-
Pseudomonas
- Oxidative gram-negative bacilli
- Produce acid from glucose or other carbohydrates
- Pseudomonas aeruginosa oxidizes but does not ferment glucose
-
Pseudomonas aeruginosa
- Non-fermentive
- Obligately aerobic
- Motile
- Straight or slightly curved rod
- Oxidase and Catalse +
- Pigments- Pyocynin (blue), fluorescein (yellow), pyorubin (red)
- Oppertunistic pathogen
-
Pseudomonas aeruginosa
Virulence Factors
- Capsule
- LPS
- Pyocyanin
- Toxins
-
Pseudomonas aeruginosa
Epidemiology
- Ubiquitous
- Simple nutritional requirements – grow where other bacteria cannot
- Colonize respiratory and GI tract of patients
-
Pseudomonas aeruginosa
Clinical Disease
- Pulmonary infect
- Skin infec
- Folliculitis/Nail
- UTI
- Ear
- Eye
- Bacteremia
- Endocarditis
-
Pseudomonas aeruginosa
Clinical Diseases
Pulmonary infections
- Risk factors
- -Cystic fibrosis
- -Use of broad spectrum Abx
- -Prior use of respiratory therapy equipment
-
Pseudomonas aeruginosa
Clinical Diseases
Skin infection
- Burn infection – localized vascular damage, tissue necrosis, bacteremia
- Burns have moist surface and lack neutrophils
-
Pseudomonas aeruginosa
Clinical Diseases
Folliculitis/Nail infections
Results from immersion in contaminated water
-
Pseudomonas aeruginosa
Clinical Diseases
Ear & Eye Infections
- Ear:
- Mild irritation of external ear
- More severe form can destroy cranial bones
- Eye:
- caused by trauma & contaminated water
-
Pseudomonas aeruginosa
Laboratory Diagnosis
- Culture:
- Simple nutritional requirements
- Identification:
- colonial morphology - (Flat colonies with spreading border)
- hemolytic activity - (beta hemolysis)
- pigmentation - (green)
- odor - (grape-like odor)
- biochem test - (oxi +)
-
Pseudomonas aeruginosa
Treatment
- Antibiotic resistance is common
- Usually use combination therapy
-
Pseudomonas aeruginosa
Prevention/Control
- Hard to eliminate from hospital environments
- Concentrate on preventing contamination of sterile equipment
-
Haemophilus
- Gram-negative bacilli liking blood
- Small, pleomorphic, aerobic and fastidious
- Requires hemin (X-factor) and NAD (V-factor) for growth
- Intact blood has V-factor inhibitor
-
Haemophilus influenzae
Virulence Factors
- Capsule –6 Sterotypes (A to F)
- Non encapsulated strains-spread from upper respiratory tract (URT) to ear, sinuses, LRT
- Encapsulated strains – URT to bloodstream, systemic spread
- Type B (Hib) is invasive – resists complement, antiphagocytic
-
Haemophilus
Epidemiology
- Asymptomatic carriers
- Hib generally not part of normal flora
- Risk factor- absence of Ab against capsule – children under 1 yr
- Crowding increases rate of disease by encapsulated strains
- Conjugated vaccine introduced in 1987
-
Haemophilus influenzae
Clinical Disease
Meningitis
- CSF 50-95% culture +
- Blood 50-95% culture +
-
Haemophilus influenzae
Clinical Disease
Epiglottitis
- Blocked airway
- Pharyngitis, fever, trouble breathing
- Blood 90-95% culture +
-
Haemophilus ducreyi
Clinical Disease
Chancroid
- STD
- Characterized by tender papule with and erthematous base
- Progresses to painful ulceration
- Lesions similar to herpes and syphilis
-
Haemophilus influenzae
Laboratory Diagnosis
- Microscopy of CSF –
- gram neg rods ranging in size from small coccobacilli to large
- pleomorphic filaments
- Culture –
- use chocolate agar (has factor X and V)
- Antigen detection – detects PRP of Hib
-
Haemophilus influenzae
Treatment
- Broad spectrum Abx - Cephalosporins, Fluoroquinolones
- Ampicillin resistance on the rise
-
Haemophilus influenzae
Prevention/Control
- Conjugated PRP vaccine against Hib
- 3 doses before the age of 6 months
-
Bordetella
- Small
- gram -
- aerobic
- coccobacillus
- Fastidious
- Nonfermentative
- Oxidize amino acids
-
Bordetella
Types
- Bordetella pertussis = Whooping Cough
- Bordetella parapertussis = milder form of whooping cough
- Bordetella bronchiseptica = respiratory disease in animals (kennel cough)
-
Bordetella pertussis
Virulence Factors
-
Bordetella pertussis
Epidemiology
- Human is only host
- Highly communicable (aerosols)
- Worldwide distribution
- Children under 1 year at greatest risk- shifting to older children and adults
- Greatest risk in non-vaccinated or inadequately vaccinated
-
Bordetella pertussis
Pathogenesis
- Mainly toxin-mediated
- Inhalation of infected droplets
- Colonization of respiratory tract – attach to ciliated epithelial cells
- Localized multiplication with localized tissue damage
- Inflammation interferes with clearance of pulmonary secretions
- Systemic toxicity – CNS effects, leukocytosis
-
Bordetella pertussis
Clinical Disease
- 7-10 days: none
- 1-2 wks: Rhinorrhea, malaise, fever, sneezing, anorexia
- 2-4 wks: Repetitive cough w/ whoops, vomiting, leukocytosis
- 3-4+ wks: less cough, pneumonia
-
Bordetella pertussis
Laboratory Diagnosis
- Extremely sensitive to drying
- DFA useful but not specific
- Culture on selective media (Bordet-Gengou medium)
- -Requires nicotinamide and charcoal, starch, blood, or albumin to absorb toxic substances
- Fastidious and slow-growing
- PCR most sensitive
-
Bordetella pertussis
Treatment
- Macrolides- reduce length of infectious stage
- -Illness not recognized during peak contagiousness
-
Bordetella pertussis
Prevention/Control
- Killed whole cell vaccine part of DTP
- Acellular vaccine now available (DTaP)
- -Use various subunits – filamentous hemagglutinin, pertactin fimbriae, etc)
-
Legionella Discovery
- Discovered in 1976
- Outbreak of severe pneumonia that caused many deaths in American Legion members attending a convention
- A previously unknown gram-neg rod was isolated
- It was spread through the air conditioning ducts
- Named Legionella after the group
-
Legionella
- Gram-negative rod
- Tissue- short coccobacilli
- Stains poorly w/ dyes
- Fastidous
obligate aerobe - Non-fermentative, metabolize amino acids
- Ubiquitous aquatic saprophyte
- L. pneumophila causes 85% of Legionella infections
-
Legionella
Pathogenesis
- Respiratory disease spread by aerosol droplets
- Facultative intracellular parasites
- Multiply in macrophages, monocytes, and free-living amoebas
- Complement initiates phagocytosis
- Phagolysosome fusion is inhibited
- Cells replicate and lyse cell
-
Legionella
Epidemiology
- Worldwide distribution
- Lives in natural bodies of water, air conditioning cooling towers, condensers, water system (showers, hot tubs)
- Survives in moist environments at high temps and disinfectant
- Parasitize amoebas and replicate in protected environmentDisease is difficult to document – incidence is unknown
-
Legionella
Clinical Disease
2 forms
- Pontiac fever -Influenza-like illness
- Legionnaire’s Disease-Severe form of pneumonia
-
Pontiac Fever
- Named after an epidemic in Pontiac, Michigan in 1968Self-limiting with symptoms of fever, chills, muscle pain, general body weakness and lethargy(malaise), headache, flu-likeNo evidence of pneumonia Symptoms develop over a 12 hour period and then stick around for 2 to 5 days, then spontaneously disappears without antibiotic treatment.There have been no deaths reported
-
Legionnaires' disease
- More severe causes morbidity and death unless treated properlyIncubates for 2 to 10 days followed by symptoms of fever, chills, dry nonproductive cough, headacheOften present is multiorgan disease, including the GI tract, CNS, liver, and kidneys.Pneumonia is the primary manifestationPulmonary function deteriorates in patients with no treatmentMortality rate is 15-20%
-
Legionella
Lab Diagnosis
- Direct microscopyClinical specimens stain poorly with Gram stainUse Dieterle’s silver or Ginenez’s stainsDirect Fluorescent Antibody (DFA) more sensitive
-
Legionella
Lab Diagnosis
- Culture on buffered charcoal yeast extract (BCYE)Contains L-cysteine and iron saltAntigen test sensitive for L. pneumophilia serogroup1 but poor for othersPCR is sensitive and specific
-
Legionella
Treatment
- Some antibiotics are incapable of penetrating macrophages Macrolides and fluroquinolones Specific treatment for pontiac fever is not necessary as it is self limiting
-
Legionella
Prevention/Control
- Identification of the environmental source and elimination of it Hyperchlorination of the water supply Maintenance of elevated water temperatures Elimination of the organism is difficult
- Hospitals -monitor their water supply
-
Clostridium
- Clostridium historically classified on four properties
- Produce endosporesStrict anaerobes
- Cannot reduce sulfate
- Gram positive cell
- Reorganization underway
-
Clostridium
Histotoxic group
- Tissue infec
- cellulilitis
- myonecrosis
- gas gangrene
- fasciitis
-
Clostridium
Enterotoxigenic group
gastrointestinal disease
-
Clostridium perfingens
- Large Gram+ bacilli
- Spores rarely seen in ivtro or in clinical specimens
- Non-motile but has rapid spreading growth on media – similar to motile organisms
- Major agent of clostridial myonecrosis – gas gangrene
- Black muscle tissue – decaying tissue
- 5 types – based on production of toxins
- Type A
- – human infections
- Types B-E
- – animal infections
-
Clostridium perfingens
Virulence Factors
- Multiple Toxins –
- α
, β, ε, ι, - Collagenase
DNaseHyaluronidase - All involved in necrosis
-
Clostridium perfingens
Epidemiology
- Ubiquitous
- Widely distributed in soil & water
- Commonly inhabits intestinal tract of humans and animals
- Endogenous or exogenous spread
-
Clostridium perfingens
Pathogenesis
Tissue infections
- Tissue trauma
- Inoculation
- Decreased oxygen tension
- Multiplication
- Toxin production and subsequent gas production
- Spread along muscle plains
- Kills all cells in path – creates more necrosis
- If untreated –
bacteremia & death
-
Clostridium perfingens
Clinical Diseases
Soft Tissue Infections
- Cellulitis– localized edema and erythema with gas formation in soft tissueSuppurative myositis – accumulation of pus in muscle with no necrosisMyonecrosis (gas gangrene) – painful rapid destruction of muscle tissueHigh mortality – death within 2 days of onset
-
Clostridium perfingens
Clinical Diseases
- Gastroenteritis
- Food poisoning –
intoxicationRapid onset of symptoms – abdominal cramps, diarrheaNo fever, nausea or vomitingLast 1-2 days - Necrotizing Enteritis
- Necrosis of jejunum – toxin mediatedSymptoms include abdominal pain, vomiting, bloody diarrhea and peritonitisMortality-50%
-
Clostridium perfingens
Laboratory Diagnosis
- Laboratory diagnosis is confirmatory – therapy must be initiated right away
- Direct microscopy of clinical specimens – large gram + rectangular rods
- Double zone of hemolysis on blood agar
- Small beta hemolysis zone
- Large alpha hemolysis zone
- Grow on egg-yolk agar
- α-toxin hydrolyzes phospholipids producing opaque precipitate
-
Clostridium perfingens
Treatment
- Rapid treatment critical for severe infections
- Debridement –
surgical removal of dead tissue and debris from wound - Clean to healthy, bleeding tissue
- High dose penicilinAnti-α-toxin and hyperbaric oxygen chamber no longer used – ineffectiveSymptomatic treatmentfor food poisoning
-
Clostridium perfingens
Prevention/Control
Proper wound care and prophylactic Abx
-
Clostridium tetani
- Causative agent of tetanusGram positive
- obligate anaerobe with prominent terminal spore (drumstick appearance)
- Vegetative cell extremely sensitive to oxygenSpores enables long-term survival
-
Clostridium tetani
Virulence Factors
- Tetanospasmin – neurotoxin
- Plasmid encoded
Intracellular toxin released by cellular autolysis during stationary phase - Heat labile (can be killed by heat)A-B toxinA subunit binds to sialic acid receptors on motor neuronsB-subunit inhibits proteins that regulate release of inhibitory neurotransmittersResults in spastic paralysis – uncontrolled contraction
-
Clostridium tetani
Epidemiology
- Ubiquitous
- Spores found in soil
- Exposure to spores is common
- Disease is uncommon in U.S. - < 40 cases annually
- Proper medical care and vaccine available
- More than 1 million cases worldwide
- Mortality- 30-50 %
-
Clostridium tetani
Pathogenesis
- Puncture woundContaminated with sporesGerminate in anaerobic environmentMultiply at site – do not invadeRelease toxinsToxins spreadsBlocks neurotransmitted
- Spastic paralysis
-
Clostridium tetani
Clinical Disease
- Generalized tetanus– most common form
- Involvement of masseter muscles – resulting in lockjawRisus sardonicus – sardonic smile resulting from sustained contractionOther signs include drooling, sweating and persistent back spasms Localized tetanus– confined to site in primary infectionCephalic tetanus –confined to the headNeonatal tetanus –initial infection of the umbilical stumpHigh mortality – 90%
-
Clostridium tetani
Laboratory Diagnosis
- Diagnosis made on the basis of clinical signs
- Very hard to isolate organism from patient
- Microscopy and culture have low sensitivity – 30%
- Neither toxin or anti-toxin antibodies are present in serum
-
Clostridium tetani
Treatment
- Debridement ofinfected area
- Antibiotic of choice– metronidazole
- Passive immunization with anti-toxin antibodies
-
Clostridium tetani
Prevention/Control
- DTP
- 3 doses of tetanus toxoid with booster every 10 years
-
Clostridium botulinum
Structure and Virulence Factors
- Gram positive
- spore forming bacillus
- Obligate anaerobe – very sensitive to oxygen
- Fastidious
- 8 distinct toxins (A-G)
- A, B, E and F associated with human disease
- Similar to tetanus toxin
- Prevents release of acetylecholine at myoneural junction (where neuron meets muscle)
- Results in flaccid paralysis
-
Clostridium botulinum
Epidemiology
Ubiquitous
-
Clostridium botulinum
Clinical Disease
Infant botulism
- C. botulimun colonized intestinal tract of infants
- Cannot colonize adults
- Initially nonspecific symptoms – constipation, weak cry, “failure to thrive”
- Progress to flaccid paralysis and respiratory arrest
-
Clostridium botulinum
Clinical Disease
Foodborne Botulism
- mostly associated with home canned foods
- Blurred vision, dry mouth, constipation and abdominal pain
- ->flaccid paralysis and bilateral descending weakness of
- peripheral muscles
-
Clostridium botulinum
Clinical Disease
Wound botulism
- Clinical presentation the same as foodborne botulism
- Less GI symptoms
-
Clostridium botulinum
Clinical Disease
Inhalation botulism
Bioterrism
-
Clostridium botulinum
Laboratory Diagnosis
- Adult cases harder to diagnose - no single test has greate than 60% specificity
- Culture organism from feces of patient or from suspected food.
- Heat to 80C for 10 mins to kill contaminating microbes
- grow on egg-yolk agar
- mouse bioassay to test for pre sence of toxin
- Infant botulism more likely to culture from feces and detect toxin in blood
-
Clostridium botulinum
Treatment
- Metronidazole- elimination of bacteria from GI tract
- Trivalent antitoxin
- Ventilator support
-
Clostridium botulinum
Prevention and Control
- Destroying spores in food – very hard for practical reasons
- Prevent spore germination – acid pH, high sugar concentration or spore at 4C
- Destroy preformed toxin by proper cooking – at least 60C for 10 min
- Infant botulism associated with consumption of spore contaminated honey – no honey to children yuonger than 1 yr
-
Clostridium difficile
Structure and Virulence Factors
- Gram +
- spore forming rod
- obligate anaerobe
- Produce two toxins
- enterotoxin
- cytotoxin
-
Clostridium difficile
Epidemiology
- Ubiquitous
- Colonizes GI tract of small percentage of healthy individuals (5%)
- Broad spectrum
Abx leads to overgrowth of C. difficile - Spores are shed in infected people
- Detected in hospital rooms – leads to exogenous spread
-
Clostridium difficile
Clinical Disease
- Antibiotic associated diarrheaAcute diarrhea develops 5-10 days post initiation of Abx treatmentAmpicillin, clindamycinUsually brief and self-limiting
- Pseudomembranous
colitis-More severe-False membrane of fibrin, mucus and inflammatory cells line intestinal mucosa -White plaques - -Profuse diarrhea, abdominal cramps and fever
-
Clostridium difficile
Laboratory Diagnosis
- Detect toxin in feces
- Commercial immunoassays
- Isolation of bacteria in feces confirms colonization but not disease
-
Clostridium difficile
Treatment
- Discontinue suspected Abx in mild disease
- Metronidazole or vancomycin for severe disease
- Kills vegetative cells not spores – relapse common
-
Clostridium difficile
Prevention and Control
Thorough cleaning of hospital room of infected patient after discharge
-
Mycoplasma
- Smallest free-living bacteria – non-intracellular parasites
- Form pleomorphicfilaments
- Have “fried egg appearance”
- Lack cell wall
- Incorporate sterols into plasma membrane
- Resistant to Penicillin, Cephalosporins
- Originally thought to be a virus
-
Mycoplasma
Bacteria like
- Divide by binary fission
- Most facultatively anaerobic
- Contain both RNA and DNA
- Grow on cell-free media
-
Mycoplasma
Virus like
- No cell wall
- Filterable
- Stain poorly
-
Mycoplasma pneumoniae
Pathogenesis
- Extracellular pathogen
- Infection by inhalation
- Adheres to respiratory epithelium by protein attachment factor
- Interacts with sialated glycoprotein receptors at the base of cilia
- Ciliostasis followed by destruction of superficial epithelial cells
- Disrupts normal clearance of upper respiratory system
- M. pneumoniae acts as superantigen
- Contributes to both clearance of cells and observed disease
-
Mycoplasma pneumoniae
Epidemiology
- Worldwide cause of pneumoniae
- No consistent increase in seasonal occurrence
- Epidemics every 4 to 8 yrs
- Most common in school-aged kids and young adults
- True incidenceunknown – not reportable, no reliable diagnostic test
- Spread by nasal secretions – close contact required
-
Mycoplasma pneumoniae
Clinical disease
- Pneumonia – walking pneumonia or typical pneumonia or atypical
- Starts out as mild fever, malaise, headache
- 2-4 days later – nonproductive cause
- May progress to tracheobronchitis – bronchial inflammation
- Develop pneumonia – patchy bronchopneumonia
- Secondary complications include otitis media, erythema multiforme, myocarditis, pericaditis and CNS involvement
- Erythema multiforme – allergic reaction of skin and mucus membranes
-
Mycoplasma pneumoniae
laboratory Diagnosis
- Microscopy – not useful due to poor staining
- Culture – slow (2-6 weeks)
- PCR – excellent sensitivity but undefined specificity (may detect non-pathogenic strains)
- Serology – detect antibodies against M. pneumoniae via complement fixation or enzyme agglutination
-
Mycoplasma pneumoniae
Treatment
- Erythromycin, tetracycline or fluoroquinolones
- Tetracylcine fluoroquinolones – adults only
-
Mycoplasma pneumoniae
Prevention/Control
- Spread byclose contact – isolation of infected individuals
- Impractical since patients are infectious for long periods of time
- Experimental vaccines have not conferred protective immunity
-
Rickettsia
- Small pleomorphic coccobacilli
- Obligate intracellular parasite – grow only in cytoplasm or eukaryotic
- Stain poorly
- Most are transmitted by vectors
- Also first thought to be a virus
-
Rickettsia
Bacteria like
- DNA and RNA
- Gram negative cell wall
- Binary fission
- Has ribosomes, makes enzymes for Krebs
- Inhibited by Abx
-
Rickettsia
Virus like
- Small
- Obligate intracellular parasite
- Poor Gram stain
-
Rickettsia
Pathogenesis
- Transmitted by arthropod bite
- Penetrates endothelial cells lining small blood vessels
- Multiplication in endothelial cells
- Cell rupture
- Leakage thrombosis and vasculitis
- Results in rash– blood in skin
- Role of endotoxin is minimal
-
Rickettsia rickettsii
Epidemiology
- Etiological agent of Rocky Mountain Spotted Fever
- 500-1000 casesannually in U.S.
- First described in Idaho and Montana
- Primarily seen in southern Atlantic state
- Principle vector– wood tick
- Seasonal occurrence– 90% of cases between April and October
-
Rickettsia rickettsii
Clinical Disease
- Rocky mountain spotted fever
- Symptoms develop 2-14 days after tick bite
- High fever, chills, headache, followed by rash – small petichial lesions
- Rash usually seen in extremities then spread to trunk – can involve palms and soles (differentiate from measles)
- Complications include GI symptoms, encephalitis and respiratory and/or renal failure
-
Rickettsia rickettsii
Laboratory Diagnosis
- Culture – tissue culture of chicken embryos
- More for research/reference labs
- Microscopy – DFA, MIF
- Microimmunofluorence (MIF) – detects specific outermembrane proteins
- Useful to detect genus, Western blot to confirm species
- PCR – also genus specific
-
Rickettsia rickettsii
Treatment
- 20% mortality if untreated
- Doxycycline drug of choice
- Fluoroquinolones as alternative
-
Rickettsia rickettsii
Prevention/Control
- No vaccine
- Avoid ticks, wear protective clothing, insecticides
-
Rickettsia prowazekii
Epidemiology
- Etiological agent of epidemic typhus (aka louse-borne typhus)
- Primary reservoir– human
- Spread by human head/body louse
- Crowding, unsanitary conditions favor spread
- Incidence in U.S. unknown (pretty low) – not reported
- More common in Central and South America and Africa
-
Rickettsia prowazekii
Clinical Disease
- Initial symptoms of high fever, severe headache, chills, myalgias (muscle pain), arthralgia (joint pain) – nonspecific symptoms
- About 40% develop petechial rash
- Complications include myocarditis and CNS disorders
- Mortality rate up to 66%
-
Rickettsia prowazekii
Lab Diagnosis
MIF
-
Rickettsia prowazekii
Treatment
tetracycline or chloramphenicol
-
Rickettsia prowazekii
Prevention
inactivated vaccine available for at risk populations
-
Spirochetes
- Thin, helical, gram negitive bacteria
- Order: Spirochaetales
- Family: Spirochaetaceae
- Genus: Treponema
- Borrelia
- Family: Leptospiraceae
- Genus: Leptospira
-
Treponema pallidum ssp pallidum
Characteristics
- Thin, tightly coiled spirochetes with tapered ends
- Causitive agent of syphilis
- Motile by periplasmic flagella
- Cannot be grown on artificial cultures
- Does not survive well outside of host
- Does not stain well
- Need to visualize with dark field or fluorescent microscopy
-
Treponema pallidum ssp pallidum
Virulence Factors
- Adherence– outermembrane proteins
- Ability to penetrate epithelial cells
- Coating of fibronectin – antiphagocytic
-
Treponema pallidum ssp pallidum
Epidemiology
- ¢Found
- Worldwide
- 3rd most common STD in U.S.
- Transmitted from direct sexual contact or from mother to fetus
- Not highly contagious - ~30% chance of acquiring disease after single exposure to infected partner
- Transmission rate dependent upon stage of disease
- Long incubation period during which time host is non-infectious
- Prostitution for drugs or for money to purchase drugs remains central epidemiologic aspect of transmission
-
Treponema pallidum ssp pallidum
Pathogenesis
- Tissue destruction and lesions primarily a result of an autoimmune response
- Syphilis is a disease of blood vessels and of the perivascular areas
- Host produces a vigorous immune response but the organisms are capable of persisting for decades
- Infection is neither fully controlled nor eradicated
- In early stages, there is an inhibition of cell-mediated immunity
- Inhibition of CMI abates in late stages of disease, hence late lesions tend to be localized
-
Treponema pallidum ssp pallidum
Clinical diseases
- Syphilis
- Primarily a STD
- Can be transferred congenitally
- Occurs in phases
-
Treponema pallidum ssp pallidum
Clinical Diseases
Primary syphilis
- Invasion of mucus membranes, rapid multiplication & wide dissemination in lymphatics and systemic circulation
- Prior to primary lesion
- Papule develops at the site of inoculation
- Erodes to become a painless ulcer with raised borders (Chancre)
- Chancre changes from hard to ulcerative with profuse shedding of spirochetes – very contagious
- Regresses in two months
-
Treponema pallidum ssp pallidum
Clinical Diseases
Secondary Syphilis
- Secondary disease 2-10 weeks after primary lesion
- Flu-like symptoms appear then skin rash
- Secondary lesions of the skin and mucus membranes are highly contagious
- Resolves slowly over a period of weeks to months
-
Treponema pallidum ssp pallidum
Clinical Diseases
Latent Syphilis
- Following secondary disease, host enters latent period
- First 4 years = early latent
- Subsequent period = late latent
- About 40% of late latent patients progress to late tertiary syphilitic disease
-
Treponema pallidum ssp pallidum
Clinical Diseases
Tertiary Syphilis
- Diffuse, chronic inflammation can cause destruction to any tissue/organ
- Often localized granulomatous dermal lesions in which few organisms are present
- Granulomas reflect containment by the immunologic reaction of the host to chronic infection
- CNS involvement – dementia, seizures, etc.
-
Treponema pallidum ssp pallidum
Clinical Diseases
Congenital Syphilis
- Congenital syphilis results from transplacental infection
- Causes septicemia in the developing fetus with widespread dissemination
- Abortion, neonatal mortality and late mental and physical problems
-
Treponema pallidum ssp pallidum
Laboratory Diagnosis
- Microscopy– Dark field or DFA of exudate from skin lesions
- Must be done right away – do not survive long outside the body
- Culture– none
-
Treponema pallidum ssp pallidum
Laboratory Diagnosis
Serology
- Treponemal tests
- Fluorescent treponemal antibody-absorption (FTA-ABS)
- Immobilized T. pallidum > patient serum > fluorescently tagged anti-human Ab.
- Treponema pallidum particle agglutination (TP-PA)
- Particles with T. pallidum antigens mixed with patient serum
- Nontreponemal test – measure Ig against lipids released from damaged
- cells
- Venereal Disease Research Laboratory test (VDRL)Rapid
- Plasma Reagin Test
-
Treponema pallidum ssp pallidum
Treatment
- Penicillin remains drug of choice
- Alternatives– tetracycline, doxycycline
- Only penicillin for neurosyphilis
- 7-10 days continuously for early stage
- At least 21 days continuously beyond the early stage
-
Treponema pallidum ssp pallidum
Prevention
- Abstinence
- Practice safe-sex
-
HIV Transmission
- Exposure to blood products
- Transfusions
- Hemophiliacs
- Transplants
- Needle sticks (health care workers)
- Other –dentist, tattoos, etc
- IV drug users – a major route of transmission of HIV in U.S.
- Perinatal-
- Before birth
- During birth
- Through breast milk
-
HIV Pathogenesis
Sexual intercourse
HIV infects and sticks to Langerhan and Dendritic cells, carried to lymph nodes
-
HIV Pathogenesis
Direct injection
Infect Dendritic cells or monocytes/macrophages, carried to lymph nodes
-
HIV Pathogenesis
Immune system responds
- Cell mediated and hemoral response
- Viremia decreases, anti-HIV antibody titers increase
- Body’s immune system clears viral particles from blood
- HIV remains in lymphoid tissue in latent or proviral form
- Incubation up to 10 years
- MORE
-
HIV Clinical Syndromes
Asymptomatic period (acute phase)
slide 17
-
HIV Clinical Syndromes
Early symptomatic
Slide 18
-
HIV Clinical Syndromes
AIDS
slide 19
-
HIV Epidemiology
homosexual men in U.S.-spread throughout world
-
-
HIV-1
- More virulent
- Responsible for worldwide epidemic
- Severity of infection varies from person to person
-
HIV-2
- Primarily found in western Africa
- Not transmitted as efficiently
- Genome more closely related to SIVmm than HIV-1
-
HIV Treatment
- Anti-HIV drugs classified into 4 categories
- Fusion-penetration inhibitors
- Nucleoside analogue reverse transcriptase inhibitors
- Non-nucleoside analogue reverse transcriptase inhibitors
- Protease inhibitors
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