion
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Toxic Shock Syndrome: S. aureus
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  • Toxic shock syndrome toxin 1:
    • SUPERANTIGEN
    • Non-specific interaction of T cells and macrophages
    • Potent inducer of TNF and IL-1, systemic inflammation
    • enterotoxin activity
    • Localized infection, systemic toxemia
  •  Local infection: tampon, wound, boil: with systemic toxemia
  • High Fever
  • Vomiting/diarrhea
  • Development of a characteristic rash
  • Systemic toxemia-induced hypotension leads to cardiac and renal failure
  • Rare bacteremia-no bacteremia classically
  • Delayed desquamation of feet and hands
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Food Poisoning: S. aureus
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  • Enterotoxins:
    • six serotypes present
    • Heat stable
    • Stimulates emetic receptor in abdominal viscera
  • Common form of food poisoning in US
  • Ingestion of pre-formed toxin elaborated by enterotoxin -producing strains growing in foods
  • Typical Foods: custard or cream filled pastries, chicken salad, processed meats, cottage cheese, sauces etc.
  • Rapid onset of symptoms 2-6 hours 
    • Vomiting, severe cramps, variable diarrhea
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Pneumonia: S. aureus
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  • Seen in Children < 1 yr and immunocompromised (cystic fibrosis etc)
  • Increased in number of highly virulent MRSA infections in apparently normal individuals (necrotizing pneumonia)
  • Fulminant disease, high mortality rate (50%)
  • Consolidation or necrosis with formation of multiple abscesses   
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Metatatic Infections: S. aureus
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  • Any area of the body
  • Often following skin/tissue infections
  • Osteomyelitis
    • Most frequent organism causing osteomyelitis
    • Male Children under age of 12
    • Especially in long bones of legs
    • Hematogenous spread from a primary focus (wound or boil)
    • Direct spread from a tissue puncture wound pentrating to the bone
    • Spine may be infected with para-meningeal involvement (aseptic meningitis) 
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Arthritis: S. aureus
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  • 50% of all cases of bacterial arthritis
  • Dissemination from skin infection or from osteomyelitis
  • Direct inoculation during intra-articular injections
  • Destruction of articular cartilage, permanent joint deformity  
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Endocarditis: S. aureus
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  • 50% are hospital acquired from bacteremia following a primary infection of the skin, respiratory tract, or other body site inculding MRSA
  • Common in patients with diabetes mellitus, cardiovascular disease, granulocyte disorders, immunological defiencies, prior valve damage
  • Mitral and aortic valve damage is most common: splinter hemorrages and janeway lesions present
  • Tricuspid valve in IV drug abusers, lung abscesses
  • Usually a continuous bacteremia
  • Difficult to treat with antibiotics
  • Often requires valve replacement
  • 40-80% mortality with antibiotics  
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Laboratory Diagnosis of S. aureus
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  • Sample must be "clean"
  • Direct Examinaion-Gram stain (sterile sites only)
  • Culture-blood agar, B-hemolytic, yellow colonies
    • Rapid Slide agglutination kids (protein A)
    • Phage typing
    • PCR assays
  • Antibiotic sensitivites: MRSA ID and molecular typing
    • 85-90% are B-lactamase positive (plasmid)
    • Some vancomycin resistance
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Treatment of S. aureus
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  • Clean wounds, drain abscesses, remove foreign bodies
  • Topical antibiotics fro impetigo (bacitracin, mupirocin)
  • HA-MRSA: Vancomycin alone or with rifampin
  • CA-MRSA:
    • skin tissue: TMP/SMX or clindamycin, doxycycline
    • Pneumonia, endocarditis, arthritis: vancomycin or linezolid
  • Prevention:
    • Proper handwashing
    • Eliminate carriers
    • 7-day treatment with combination of
      • Daily Bactroban Nasal (mupirocin)
      • Daily chlorhexidine baths
    • NO VACCINES
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HA-MRSA
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  • Primarily USA 100
  • NO increased virulence
  • exreme antibiotic resistance

 

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CA-MRSA
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  • USA 300 and USA 400 strains
  • INCREASED virulence
  • Moderate antibiotic resistance  
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Streptococcus pyogenes
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  • Gram positive cocci
  • Never considered norma flora
  • Cellular Antigens
    • Peptidoglycan- inflammatory
    • Teichoic Acid
    • Lipoteichoic Acid
    • M Protein- Major protein antigens > 60 serotypes
      • Main virulence factor
      • Fibrillar molecule composed of two alpha helical cahins
      • Inhibits complement fixation, resistance to phagocytosis
    • Protein G
    • Capsule-anti-phagocytic
  • Cytolytic Toxin: RBC hemolytic, kills phagocytic cells, tissue nerosis
    • Streptolysin O:
      • Produced by nearly all strains
      • Oxygen Labile
      • Channel forming toxin
      • Potent antigen
    • Streptolysin S
      • Produced by nearly all strains
      • Oxygen Stable
      • Small peptide
      • Non-antigenic
  • Pyrogenic Exotoxins-fever producing
    • SpeA and SpeC
      • Super antigens
      • Inflammatory
      • Erythrogenic toxins- rash and fever of scarlet fever
      • SpeA associated with most severe disease
      • Only by strains lysogenized by specific phage
      • Shock and organ failure of strep toxic sock syndrome
      • Stimulates cytokine production in macrophages
    • SepB- inflammatory
  • Transient on the skin surface
  • Transmission is person-to-person
    • Respiratory Droplets
    • Exchanging Secretions
    • Touching skin, carrier on hands
  • URT and skin infections primarily inc children (5-15 yr old)
  • Healthy people can get invasive GAS but immunocompromised are more likely to get GAS
  • Clinical Manifestations and Pathogenesis
    • Pharyngitis
    • Scarlet Fever
    •  Pneumonia
    • Impetigo
    • Erysipelas
    • Necrotizing fascitis
    • Streptococcal toxic shock syndrome
    • Puperal sepsis
    • Acute rheumatic fever
    • Acute glomerulonephritis
    • PANDAS
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Impetigo: S pyogenes
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  • Encrusted pustules on superficial layers of skin
  • Associated with certain M protein serotypes

 

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Erysipelas: S. pyogenes
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  • Acute lymphangitis of the skin (may be complication of impetigo)
  • Painful, hot, rapidly spreading, inflamed area with an advancing bright red margin-may spread to fascia (spreads laterally)
  • Most often present on the face and lower extremities (primarily infants, elderly) 
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Necrotizing Fascitis: S. pyogenes
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  • Enter throuh a break in the skin
  • Bacteria follow a path along the fascia between the subcutaneous tissue and muscle
  • Rapid swelling, red-to-purple-to blue, large blisters
  • Skin dies, muscle may be infected, gangrene
  • Bacteremia (60%),
  • May progress to streptococcal toxic shock syndrome  
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Sreptococcal Toxic Shock Syndrome
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  • Complication of bactermia and or agressive soft tissue infection
  • Historically in older patients with multiple medical problems
  • Now seen in persons of all ages with no underlying disease
  • Associated with systemic production of  pyrogenic exotoxins
  •  Fever, rash, vomitign/diarrhea/ hypotension, leading to cardic and renal failure, shock and death
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Puerperal Sepsis
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  • Historical "child-bed-fever"
  • Spread to uterus after delivery
  • Endometritis, bacteremia
  • Toxic Shock Syndrome  
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Acute Rheumatic Fever

ARF

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Only after an Group A step pharyngeal infection
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Acute Glomerulonephritis

AGN

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  • Inflammatory reaction seen after a Group A skin or pharyngial infection
  • Seen primarily in children
  • Average of 1-2 weeks in pharyngeal
  • 2-3 weeks in skin
  • Well defined group of M serotypes
  • Deposition of immune complexes in kidney, fix C, inflammation
  • Must document Step A etiology to confirm origin

 

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PANDAS
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Seems to be associated with pharyngeal infections not skin infections
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Laboratory Diagnosis of S. pyogenes
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  • Direct Examination-Gram stain-sterile sites only
  • Culure-blood agar (24 hours) 
  • Serology-important for establishing streptococcal etiology for AGN
  • Antibiotic Sensitivity-usually unnecessay b/c almost all strains are sensitive to penicillin
    • Most resistant to TMP-SMX
    • Resistance to macrolides increasing
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Treatment/Prevention of S. pyogenes
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  • Penicillin G or V
  • Any B-lactams
  • Invasive disease-higher doses of penicillin often better response with added clindamycin or erythromycin
  • Surgical debridement
  • Typically resistant to TMP/SMX
  • No Vaccines 
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Propionibacterium acnes
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  • Gram (+) rods
  • Chinese characters
  • Not acid Fast
  • Produce lipases to degrade lipis for cutrients
  • Anaerobic
  • Normal flora of skin (sebacecous follicles)
  • Overgrowth of normal flora in response to nutrient stimulation (lipids) causing inflammation
  • Disease follows increase in bacterial numbers, usually 1-3 years before sexual maturity
  • Bacterial numbers are in direct relation to the amount of lipid sebaceous gland sebum secretions at the time of pubrty
  • Less common in people over 25 yrs 
  • Inflammatory mediators from bacterial cell wall products and extracellular enzymes along with faty acids from pliase action on lipids
  • Intense local inflammatory response
  • Papules, pustules, and nodulocystic lesions typical of this disease
  • Treatment:
    • Comedonal acne-blackheads, white heads, no inflammation
      • Topical lipid dyring colutions-tretinon
    • Mild inflammatory acne-small papules or pustules
      • Topical for above + topical antibiotics/antiseptics: erythmycin or clindamycin _ benzoyl peroxide
    • Inflammatory acne, commedones, papules or pustules
      • Tpoical for above + oral antibiotics (doxycycline, minocycline, tetracycline, etc)
  • Accutane is bad: birth defects, depression, IBD
  • NO vaccine
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Atypial Mycobacteria
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  • Free-living in the soil and water
  • Growth within amoebae
  • Chronic diseases
  • Opportunistic infections only
  • Number of cases increasing, particularly in AIDS patients
  • Tuberculosis-like disease in presentation and pathogenesis
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Mycobacterium marinum
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  • Superficial skin lesions
  • Associated with fish tanks
  • "Swimming pool granulomas"
  • Growth in macrophages
  • Pigmented
  • Optimum temp is 32 C
  • Nodular skin lesions, break in skin is necessary
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Mycobacterium fortuitum
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  • Fast growing
  • wound
  • systemic
  • pulmonary disease
  • non-pigmented
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Nocardia species
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  • Pulmonary disease (AIDS patients)
  • Skin/tissue granulomas
  • Break in skin with exposure to soil necessar
  • An example is a puncture wound with rose thorn

 

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Mycobacterium ulcerans
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  • Acid Fast
  • Slow growing
  • Extracellular pathogen
  • DNA analysis suggests a recent divergence from M. marinum with the acquisition of a plasmid that codes for a potent lipophilic toxin (mycolactone)
    • Cytotoxic-tissue necrosis, leading to spreading ulceration.  Lethal for most cells
    • Anti-inflammatory/immunosupressive-little fever, no early granulomatous lesion
      • fills phagocytic cells etc
    • Mycolactone toxins are found in fish//amphiban pathogens but this is the only human pathogen mycolactone is found in
  • Aquatic environmental habitat
  • Human to human transmission
  • Aquatic environmental habitat following trauma usually on the legs or arms
  • Buruli ulcer disease (Bairnsdale ulcer disease in Australia)
    • Higher incidence in Children < 12 years
    • Swimming in rivers is a risk
    • In US only seen in recent immigrants
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Buruli Ulcer Disease
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  • Caused by Mycobacterium ulcerans
  • Pre-Ulcerative Stage
    • Inoculation into the tissue via a break in the skin
    • Incubation period: 2 weeks to 3 years
      • Average 2-3 months
    • Replication extracellularly in dermis and subcutaneous tissue with production of the mycolactone toxin
      • Tissue necrosis
      • Immunosupression
    • Disease manifests initially as a firm, non-tender nodule (1-2 cm) at site of trauma
  • Ulcerative Stage
    • Within 1-2 months the nodules erode forming a painless, continuously spreading ulcerative lesion as the bacteria spread into new tissue
    • Ulcerations can involve as much as 15% of the patients skin surface
    • Inflammatory cels are scarce in the active lesions
      • phagocytic cells that migrate to the lesion are killes by the mycolactone toxin
    • May include dissemination via bloostream with widespread damage
    • Infection may destroy nerves, appendages,and blood vessels
    • Ocassionally invade the bone
    • Delayed treatment leads to significant cosmetic and or functional disabilites
    • Untreated lesions tend to heal over months or years by a cell mediated granulomatous response with delayed-type hypersensitivity and scarring
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Mycobacterium ulcerans

Diagnosis/Treatment/Prevention

answer
  • Diagnosis: made on presentation
    • Acid fast stain of tissue
    • Culture (6-8 weeks(
    • PCR
  • Treatment: Requires rapid diagnosis and initiation for good response
    • Surgery to remove infected tissue
    • Skin grafts may be required
    • Combined antibiotic therapy: rifampin plus streptomycin or amikacin for 8 weeks
    • Heat packs 40 C on wounds or skin gradts
      • M. ulceranshas poor growth at 37 C
  • Prevention:
    • No vaccines
    • Preventative wound care
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Mycobacterium leprae
answer
  • Not Gm (-) but outer membrane has glycolipids
  • Can NOT be grown on lab media
  • Does NOT grow well at 37 C
  • Optimum growth at 25-33 C
  • Obligate intracellular pathogen that multiplies slowly
    • Mononuclear phagocytosis especially histiocytes in the skin
    • Schwann cells of the nerves
  • Humans are the primary natural host
  • Also foung in armadillos, and certain Monkeys
  • Person-person transmission
    • Respiratory droplets
    • Long incubation period-average 2-5 years
      • Range 3 months - 20 years
  • Most people are resistant to infections, children are more suspectible
  • Anyone with a defect in cell mediated immunity is at risk

 

 

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Leprosy
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  • Caused by Mycobacterium leprae
  • After respiratory exposure the bacteria are able to invade into the bloodstream
  • Bacteremia but no systemic inflammation
    • No sepsis
  • Migration to the skin-preference for cooler areas of the body with the temperature < 37 C
  • Growth as an obligate intracellular pathogen that multiplies very slowly
      • Mononuclear phagocytes, especially the histiocytes in the skin
      • Schwann Cells of the nerves
  • Tuberculoid leprosy
    • Benign, non-prgressive
    • Rapid onset of asymmetric loss of nerve functions
    • Macular skin lesions-may have hypo-pigmentation
    • Few bacteria in the lesions
    • Positive lepromin skin test
    • Cell mediated immune response intact
  • Borderline leprosy
    • Transition from tuberculosis to lepromatous stages
    • Skin lesions more extensive
    • Bacteria increasing
    • Cell mediated immunity is decreasing
  • Lepromatous Leprosy
    • Rapid progressive course
    • Nodular skin lesion
    • Slow, symmetric nerve involvement with loss of the sense of touch, leading to injury with hands and feet
    • Abudant bacteria in skin lesions, continuous bacteremia
    • Negative lepromin skin test
    • Cell mediated immune response is markedly depressed
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Mycobacterium leprae

Diagnosis/Treatment/Prevention

answer
  • Diagnosis:
    • Symptoms, type, and distribution of lesions, endemic area
    • Acid-fast stains: skin lesions and tissue
    • Lepromin skin test useful only for tuberculoid leprosy
    • New DNA probes with PCR
  • Treatment
    • Traditional therapy: 4,4-diaminodiphenylsulfone (DDS or dapsone)
      • Life time treatmet
      • Resistance is increasing (40%)
    • Combined Treatment
      • Dapsone/rifampin/clofazimine-lepromatous
      • Dapsone/rifampin-tuberculoid
      • 1-2 years or until skin smears are negative
  • Prevention
    • Early detetion and treatment
    • No Vaccine
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Epidermophyton
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  • Dermatophytes
  • Grow only as septate filamentous fungi
  • Smooth walled, club shaped macroconidia
  • ABSENCE of microconidia
  • Chlamydospores and arthrospores
  • Arthrospoores are significant in transmission
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Microsporum
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  • Dermatophytes
  • Grow only as septate filamentous fungi
  • Prominent microconidia
  • Rough walled, spindle shaped macroconidia
  • Arthrospores ae more significant in transmission
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Trichophyton
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  • Dermatophyte
  • Grow only as septate filamentous fungi
  • Prominent microconidia
  • Few smooth-walled cylindrical, club-shaped or cigar shpaed macroconidia
  • chlamydospores and arthrospores
  • Arthrospores are significant in transmission
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Dermatophytes
answer
  • Keratinophilic fungi
  • Keratinase t degrade keratin in the skin, hair, and nails
  • Elastase and proteinases present
  • Microsporum species secrete pteridine that fluoresces bright blue-green under long wave UV light
    • Woods lamp-diagnostic
  • Associated with humans, animals, or soil
  • Transmitted to humans via
    • direct contact with infected tissue (human or animal)
    • Human contact with soil
      • Indirectly through contaminated surfaces or objects (hair brushes)
  • Arthrospores are produced in high amounts in tissues are are VERY infectious
  • Microconidia and macroconidia are potentially infecios
  • May affect both normal and immunocompromised
  • Risk of invasion deeper into the body in immunocompromised
  • Moist areas provide the most favorable environment for establishment of fungal infections
  • When arthospores or conidia are transmitted to the new host they germinate and the hyphae invade into the keratinized tissue in order to obtain nutrients
  • Endothrix Pattern of growth: fungal hyphae grow inside the hair shaft, eventually breaking off the hair and leaving a block dot (T. tonsurans)
  • Ectothrix growth: Fungal hyphae grow on the outer surface of the hair shaft an results in scaly patterns with ahir loss ( M.canis)
  • Favus pattern of growth: Most aggressive type of scalp hair infection, hyphae growing inside the hair shaft, with production of air bubbles withn the hair.  yellow thick crusts and inflammation produce scarring. (T. schoenleinii)
  • No invasion into healthy living tissue, except in severely immunocompromised patietns
  • Inflammation and pathology result from the production of extracellula enzymes and other metabolic by-products that induce an inflammatory response, with redness, swelling, and itching
  • The classic lesion is red, scaly with an advancing border with a greater degree of inflammation at the margins (termed an actived border), often with central clearing.
  • Seen on the trunk, arms, legs
  • Itching is a major symptoms
  • Scalp infections may lead to patches of hair loss (alopecia)
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Tinea capitis
answer
  • Infection of the scalp hair and skin
  • Transmission fostered by poor hygiene, ovrcrowding, and contaminated items
  • Seen mainly in children
  • Scalp scaling, scalp pruitus, occipital adenopathy, and diffue or pathy alopecia
  • Most caused by T. tonsurans
    • Non-fuoescent
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Tinea faciale
answer
  • Infection of the face
  • Lesions seen on non-bearded parts of the face
  • Some classic lesions, others less distinct
  • May be confused with other skin lesions
  • T. tonsurans most common in US
  • T. mentagrophytes and T. rubrum in Asia
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Tinea barbae
answer
  • Infection of the mustache, beard area, and neck
  • Caused by zoophilic and anthropophilic species
  • Farm workers often effected from exposure to animals
  • T. verrucosum (cattle) most common
  • M. canis, M. mentagrophytes
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Tinea Corporis
answer
  • Infections of the trunk, arms, legs
  • Usually demonstrates the classic "ringworm" lesion with central clearing
  • Seen in adults and children
  • Hot humid climates
  • T. rubrum, M. tonsurans (anthropophillic) and M. canis, T. verrucosum (zoophilic), M. gypseum
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Tinea manuum
answer
  • Infection of the palms of the hands
  • Diffusely dry, scaly, erythematous
  • T. rubrum-may be an extension of Athlete's foot
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Tinea cruris
answer
  • Infection of the groin "jock itch"
  • E. floccosum, T. rubrum
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Tinea pedis
answer
  • Infection of the soles of the feet and interdigital web "Athlete's foot"
  • Interdigital form: most common, lesions with fissuring, maceration between toes
  • Plantar skin becomes clinically scaly and thickened with hyperkeratosis and erythema of soles, feet and sides of feet
  • Vesiculobullous form: characterized by vesicles, pustules, and coems bullae in an inflammatroy patern on the soles
  • T. rubrum
  • T. interdigitale
  • T. mentagrophytes
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Tinea unguium
answer
  • Infection of the nails (onychomycosis)-feet (most common) or hands
  • Thickened, broken, discolored, and dystrophic nails
  • Nail plate may be separated from the nail bed
  • T. rubrum
  • T. mentagrophytes
  • Dermatophyte form and non-dermatophyte forms
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Pityriasis (tinea) versicolor
answer
  • Non-dermatophyte
  • Malassezia furfur
  • Lipophilic yeast that is normal flora of the skin
  • Hyperpigmented macules thatcoalesce to form scaling plaques, usually NOT itchy
  • Stimulus for the disease unknown
  • Often resolves spontaneously
  • Also associated wtih seborrheic dermatitis and dandruff
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Tinea nigra
answer
  • Hortaea werneckii
  • Inoculation onto the skin from soil, growing as a filamentous fungus in the stratum corneum in moist areas
  • Growth on lipids
  • Tolerates increased salt, low pH
  • Generally the infection is asymptomatic (rare itching), appears as brown-to-black macule, beginning as a small; dark spot and enlarging slowly (weeks to months) to several centimeters with times
  • Lesionsare typically located on the soles of feet or palms of the hands
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Black piedra
answer
  • Piedra hortae
  • Inoculation onto the skin and hair from the soil growing as a filamentous fungus on the hair shaft, particularly the scalp hair.
  • Infection is asymptomatic, but the fungal growth and firm adhering black to brown;nodules on the hair shafts can weaken the hair causing breakage
  • Rare in US occurs in tropical and subtropical regions
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White piedra
answer
  • Caused by Trichosporon
  • The dimorphic yeast is common in the soil but being recognized as a member of the normal flora of the human skin, nails, mouth, and GI tract
  • Transmission of infection is not known
  • Infected hair occurs minly in the pubic, beard, scalp areas
  • Fungal noduleson the hair shaft are white-to-light brown, easily removed
  • Infections are most common in temperat climates, common in parts of southern US
  • T. cutaneum causes superficial skin infections
    • Cutaneous lesions
    • Onychomycosis
    • Disseminated infections-resulting in positive blood cultures
    • endocarditis
    • meningitis
    • Has significant intrinsic resistnace to amphotericin B, azoles, and echinocandins
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Diagnosis/Treatment/Prevention

of

Dermatophyte and Non-Dermatophyte Fungi

answer
  • Acute and Chronic inflammatory response are important for maintaining the superficial nature of the infections
  • Inflammatory environment with iflux of neutrophils is not favorable for fungal replication
    • Diseases with impaired neutrophil response (diabetes) have a higher risk for dermatophyte infection, particularly onychomycosis
  • Cell mediated immune response seems to be critical for defense and recovery
  • AIDS patients may be extensively infected and disseminated dermatomycoses are also observed only in AIDS patients
  • Diagnosis
    • Woods light examination-only useful if + M. canis infection
    • Direct microscopic examination-skin scrapings, hair, nail scrapings
    • KOH treatment to degade keratinized tissue, observe directly or stained
    • skin biopsy
    • Observe for branching, septate hyphae, with arthospores, for skin biopsy observe for prominent neutrophils in stratum corneum
    • Culture-results are slow-2 weeks
  • Treatment
    • Historically treated with oral griseofulvin
    • Newer azoles and allyamines are more effective and work well together
  • Tinea corporis, cruris, or pedis treatment
    • mild: topical butenafine Lotrimin Ultra, terbinafine (Lamisil)
      • 2-3 weeks
    • extensive: oral terbinafine (Lamisil)
      • 2 weeks- 4 months
  • Tinea capitis treatment: oral terbinafine-4-8 weeks
  • ;Onychomycosis Treatment: oram terbinafine-6-12 weeks
  • Pityriasis (tiea) versicolor treatment- topical or oral ketoconazole or fluconazole
  • Trichosporon treatment- intrinsic resistance to many anti-fungal drugs
  • Hortaea/Piedraia treatment- topical anti fungals
question
Sporotrichosis
answer
  • Organsim: Sporothrix schenckii
    • Thermally dimorphic fungus
  • "Rose handlers disease"
  • 37 C: Growth as oval to cigar shaped yeast cells. This is observed is tissue
  • 25 C: Growth as filamentous fungi with hyaline hyphae (septate), conidophores and conidia.
    • Conidiophores are sympodial and arise at right angles to the hyphae. Conidia are arranged in rosette like clusters at the tip of conidiophores
  • Skin trauma, usually to extremities
  • Appearance of a reddish, necrotic, nodular papule at the inoculation site.; Appears 1-10 weeks after the injury
  • Lesion will usually suppurate, ulcerate, anc become chronic
  • Frequent spread along the lymphatics with additional ulcerating nodules appearing
  • Disseminaton may occur in AIDS patients and other immunocompromised persons
    • May also cause a primary inhalaton pneumonia in these latter patients
  • Diagnosis:
    • Direct microscopic examination: observe for yeast vs. hyphae (pigmented vs. hyaline)
    • Culture: results are slow
  • Treatment:
    • Surgical excision or cryocurgery of infected lesions is usually necessary
    • Recommended antimicrobial therapy (generall long term due to slow response)
    • Cutaneous/lymphonodular-itraconazole (3-6 months)
    • Pulmonary-itraconazole (6-12 months)
    • Meningitis-amphotericin B followed by itraconazole
question
Chromoblastomycosis
answer
  • Organsims: Fonsecaea, Phialophora, Cladosporium, Rhinocladiella
  • Dimorphic (nutrient not temperature)
  • Tissue: thick walled, dark brown rounded sclerotic cells known as Muriform cells or Medlar bodies. Divide by planar splitting not budding
  • Lab agar media- grow as dematiaceous (dark brown) hyphae (septate) forming slow growing, dark, velvety colonies with a black reverse at 25 or 37 C.;
  • Seen world wide but higher in tropics and subtropics
  • Commin in men who work outside in rural areas
  • Skin trauma from thorns or splinters usually to extremities. Often not remembered since skin trauma occurs several years before lesions appear
  • Lesions start as a small scaly bump that slowly develops; into a raised crusted lesion with a dry warty appearance. The center of the lesion may clear partially
  • Slow spread (2mm/year) to healthy skin with new satellite nodular lesions and plaques
  • The limb may be very swollen (elephantiasis) and covered with various nodular scaly or verrucous lesions that resemble cauliflower
  • Rarely disseminates via bloodstream to the brain.
  • Treatment:
  • Surgical excision or cryocurgery of infected lesions is usually necessary
  • Recommended antimicrobial therapy (generall long term due to slow response)
question
Phaeohyphomycosis
answer
  • Organisms: Exophiala, Wangiella, Phialophora, Alternaria, Bipolaris etc
  • All species grow with dematiaceous hyphae septate in tissue.;Some species produce both hyphae and yeast in tissue
  • Very diverse group of at least 71 species from 39 genera.; Identification based on microscopic sporulation in conidia production
  • Subcutaneous Infection:
    • Skin trauma from thorns, splinters, or soil
    • Generally a single swollen cystic granulomatous lesion or abscess develops at the site of implantation.;
    • Immune compromised patients can develop multiple lesions with odules and ulcers
    • Similar implantation of spores can occur in the eyes, corneal lesions
  • Respiratory/Disseminated Infections
    • Inhalation of fungal spores to:
      • Nasal cavity-lesions on the nasal septum
      • Sinuses-Sinusitis, often associated with allergic rhinitis or immunosupression
      • Lungs-pneumonia seen with immunosupression
    • Dissemnation via the bloostream to brain. Meningitis is most common
  • Treatment:
    • Surgical excision or cryocurgery of infected lesions is usually necessary
    • Recommended antimicrobial therapy (generall long term due to slow response)
question
Mycetoma
answer
  • Organisms: Pseudoallescheria, Madurella, Acremonium
  • Diverse group of fungi
  • All species grow as filamentous fungi in tissue but form masses of fungi that appear as tiny balls or grains with white or black draining pus
  • Madura Foot
  • Usually involves;the feet, following implantation of fungal spores from the soil
  • Initially a simple primary lesion, develops as a small painless lump under the skin.; Fungal growth is slow but is locally invasive, indolent and tumor like, eventually involving the underlying muscle and bone.
  • Eventually multiple subcutaneous lesions consist of abscesses, granulomatous lesions
  • Middle of the lesion caves in, ulcerates and discharges pus (white or black grains).; The grains are the hallmark.
  • Lesions can eventually cause considerable deformity
  • Treatment:
    • Surgical excision or cryocurgery of infected lesions is usually necessary
    • Recommended antimicrobial therapy (generall long term due to slow response)
question
Spirochetes Properities
answer
  • Spiral shape due to peptidoglycan
  • Outer envelope similar to GM (-) bacteria but NO LPS
  • Periplasmic flagella- very actively motile, seems to be required for virulence
  • Very long, very thin (too thin to see with light microscope)
  • Must use dark field microscopy or silver impregnation for Treponema and Leptospira
  • Blood smears-wright or giemsa for Borrelia
  • Difficult to grow in vitro
  • Extracellular pathogens
  • How they evade the host immune response is now known in most cases
question
Treponema pallidum-Syphilis
answer
  • Seen in humans with disease
  • Transmission is person-person via sexual contact
  • Rate 6X more commin in men
  • Biggest increase seen in men having sex with men
  • HIV/AIDS have accelerated stages, increased severity, increased neurosyphilis
question
Primary Syphilis
answer
  • Penetration of mucous membranes by T. pallidum, multiplication at site of infection with proliferation in regional lymph nodes.;
  • Extracellular
  • Development of chancre at site of entry within 2-10 weeks
  • Sinlge lesion at site of contact (may be oral)
  • Smooth base, sharply demarcated walls "hard chancre"
  • Painless
  • Enlarged inguinal lymph nodes
  • Highly infectous, full of spirochetes
  • Darkfield/silver stain of skin scrapings-positive
  • If untreated spontaneous healing within 3-6 weeks
  • Some patients do not develop disease beyond primary stage
  • Good antibody response against organism-positive serology
question
Secondary Syphilis
answer
  • Dissemination of T. pallidum throughout the body with multiplication in lymph nodes, liver, joints, muscles, skin, and mucous membranes
  • Extracellular
  • Development of muco-cutaneous lesions within 1-3 months after the primary chancre
  • Rash on palms and soles
  • Alopecia-pathy hair loss
  • Papules in genital area
  • Skin lesions any where on body
  • Lesions in the mouth
  • Highly infectious
  • Painless
  • Flu like illness, fever, sore throat, headache, and lymphadenopathy
  • May last 2-6 weeks
  • 1-3 relapses in 25% of untreated patients
  • Some patients do not develop disease beyond the secondary stage
question
Latency-Syphilis
answer
  • Asymptomatic period between secondary and tertiary disease
  • Early latency;; 4 years
  • Long latency ; 4 years
  • No clinical symptoms but positive serology
question
Tertiary Syphilis
answer
  • Varied symptoms " The great pretender"
  • Development of gummas (granulomatous lesions) ; 10 years after primary syphilis
  • Spirochetes absent (immunopathology)
  • occurs in 25-40% of untreated patients
  • Skin and bone affected
  • CNS (neurosyphilis)-brain and or spinal cord (tabes dorsalis)
    • Progressive mental deterioration, insanity
    • Muscular incoordination, sensory disturbances
    • Acute pain
    • Paralysis of leg muscles
    • Acute abdominal pain
  • cardiovascular system (commonly aorta)
question
Congenital Syphilis
answer
  • Infection of te fetus-usually after 16th week of gestation
    • 100% risk of transmission if woman has primary
    • 90% risk of transmission if woman has secondary
    • 30% with ealy latent
    • no risk with late latent or tertiary syphilis
  • Fatal in 25-50% of cases without antibiotic syphilis
  • Early congenital symptoms (; 2 years of age, chronic infection)
    • low birth weight
    • Cutaneous lesion and mucoid patches on palms and soles
    • Snuffles-highly infectous mucoid nasal discharge
    • Hepatosplenomegaly
    • nephritis
    • Long bone involvement
    • multiple organ failure
  • Late congenital symptoms (; 2 yrs of age)
    • Stigmata (visible evidence of disease, permanent defects)
    • Hutchinson triad:
      • Hutchinson's teeth-notched permanent incisors
      • Interstitial keratitis-chronic inflammation of the cornea
      • Deafness
    • Saddle nose
    • Boney deformities
    • Similar to tertiary syphilis
question

Diagnosis/Treatment/Prevention

Syphilis

answer
  • Culture and Gm stain NOT possible due to small size
  • Non-treponemal antigen tests-screening
    • Cardiolipin-lecithin-cholesteol suspension as antigen
    • Detects nonspecific IgM, IgG antibodies called reagin
    • May be negative in tertiary syphilis
    • Subject to false positives
  • Treponemal antibody test-confirmation
    • Fluorescent treponemal antibody absorbed (FTA-ABS)
    • T. pallidum as antigen
    • Once positive remains so for life
    • Reported as negative or positive
    • Specific and sensitive
  • Treatment:
    • Penicillin G-preferred for treatment of all stages of syphilis
    • Primary/seconday/early latency-1 dose of 2.4 million units IM
    • Neurosyphilis-3-4 million units IV every 4 hours for 10-14 days
    • Jarisch-Herxheimer reaction-acute febrile reaction < 24 hours of start of penicillin
    • Alternative: azithromycin
question
Other Treponemal Diseases
answer
  • Non-venereal contact
  • Bejel (endemic syphilis):
    • caused by endemicum
    • middle east, africa
    • Acquired in early childhood
    • Lesions primarily in the mouth
    • Mouth to mouth transmission
  • Pinta
    • Caused by T. carateum
    • Central and South America
    • Hyperpigmented lesions
    • Skin to skin transmission
  • Yaws
    • Caused by T. pertenue
    • Tropical forests worldwide
    • Resembles syphilis in course of disease
    • skin to skin transmission
    • Dissemination like T. pallidum possible
question
Klebsiella granulomatous
answer
  • Granuloma inguinale (Donovanosis)
  • Intracellular, pleomorphic Gm (-) bacteria
  • One of more nodules that erode to form beefy-red, painless, slowly spreading granulomatous ulcers that bleed easily
  • Uncommon in US but much more connon in tropical/subtropical regions such as India, New Guinea, Austilia, Caribeban, Brazil
  • Dianosis - microscopic observation of Donovan bodies (intracellular bacteria)
  • Treatment- doxycycline, fluoroquinolones
question
General Properities of Genus Nisseria
answer
  • Gm (-) diplococci
  • Obligate parasites of the respiratory and genital tract of humans
  • Obligate aerobes (do NOT ferment carbohydrates), catalase (+), oxidase (+) (high cytochrome oxidase activity)
  • Sensitive to adverse environemntal conditions-drying, cold, UV light
  • Special growth media (chocolate agar) required
  • Increased CO2 required
question
N. gonorrhoeae
answer
  • Gm (-) diplococci
  • Obligate parasites of mucosal surfaces (female genital, intestinal, URT)
  • Never considered normal flora
  • LPS- endotoxin, cytotoxin, no O-antigen
  • Outer Membrane Proteins- major adhesins, vaccine development
  • Pili (fimbriae)-major adhesin, major virulence factor, Vaccine target
    • Large strain to strain antigenic variation (problem for vaccine)
  • NO capsule
  • Exoenzymes- IgA protease, B-lactamase (10% os strains)
  • Sexual transmission, transmission to newborn during birth
  • 25% risk of transmission from a single exposure
  • Uncomplicated Infections- mucosa surface/ submucosal invasion, inflammation
    • Lots of pus present
    • Males
      • Urethra, pharynx (homosexuals), conjunctiva (newborn)
      • Urethritis is painful, very likely to be diagnosed early
    • Females
      • Endocervix, rectum, conjunctiva (newborn)
      • Infection is often asymptomatic, leading to delayed treatment
  • Complicated infections- Chronic infections, spread to adjacent tissues if primary infection is not treated
    • Males
      • Chronic prostatitis
      • Urethral strictures
      • Uncommon in US
    • Females
      • Pelvic inflammatory disease-often a mixed infection with syphilis
      • Occurs in 20% of untreated primary infections
      • Infertility, ectopic pregnancies
      • Abscesses, peritonitis
  • Disseminated Infections
    • Spread via lymphatics to bloodstream
    • No sepsis due to lack of capsule
    • Foci of infection at other body sites
    • 1% of untreated primary infections
    • Arthritis and or tenosynovitis-extremities
    • Dermatitis-often a single lesion on arms or hands
    • Endocarditis-rare occasions
    • No sepsis
    • If arthritis/tenosynovitis and dermatitis is present this is diagnostic

 

question

Diagnosis/Treatment/Prevention

N. gonorrhoeae

answer
  • Diagnosis in MEN
    • Urethral exudate, pharyngeal swab
    • Gm stain(Gm (-) diplococci and nertrophils) on urethral exudate-diagnostic
    • Culture on chocolate agar with antibiotics, increased CO2
      • Identification of isolates: + oxidase test
    • DNA amplification/detection: Urine test can also identify syphilis
  • Diagnosis in Females-endocervical swab, rectal swab
    • Gm stain-not appropriate
    • Culture on chocolate agar with antibiotics, increased CO2
      • Identification of isolates: + oxidase test
    • DNA amplification/detection: Urine test can also identify syphilis
  • Disseminated infections (male or female)- blood, synovial fluid
    • Gm stain on synovial fluid
    • Culture-chocolate agar + CO2 (no normal flora)
  • Treatment of uncomplicated Infections: two drug therapy due to drug resistance and co-infection with chlamydiae
    • Ceftriaxone (250 mg IM single dose) + doxycycline ( 7 days)
    • Fluoroquinolones-increased resistnace
    • Spectinomycin-especially for penicillinase producing strains
  • Treatment of Neonatal and Disseminated Infections- Penicillin G (IV) and ceftriaxone (IV, IM)
  • Pelvic Inflammatory Disease- combined broad spectrum antimicrobial therapy
    • Ceftriaxone/cefoxitin (IM/IV) + doxycycline (oral) ±metronidazole
    • Clindamycin (IV) + gentamicin (IV or IM) + doxycyline (oral)
  • Prevention
    • No successful vaccine
    • Public Health offcials-trace all sexual contacts
    • Education
    • Prophylaxis-erythromycin ointment for newborn eyes
question
General Chlamydia characteristics
answer
  • Obligate intracellular bacteria
  • Host target cell-columnar epithelial cells lining mucous membranes of humans and animals
    • Urethra
    • Endocervix
    • Endometrium
    • Fallopian Tubes
    • Rectum
    • Respiratory Tract
    • Conjunctiva
  • Cellular Location-phagosome of the host cell
    • Inhibit phagosome-lysosome fusion
    • Appears as an inclusion in the cell
  • Pathogenesis of infections if due to persistent inflammation-alternating cycles of host cell destruction and chlamydial growth.
  • Elementary Body (EB)
    • Infectious
    • Responsible for attachment and entry
    • Inhibits phagolysosomal fusion
    • Rigid cell wall-lacks traditional peptidoglycan but has disulfide cross-linking of the major outer membrane protein
    • Tough, survives environmental stress "spore like"
  • Reticulate Body (RB)
    • Metabolically active form within phagosome
    • Divides by binary fission
    • Osmotically fragile-do not survive in environement
    • Enlarging phagosome full of dividing and differentiating RBs is called an inclusion
    • Gm (-) membrane but no peptidoglycan (LPS is present)
  • Genus specific LPS (all Chlamydia have the same major LPS antigen)
  • Species specific antigen-heat labile protein
  • Type specific antigen (serovars)-MOMP a heat liabile protein on the surgace of EB.  Each serovar cause different disease
question
Developmental Life Cycle of Chlamydia
answer
  • Phase 1
    • Transmission of mucosal secretions from an infected person or animal
    • Attachment of infectious RBs to host epithelial cells
    • Endocytosis within phagosome
    • Inhibition of phagolysosomal fusion
  • Phase 2
    • Primary differentiation of EBs into RBs by 9 hours post infection
  • Phase 3
    • Growth and Binary fission of RBs
    • Genus specific antigen on surface of infected cells within 18 hours
    • Inclusions are present (phagosome filled wiht RBs)
  • Phase 4
    • Secondary differentiation of RBs to EBs bu 24 hours post infection
  • Phase 5
    • Release of infectious EBs by host cell lysis or exocytosis at 40 hours post infection, transmission to other susceptible hosts
question
Diagnosis of Chlamydia
answer
  • Direct microscopic examination of specimens for cytoplasmic inclusions-Giemsa or iodine
  • Direct microscopic detection of chlamydial antigens in epithelial cell inclusions
    • Fluorescein or enzyme labeled monoclonal antibody
  • DNA amplification/detection-in combinaton with ghonerra
  • Isolation in cell culture- McCoy fibroblasts or epithelial cells-examine for inclusions
question

Chlamdia trachomatis servars A-C

Trachoma

answer
  • Leading, preventable cause of blindness in the world
  • Common in poverty-stricken regions of Africa and southeast Asia
  • Spread from child to child in a household by flies, dirty clothing, fingers
  • Early Disease in children (< 2 years of age)
    • Inflammation within the epithelial cells of the conjunctivae
    • Begins as purulent conjunctivtis and develops into a follicular keratoconjunctivitis
  • Development of Blindness-may no occur into 40 yrs of age, chronic disease
    • Scarring of the conjunctiva as a result of follicular necrosis
    • Deformity of the eyelids- turning in of eyelashes
    • Abrasion of the cornea-ultimately resulting in blindness
    • Ingrowth of new blood vessels into cornea
    • Repeated infections over time-extensive lymphoid proliferation with formation of lymphoid follicles
  • Treatment:
    •  Topical tetracycline ointment 2X day for 6 weeks- compliance problem
    • Erythromycin-single oral dose (expensive but more reliable
    • Surgery to correct lid deformities
    • No vaccines
question

Chlamydia trachomatis servars D-K

Genital Tract Infections

answer
  • Human to human transmission via sexual contact
  • Most common sexually transmitted pathogen
  • Replication in epithelial cells
  • Nongonococcal Urethritis (NGU)- males
    • Infection of the urethra-causes inflammation
    • Clear to purulent discharge-sometimes not noticeable
    • Begins 7-10 days after sexual contact
    • Gm stain reveals neutrophils and NO organisms
    • Pain upon urination in 50%
    • If left untreated it may be followed by epididymitis
  • Cervicitis-females
    • Cervix most commonly affected site with inflammation
    • May have mucoid or purulent discharge-often not noticeable
    • 75% asymptomatic with no noticeable discharge
  • Acute Pelvic Inflammatory Disease- often co-infected with N. gonorrhoeae
    • Untreated infections may spread to the uterus and Fallopian tubes
    • Inflammation in these new areas of colonization
    • subacute or chronic with mild abdominal pain and unimpressive tenderness
    • Scarring of Fallopian tubes leading to infertility and ectopic pregnancy
  • Reiter's Syndrome "The patient can't see, can't pee, and can't bend the knee"
    • Primary bacterium wiht this syndrome
    • HLA-B27 linkage
    • reactive arthritis, urethritis and uveitis following active disease
    • Occurs most often in men
    • Also seen in infections from Salmonella, Shigella, Campylobacter, and Yersinia
  • Treatment is prescribed on the basis of clinical diagnosis or as a co-treatment for gonorrhea
    • Doxycycline is most widely used
    • Erythromycin/Azithromycin-alternative for pregnant women
    • No vaccines
    • Treat sex partners of infected pateints (contact within 30 days of onset of symptoms)
question

Chlamydia trachomatis serovars D-K

Venereal Infections in Neonates

answer
  • Inclusion Conjunctivitis
    • Purulent conjunctivitis that heals without scarring
    • Eyes become infected during passage through the birth canal
    • Incubation of 5-21 days after birth
  • Opthalmia Conjunctivitis
    • Purulent conjunctivitis occuring usually within the first 10 days of life
  • Pneumonia
    • Infected during passage through birth canal
    • Develops at 3-11 weeks of age
    • Cough and little fever
    • Often preceded by inclusion of conjunctivitis
question

Chlamydia trachomatis serovars L1-L3

Lymphogranuloma Venereum (LGV)

answer
  • Seen in tropical and subtropical areas of Africa and Asia
  • Seen in homosexual males in US
  • Incubation period usually 1-3 weeks after intercourse
    • Incubation period may be longer
  • Small painless ulcer at the site of sexual contact (angogenital area in male homosexual)
  • Ulcer heals in a few days but bacteria invade systemically
  • 2-6 weeks later development of inguinal lymphadenopathy with painful lymph nodes
  • Granulomatous micorabscesses in lymph nodes
  • If untreated: leads to chronic infection
    • Colorectal fistulas and strictures
  • Difficult to dianose because it is rare and can look like other diseases
  • Genital or lymph nodes swap or aspirates-nucleic acid detection, serology
  • Treat with Doxycycline
    • 3 weeks
  • No vaccine
question

Chlamydia pneumoniae

Community Acquired Pneumonia

answer
  • Person to person spread via respiratory secretions
  • Most infections in school aged children and young adults
  • Accountss for 10% of community acquired pneumonia
  • Also infects animals
  • Begins with URT symptoms: pharyngitis, sinusitis, otitis media
  • Progresses to bronchitis-mild to severe atypical pneumonia
  • Must distinguish from Mycoplasma pneumoniae
  • Treat with doxycycline
  • Can treat with Azithromycin-will cover other atypical pneumonia agents: Legionella and Mycoplasma
  • No vaccines
question

Chlamydia psittaci

Psittacosis-Community acquired Pneumonia

answer
  • Inhalation of chlamydiae from infected birds (dead or alive) and their droppings
  • Psittacine birds: parrots, parakeets, pigeons, turkeys
  • Infection is often mild or aymptomatic but can be fatal
  • Elderly are more likely to have a symptomatic infection
  • Unilateral, lower lobe interstitial pneumoniae
    • Atypical pneuomonia
  • Can disseminate systemically to liver, spleen, heart, and CNS
    • More common in immunosupressed pateints
  • Treat with doxycycline
  • Azithromycin-covers the other atypical pneumonia pathogen-Legionella and Mycoplasma
  • No Vaccine
question
General Properities of Rickettsiae
answer
  • Gm (-)
  • Obligate intracellular growth
  • Rickettsial genome: Similar to mitochondria.; Thought to be the closest living relative to mitochondria and are believed to be involved in the endosymbiotic process of eukaryotic evolution.;
    • No genes for glycolysis
    • No genes involved in biosynthesis
    • No genes involved in regulation of amino acids and nucleosides
      • All of these functions are provided by the host
question
Rickettsia rickettsii
answer
  • Rocky Mountain Spotted Fever
  • Host Target Cell: Vascular Endothelium
  • Intracellular location: Cytoplasm
    • Can travel cell to cell without exiting hose cell via actin polymerization
  • Transmitted to rodents, dogs, and humans;by the bite of the adult domestic dog tick.
  • Most common and most severe tickettsial disease in Western hemisphere
  • Found in 38 states including KY.; Most common in South Atlantic and Ozark regions (North Carolina and Oklahoma)
  • 2/3 in children under age of 15
  • Tick must be attached for 24-48 hours for bacterial transfer
  • Spring-summer transmission
  • Symptoms appear 5-7 days after tick bite
  • Fever, headache (severe and frontal)
  • Macular, maculopapular, petichial rash
    • extremities to trunk-centripetal
    • may become necrotic
  • Vasculitis- growth of Rickettsia in endothelial cells causing ststemic inflammation
  • Perivascular infiltration of mononuclear cells, plasma cells, and macrophages ; leakage ; thrombosis ; microinfarction ; vascular necrosis
  • Shock, multiple organ failure (especially renal)
  • Death in 20% if untreated or delayed treatment
  • Diagnosis
    • Clinical Presentation-progression of rash from extremities to trunk
    • History of tick bite
    • Rapid detection in tissue (skin scraping)
      • Direct immunofluorescence microscopy
      • PCR
    • Serology to confirm diagnosis-to slow for primary diagnosis
  • Treatment-doxycycline
  • Treatment needs to be intitiated early to get a goodresponse
  • No Vaccine
question
Rickettsia conorii
answer
  • Boutonneuse fever- Southern Europe, Africa, Middle East
  • Transmitted from rodents and dogs by tick bite
question
Rickettsia akari
answer
  • Host Target Cell: Vascular Endothelium
  • Intracellular location: Cytoplasm
    • Allows cell to cell spread via actin tail to avoid the immune response
  • Rickettsial Pox
  • First identified in NY in 1946
  • Transmitted from house mice by the bite of a mite
  • Highest risk in urban areas with mice infecstations
  • Replication in endothelial cells, less sever tehn rocky mountain spotted fever
  • Lesion develops with a black crusty scab at the site of tick or mite bite
  • Lymph node swelling
  • Chills, fever, adn headache accompanied by a maculopapular rash
  • Usually mild course with rare fatalities
  • Lesion to recovery period is over three weeks
question
Rickettsia prowazekii
answer
  • Epidemic Typhus-louse borne
    • Africa, Asia, South America
    • Human louse vector (no animal reservoir)
    • Human to human disease
    • Louse feces-rubbed into bite, suberficial abrasion or inhaled
    • Delousing with DDT helped to lower deaths in WWII
  • Sylvatic typhus-exposure to flying squirrels
    • Eastern US
    • Louse or flea vector (animal to human)
    • Milder disease than epidemic typhus
  • Brill-Zinsser-reoccurance of a mild disease months or years after primary epidemic typhus
  • Rickettsai typhi and R. felis
    • Endemic typhus (Murine typhus)
    • Flea borne from rodents
    • Risk for travelers
  • Clinical Manifestations of all typhus disease are similar only differing in speed and severity
    • Symptoms appear 5-10 days after louse or flea bite
    • Fever, headache, myalgia
    • Macular, papular rash
      • Trunk to extremities-centrifungal
    • Vasculitis of small vessels of many organs (especially the liver)-causing systemic inflammation
    • Clotting abnormalities, shock, multiple organ failure, death
    • Milder symptoms in Brill-Zinsser disease, sylvatic typhus, and murine typhus
  • Diagnosis
    • Clinical presentation-progression of rash from trunk to extremities
    • Rapid detection in tissue (skin scrapings0-speed is important
      • Direct immunofluorescence microscopy
      • PCR
    • Serology to confirm diagnosis-too slow for primary diagnosis
  • Treatment-doxycycline
  • No Vaccine
question
Orientia tsutsugamushi
answer
  • Scrub Typhus
  • Mite (chigger) vector from mice or other rodents
  • Seen in areas of low vegetation or "scrub"
  • Typhus like disease
  • Incubation period 6-21 days
  • Fever and headache
  • Localized escher at site of bite
  • Macular, papular rash
    • Trunk to extremities (centrifigal)
  • Usually mild, rare fatalities
question
Ehrlichia chaffeensis
answer
  • Human Monocytic ehrlichiosis (HME)
  • Common in KY, common in eastern US
  • Incidence highest in adults
  • Lone star and dog ticks-deer is natural host
  • Replication in bloodstream monocytes and tissue macrophages
  • Incubation period 3-4 weeks after tick bite
  • Rash seen in 50% of patients
  • Leukopenia and thrombocytopenia
  • Systemic inflammation
  • Fever, Headache, Vomiting
  • Death in 2-5 % of cases
  • Diagnosis:
    • Presentation with history of tick bite
    • Part of Tick-borne serology panel
  • Treatment-doxycycline
  • No Vaccine
question
Anaplasma phagocytophilum
answer
  • Human granulocytotropic anaplasmosis (HGA)
  • Diagnosis:
    • Presentation with history of tick bite
    • Part of Tick-borne serology panel
  • Treatment-doxycycline
  • No Vaccine
  • Common in KY, common in upper midwest
  • Deer ticks (cotransmitted with Lyme disease)
  • Deer is natural host
  • Repliation in circulating granulocytes
  • More acute than HME
  • Incubation period 1 week after tick bite
  • Rash is rare
  • Leukopenia and thrombocytopenia
  • Systemic inflammation
  • Fever, headache, confusion
  • Death in 7-10%
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Ehrlichia ewingii
answer
  • Newly discovered
  • Replication in granulocytes
  • Same tick vector as HME
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Bartonella henselae
answer
  • Cat-Scratch Disease
  • Cats are often asymptomatically infected
  • Transmitted by a cat bite or scratch (contaminated with saliva)
  • Normal humans can be infected but peopel with immunocompromised conditions are more likely than others to have complications
  • Extracellular pathogen
    • Some new evidence for replication in endothelial cells
  • Cat scratch disease- normal individuals
    • Primary skin papule or pustule at inoculation sire (3-10 days after scratch/bite)
    • Painful lymphadenopathy in axillary or cervical lymph node
    • Fever
    • Most resolve without treatment but may become chronic if untreated
  • Cat Scratch Disease in Immunocompromised
    • Bacillary angiomatosis-vascular proliferative disorder of the skin and visceral organs.;Appears as red nodular lesions
    • Bacillary peliosis hepatitis (also spleen)- cystic, blood filled spaces in the liver
    • Bacteremia
    • Sepsis
    • Endocarditis
  • Diagnosis
    • History of contact with a cat and the presence of a scratch/bite
    • Histopathology of lymph nodes, serology, slow growth on lab media.; Extracellular bacterium
  • Treatment-azithromycin, FQs
    • Treatment of HIV patients is slow and relapses are common
  • No vaccine
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Bartonella quintana
answer
  • Trench Fever
  • Extracellular pathogens
  • Human to human via body lice
  • Unusual in US
  • Distinctive symptom is bone pain especially in shins
  • Macular rash, headache, fever
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Bartonella bacilliformis
answer
  • Oroya fever
  • Intracellular in RBC
  • Human to human via sandfly vector
  • Andes Mountains
  • Severe hemolytic anemia
  • High fatality
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Coxiella burnetii
answer
  • Q fever
  • Rarely associated wtih an insect vector
  • Primarily an infection in aminal populations
    • Spread via contact with urine, feces, milk, placentas
  • Human disease is via inhalation of aerosols or dust contaiminated with C. burnetti
  • "Spore Like"- very hardy in the environment
  • One of the MOST infectious known bacteria
    • 1-10 bacteria infectious dose
    • Potential biological warfare agent
  • Ingestion of infected unpasteurized milk or food
  • Patients wtih prosthetic or damaged heart valves are at high risk b/c endocarditis is a clinical manifestation
  • Clinical Manifestations
    • Mild asymptomatic disease
    • Acute Disease-respiratory with systemic spread-typical presentation
      • Febrile illness, fever, chills, headache, chest pain
      • Mild atypical lobar or interstitial pneumonia
      • Hepatosplenomegaly with granulomas
      • Usually self limited, lasts several weeks
    • Chronic disease-months to years after primary infection
      • Endocarditis-typical presentation
      • Chronic hepatitis
      • osteomyelitis
      • Poor prognosis, may be fatal
    • No rash in any disease presentation
    • Replication in macrophages (live, lung, spleen)
    • No vasculitis
  • Serology is useful to diagnosis chronic disease
  • New rapid PCR based test approved for defense department
  • Treatment: doxycycline
    • Q fever endocarditis: doxycycline + hydrochloroquine for 18 months
  • Vaccin is available in Australia for high risk occupations
    • killed whole cell preparation
    • Not approved in US
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Borrelia burgdorferi
answer
  • Spirochete
  • Lyme Disease
  • White-footed mouse and deer-main animal reservoirs
  • Primary tick borne disease in US
  • Transmitted by deer ticks-nymphal life stage
  • Highest risk in Northeast adn upper midwest
  • In California transmitted by western black legged tick
  • Tick must be attached for 24-48 hours for transmission of bacteria
  • May-August transmission
  • Extracellular pathogen
  • Primary Stage- erythema migrans (EM)
    • Annular bulls eye skin rash
    • Rash occurs in 60-80% but most often is atypical form
    • Rash may fade or reoccur at sites distant from tick bite
    • Headache, fever, myalgia, lymphadenopathy
    • Proliferation of bacteria in the tissue at the site of the tick bite, initial dissemination
  • Seconday Stage-Early disseminated, neurologic and cardiac symptoms
    • Usually 2 weeks - 3 months after the initial tick bite
    • Result of dissemination and replication of the bacteria throughout hte body
    • May be a disseminated rash-not at the site of bite
    • Chronic fatigue
    • Neurologic symptoms-facial nerve palsy, peripheral neuropathy, meningitis
    • Cardiac symptoms-carditis, atrioventricular block
  • Tertiary Stage-late or chronic lyme disease-arthritis
    • Weeks-years after the primary infection
    • Migratory pain in joints, especially knees (arthritis)
    • Chronic memory loss, other neurologic complaints
    • Chronic muscle pain
    • Chronic and destructive in patients with HLA-DR4 or HLA-DR2
    • Immunopathological process
    • Cannot culture bacteria from the joint fluid
  • Post lyme Syndrome
    • Chronic lyme disease even after appropriate treatment
    • 10-20% of patients
    • Fatigue
    • joint pain
    • Muscle aches
    • cognitive impairments
    • "Antibiotic therapy has not proven to be useful and is not recommended"
  • Congenital Lyme Disease
    • Transplancental transmission
    • Stillbirths, birth defects, mental retardation
    • Rare
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Diagnosis/Treatment/Prevention

Lyme Disease

answer
  • Diagnosis
    • Based on clinical grounds-classical rash
    • Medical history of tick bite or travel to sites of likely exposure
    • Serology-Elisa followed by western blot
  • Treatment
    • Prophylaxis-engorged tick in endermic area: doxycycline
    • Primary Stage: oral doxycycline or amoxicillin or cefuroxime 14-21 days
    • Early neurological symptoms: oral doxycycline or amoxicillin or IV deftriaxone (14-21 days)
    • Lyme carditis- IV ceftriaxone or Pen G (14-28 days)
    • Meningitis/encephalitis: IV ceftriaxone or Pen G (14-28 days)
    • Lyme arthritis (without neurological symptoms): oral deoxycycline or amonicillin (30-60 days) or IV ceftriaxone or Pen G (14-28 days)
    • Late Neurological symptoms-no treatment
    • Post Lyme syndrome-no treatment beyond standard therapy
  • No vaccine
  • Old vaccine: LYMErix-recombinant outer surface protein
    • Two IM doses 1 month apart and third dose one year later
    • Very effective no longer available ince 2002
    • Reported side effects: arthritis, myalgia
question
Borrelia-Relapsing Fever
answer
  • B. recurrentis- transmitted by human body louse (human to human) not common in US
  • B. hermsii, B. parkeri-transmitted by sfot ticks in US
    • Tick Born Relapsing Fever (TBRF)
    • Most cases are in the summer months
  • Incubation period: 1 week after louse of tick bite
  • Primary febrile attack-persists for 3-6 days with high fever, headache, muscle pain
  • Asymptomatic interval of 6-10 days
  • 1-4 relapses due to antigenic variation
  • Spirochetes disseminate in the body replicating extracellularly
  • Spirochetes express surface exposed immunodominant antigen called variable major proteins. ; 26 different VMP
  • Antibody response to initial VMP develops and removes borreliae from blood causing asymptomatic interval
  • Transposition of new vmp into expression site: immune response does not recognize new vmp; borreliae will multiply and disease symptoms will relapse
  • Diagnosis-blood Giemsa stain-microscopic observation of spirochetes in bloos
  • Serology and culture are difficult due to antigenic variation
  • Treatment-Doxycycline
  • No Vaccine
question
Leptospira interrogans
answer
  • Leptospirosis (Weil's disease)
  • Reservoir: dogs are a major source; other domestic animals too
  • Animals are infected and shed large numbers of spirochetes in their urine contaminating water and soil where they survive for months
  • Swimming or washing in natural bodies of water is a risk
  • Worldwide distribution
  • Site of entry: skin and mucus membranes
  • No lesions
  • Incubation period: 8-12 days
  • Primary Disease:
    • mild septicemia
    • Fever, headache
    • Diverse presentaton and symptoms
    • Asymptomatic interval due to antibody clearance of leptospires from all tissues except kidneys and aqueous humor of eye
  • Secondary disease
    • return of symptoms (immune stage)
    • Depends on organs involved
    • Anicteric (90% of patients)-fever, mild meningitis, uveitis, other organ involvement
    • Icteric (Weilds disease) (10% of patients)
      • Jaundice
      • Hemorrhage
      • renal failure
      • death in 5-40% of cases
  • Diagnosis-blood or urine cultures
  • Treatment: Pen G or doxycycline
  • No Vaccine
question
Yersina pestis
answer
  • Gm (-) rods and coccobacilli
  • Bipolar staining "safety pin appearance"
  • PLAGUE
  • LPS endotoxin-septic shock
  • Capsule (Fral glycoprotein) essential for growth
    • Anti phagocytic
    • Extracellular
  • V and W antigens: outer membrane proteins
    • Anti phagocytic
    • Extracelular
  • Intracellular growth in macrophages
  • Has both intracellular and extracellular periods in disease process
  • Facultative intracellular parasite
  • Wild rodents are a reservoir (prairie dogs0
  • Trasmission to humans via
    • Bites of rodent fleas
    • Direct contact
    • Aerosols
  • Bubonic Phase-2-6 days after flea bite
    • Y. pestis travels vai lymphatics from site of the flea bite to lymph nodes (intracellular phase)
    • Inguinal or axillary lymph nodes usually
    • Survives and grows in macrophages- intracellular phase
    • Production of bubo (swollen lymph nodes becomes filled with pus)
    • Will eventually spread to blood stream
  • Septicemic (extracellular) Phase-LPS endotoxin induced
    • Disseminated intravascular coagulation- necrossi "black death"
    • Septic Shock
  • Pneumonic (extracellular phase)-systemic spread to lungs
    • Pneumonia with organisms in alveolar spaces and sputum
    • May arise from inhalation of infectious respiratory droplets (bio terrorism agent)
    • Person to person spread
  • Diagnosis-
    • culture in biosafety level 3 labs
    • Immunofluorescence using Fral antibody: rapid
    • Serology: 4 fold rise in antibody to Fral antigen
  • Treatment/Prevention
    • Isolationg of patients
    • Streptomycin or gentamycin
    • Poor prognosis is therapy is delayed
    • Vaccine: killed whole bacteria contains Fral fragement
    • Only in high risk situations
question

Yersinia enterocolitica

Yersinia pseudotuberculosis

 

answer
  • Enterocolitis
  • LPS endotoxin
  • Gm (-) rods and coccobacilli
  • Bipolar staining "safety pin appearance"
  • Yops-anti-phagocytic
  • Do not replicate in macrophages
  • No capsule
  • Present in aquatic and animal reservoirs
  • Fecal-oral transmission via ingestion of food or water contaminated (often times milk)
  • Occurs in children mostly
  • Reiter syndrome: Can't see, can't pee, can't bend the knee.; HLA-B27 positive individuals
  • Gastroenteritis
  • Following ingestion, invasion of the mucosathrough M cells multiply in Peyes patches
  • Enter mesenteric lymph nodes-intense inflammation (pain resembeling appendicictis)
    • May have septicema (abscesses in liver and spleen)
question
Francisella tularensis
answer
  • Tularemia
  • Small Gm(-) coccobacillus
  • bipolar staining
  • Capsule-antiphagocytic, protects while bacteria is extracellular
  • Facultative intracellular parasire-macrophages
  • Widely distributed in animals especially rabbits
  • Transmission via handeling of infected animals, tick bite from infected animal, ingestion of animal meet
  • Ulceroglandular disease-most common
    • focal ulcer at the site of entry
    • Regional lymphadenopathy
    • Intracellular growth in macrophages
    • Resembles bubo plaque
  • Typhoidal Disease-acquired by eating undercooked infected meat. Intracellular
  • Oropharyngeal Disease-pneumonia, intracellular;(bioterrorism agent)
  • Ocularglandular Disease-wiping eyes with contaminated hands. Intracellular
  • All infections can enter the blood stream and become extracellular
  • May be fatal without treatment
  • Diagnosis-culture specimens in lab-biosafelty level 3
  • Treatment: streptomycin or gentamycin
  • Prevention: Live attenuated vaccine-only for high risk
  • No person to person transmission
question
Brucella
answer
  • Brucellosis
  • Undulant Fever
  • Small Gm(-) coccobacilli, weakly staining
  • Faculative intracellular pathogens within macrophages
  • Taxonomy is based on the animal they primarily infect
  • Grow slowly on complex media containing serum or blood
  • Growth of B. abortus is enhanced by erythritol-found in uterus and placental tissue
  • Found in wild domestic animals
  • Transmission is from infected animals in urine, milk, vaginal secretions, placental tissue
    • Ingestion
    • Direct Contact
    • Inhalation
  • Chronic febrile illness with either an abrupt or more often insidous onset
  • Symptoms are severe and prolonged with B. melitensis and self-limtied with B. abortus
  • Fever and malaise may persist for weeks
  • Series of relapses "undulant fever"
  • Targer organs
    • lungs if inhales
    • Lymph nodes
    • Spleen
    • Liver
    • Bone marrow
  • minute granulomas-hallmark lesions
  • Diagnosis is based on immunological reactions
    • Serology
    • Brucellergin DHT skin test
  • Treatment: ; 6 weeks: doxycycline + streptomycin or gentamycin
  • Prevention: Aminal immunization-live attenuated
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