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Dr. Miller Block 4 – Flashcards

Ewan Knight

7 July 2022

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Staphylococci epidermidis

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Staphylococci saprophyticus

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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

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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

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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

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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

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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

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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

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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

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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

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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

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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

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Infection of the groin "jock itch"
E. floccosum, T. rubrum

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Tinea pedis

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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

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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

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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

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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

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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

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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

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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

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Sporotrichosis

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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

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Chromoblastomycosis

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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)

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Phaeohyphomycosis

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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)

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Mycetoma

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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

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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

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Latency-Syphilis

answer

Asymptomatic period between secondary and tertiary disease
Early latency;; 4 years
Long latency ; 4 years
No clinical symptoms but positive serology

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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)

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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

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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

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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

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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

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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%

question

Ehrlichia ewingii

answer

Newly discovered
Replication in granulocytes
Same tick vector as HME

question

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

question

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

question

Bartonella bacilliformis

answer

Oroya fever
Intracellular in RBC
Human to human via sandfly vector
Andes Mountains
Severe hemolytic anemia
High fatality

question

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

question

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

question

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

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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

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Yersinia enterocolitica
Yersinia pseudotuberculosis

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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)

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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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