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Arthropod-Borne Diseases. Lyme Disease (Lyme Borreliosis). Borrelia burgdorferi. Lyme disease (LD, Lyme borreliosis) - Borrelia burgdorferi, B. garinii and B. afzelii New syndrome – 1975 Cluster of arthritis cases in Lyme, Connecticut area Plasmid-encoded virulence factors

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slide3
Lyme disease (LD, Lyme borreliosis) - Borrelia burgdorferi, B. garinii and B. afzelii
    • New syndrome – 1975
      • Cluster of arthritis cases in Lyme, Connecticut area
    • Plasmid-encoded virulence factors
    • Tick-borne, with deer, mice, or the woodrat as the natural reservoir
      • Tick must be attached for ~48 hours
      • Tick larvae (nymph) is small – may be hard to detect
      • Ixodes dammini in N.E. U.S.A.
slide4
Symptoms include localized rash, flu-like symptoms
    • Three stages
      • 1. Skin lesion
        • Erythema chronicum migrans
        • Skin rash, fever, stiff neck, malaise and lymphadenopathy
      • 2. Weeks to months later:
        • Cardiovascular manifestations
        • Neurologic changes (memory loss, mood changes, insomnia, hearing loss)
        • Migratory musculoskeletal pain
      • 3. Later  Intermittent arthritis
        • Over a period of years or chronic
    • 8% develop cardiac symptoms, 15% develop neurologic symptoms and 60% develop joint disorders (autoimmune reactions)
slide5
Years later, it can cause symptoms resembling Alzheimer’s disease and multiple sclerosis with behavioral changes as well
  • Laboratory diagnosis
    • Isolation of the spirochete
    • PCR to detect DNA in the urine
    • Serological testing (ELISA or Western Blot)
  • Treatment with penicillin or tetracycline is effective if administered early
plague
Plague
  • Yersinia pestis
    • Ring a ring of rosies
    • Pocket full of posies
    • Achoo, Achoo
    • All fall down
history
History
  • Old Testament – 1325 B.C.
  • Earliest documented evidence: 430 B.C. – Peloponnesian wars (1/3 -2/3 died)
    • Athenian Empire destroyed
  • 100 million killed in an epidemic in the 6th century
  • ~25% of European population in 14th century
  • 70,000 in London plague in 1665
  • Hong Kong  India epidemic in 1893 killed 10 million over a 20 year period
    • Eventually reached San Francisco in 1900
      • Now established in SW USA (prarie dogs, ground squirrels, wood rats, chipmunks and mice)
slide8
Plague - Yersinia pestis
    • Flea-borne, from rodents
    • Small, Gram negative, non-motile, coccobacillus, bipolar staining
    • Sporadic in the U.S. (about 25 cases per year)
    • Bacteria survive and proliferate inside phagocytic cells
    • Symptoms include subcutaneous hemorrhages, fever, and enlarged lymph nodes (buboes)
slide9
Mortality rate is 50 to 70% if untreated
    • High fatality rate associated with septic shock (bacteremia – endotoxin – TNF-alpha and IL-1)
  • Virulence factors
    • Fraction I capsule – capsular antigen
    • Fibrinolysin  dissemination of deeper tissue
slide10
Outer membrane proteins (YOPS)
    • YOP E, H, K, L and M
    • Encoded on a low calcium-response plasmid (LCR)
      • E = actin degradation
      • H = Trytophan phosphatase
      • K/L = Inhibition of phagocytosis
      • K/L = Inhibition of cell=mediated immune responses
      • M = Inhibition of platelet aggretation
  • V/W antigens
    • Suppress granuloma formation
      • Decrease in gamma interferon and tumor necrosis factor alpha cytokines
slide11
Lab
    • Grown from aspirates of buboes (bubonic plague)
    • Grown from sputum (pneumonic plague)
  • Treatment - streptomycin or tetracycline
    • If untreated it may invade lungs (pneumonic plague), resulting in 100% mortality if unrecognized within 12 to 24 hours
  • A vaccine is available for people at high risk
    • Short term protection
    • Ab production
anthrax

Anthrax

Bacillus anthracis

slide15
Anthrax - Bacillus anthracis
    • Facultative anaerobic rod, Gram positive, spore-forming
    • Mainly a disease of sheep, goats and cattle
      • Once established in an area, bacterial endospores from infected or dead animals contaminate the soil in the pasteur area for many years
      • Enter the animal through oral or intestinal abrasions  enter bloodsteam  replicate  death in 2-3 days
slide16
Humans acquire skin infection by:
    • Handling hides: cutaneous form (Wool sorters disease - malignant pustule)
    • Inhaling spores: pulmonary form
    • Ingestion: gastrointestinal form
  • Causes ulcerated skin lesions or influenza-like symptoms; headache, fever, and nausea are major symptoms
slide17
Diagnosis
    • Gram stain: Gram positive
    • The cells have characteristic squared ends.
    • The endospores are ellipsoidal shaped and located centrally in the non-swollen sporangium.
    • The spores are highly refractile to light and resistant to staining.
slide18
Treatment - penicillin, usually in combination with streptomycin; other treatment possibilities are erythromycin or tetracycline; cephalosporins or chloramphenicol; ciprofloxacin
  • Vaccine - available for animals and persons with high occupational risk (e.g. military personnel, veterinarians)
the philadelphia inquirer
The Philadelphia Inquirer
  • Anthrax Case Heightens Alert
    • NBC news worker in N.Y. is fourth case(10/13/01)
  • Anthrax Worries Strike Deeper
    • Letter sent to Daschle; N.Y. baby infected(10/16/01)
  • New Clues on Anthrax Emerge- Mailings bear similar writing
    • Germ strain in Senate case called very potent(10/17/01)
  • Anthrax threat leads U.S. House to adjourn
    • In D.C., calm now a challenge(10/18/01)
  • N.J. Anthrax Case Offers Lead
    • $1 million reward is announced(10/19/01)
slide22
FBI digs up mailboxes in N.J. anthrax probe
    • Officials: Anthrax found in 3 cities is same strain(10/20/01)
  • Postal staff in region gets antibiotics
    • Hundreds received medicine in N.J. as FBI agents questioned residents of West Trenton for clues to an anthrax mystery(10/21/01)
  • Anthrax Likely in Two Deaths
    • Four cases suspected at a D.C. post office (10/23/01)
  • Anthrax taints White House mail site; inhalation form suspected in N.J. case
    • Mail handler near Trenton in stable condition
    • Traces are found at a base serving executive offices
    • CDC comes under fire for response to anthrax (10/24/01)
slide23
U.S. Tries to Ease Mail Fears
    • Public is told to be alert; masks; gloves for handlers (10/25/01)
  • Anthrax Found at More Federal Sites
    • Number to receive antibiotics increases
    • Bush signs law to help authorities halt terrorism (10/27/01)
  • Traces of anthrax are found at more federal sites in D.C.
    • New Mystery: N.J. victim has no postal or media ties (10/30/01)
  • Anthrax Reported in South Jersey
    • Mail facility is closed after positive test
    • Latest anthrax cases confusing investigators (11/1/01)
  • Anthrax Confirmed at Bellmawr
    • Spores found, mail center is closed again(11/4/01)
  • Postal worker heads home, sharing her spirit of survival
    • Anthrax search at federal sites widens (11/6/01)
the emerging threat of bioterrorism
The Emerging Threat of Bioterrorism
  • The systematic use of terror to:
    • Demoralize
    • Intimidate
    • Subjugate
  • Intentional or threatened use of viruses, bacteria, fungi or toxins from living organisms to produce death or disease in humans, animals or plants.
agents of bioterrorism and biological warfare
Agents of Bioterrorism and Biological Warfare
  • Anthrax (Bacillus antracis)
  • Plague (Yersinia pestis)
  • Smallpox (Variola virus)
  • Tularemia (Francisella tularensis)
  • Brucellosis (Brucella spp.)
  • Botulinum toxin (Clostridium botulinum)
  • Cholera (Vibrio cholerae)
  • Marburg virus
world war ii marks the modern era of biological weapons
World War II Marks the Modern Era of Biological Weapons
  • Japanese facility – Unit 731: Scientists developing biological weapons including anthrax, cholera, plague
gruinard island a monument to the effects of biological warfare
Gruinard Island: A Monument to the Effects of Biological Warfare
  • British forces test their own biological weapons
  • 1942: Bomb disperses anthrax spores overhead
  • 1971: Spores still viable
  • 1986: Decontamination of Gruinard Island
united states develops biological weapons
United States Develops Biological Weapons
  • 1943 – Anthrax weapons developed
  • 1950-60s – U.S. biological warfare program continues after WWII at Fort Detrick, Maryland
  • 1969 – President Nixon ends U.S. offensive biological weapons program. Defense work continues.
slide29
1972 - Biological Weapons Convention on the Prohibition and Stockpiling of Bacteriological and Toxin Weapons and their Destruction
  • Treaty outlaws development or stockpiling of biological weapons
  • Soviet Union and U.S.A. sign this treaty
slide30
1979 - Compound 19 Sverdlovsk (Ekaterinburg), Soviet Union: Aerosolized anthrax spores released accidentally, killing 68 people
biopreparat the biological weapons empire of the former soviet union
Biopreparat: The Biological Weapons Empire of the former Soviet Union
  • Yeltsin admits the former Soviet Union had manufactured arsenals of deadly germs and diseases in violation of the Biological Weapons Convention at Obolensk and Koltsovo
slide32
“What we know about the effect of nuclear weapons is largely from studying what happened to human populations in Hiroshima and Nagasaki. What we know about anthrax is largely what we can tell from what happened in Sverdlovsk.”

Richard Preston

why anthrax
Why Anthrax?
  • Robert Koch (1843-1910)
    • Develops Koch’s Postulates
    • Proves that Bacillus anthracis is the causative agent of anthrax (1876)
anthrax life cycle
Anthrax Life Cycle
  • Entry
    • Clumps of dormant spores enter the animal’s body
  • Reproduction
    • Spores germinate into vegetative forms in nutrient-rich environment
  • Assassination
    • Millions of bacteria produce and secrete toxins that destroy cells
  • Hibernation
    • Deprived of nutrients by the decaying body, the bacteria sporulate and reform spores
  • Ambush
    • As the body decomposes, the spores drop into the soil and wait for an animal to inhale them – Cycle repeats itself
virulence factors of bacillus anthracis why is b anthracis pathogenic
Virulence Factors of Bacillus anthracis:Why is B. anthracis pathogenic?
  • Endospores
    • Resistant to heat, disinfectants, UV, desiccation
    • Can remain dormant and survive for decades
slide37
Capsule
    • Layer of poly-D-glutamic acid
    • Protection from phagocytosis by host macrophages
slide38
Exotoxins
    • Protective antigen (vaccines)
    • Lethal toxin
    • Edema factor
fear of anthrax attack boosts sales of antibiotics
Fear of Anthrax Attack Boosts Sales of Antibiotics
  • What is cipro?
    • Ciprofloxacin is a fluoroquinolone antibiotic
    • Inhibition of bacterial DNA gyrase (required for DNA replication and gene transcription)
    • More side effects than penicillin or doxycycline
human vaccine made by bioport in lansing michigan
Human Vaccine made by Bioport in Lansing, Michigan
  • Cell free vaccine (Anthrax Vaccine Absorbed)
  • Contains purified Protective Antigen from attenuated B. anthracis strains
  • Available only to medical personnel and those at high risk
military receive anthrax vaccine
Military Receive Anthrax Vaccine
  • 1991 – U.S. troops vaccinated for anthrax in preparation for Gulf War
  • 1995 – Iraq admits it produced 8,500 liters of concentrated anthrax as part of biological weapons program
  • 1998- U.S. Secretary of Defense William Cohen approves/mandates anthrax vaccination plan for all military service members
  • 2001 – Are supplies adequate for civilian populations?
slide42
Preparedness
    • Surveillance
      • CDC
      • Epidemiology
      • Diagnostics
      • Electronic communication links for hospitals, public health departments and laboratories
        • Some remote hospitals lack internet or FAX
        • Real time
        • Link information efficiently
        • Natl. Electronic Disease Surveillance System (NEDSS) underway
    • Medical and Public Health Response
      • Early warning bioterrorism systems
      • Faster detection methods required
        • Mayo clinic reports 1 hour detection test (11/5/01)
slide43
Preparedness
    • Stockpile drugs, vaccines and supplies
    • Research and Development
      • Genomics – ID
      • Vaccines
      • Antibiotics
      • Monoclonal antibodies
        • Anti-toxin antibodies
        • Anti-cytokine antibodies
slide44
Medical and Public Health Officials
    • “First responders” – Front lines of defense
    • Identify syndromes
    • Laboratory diagnoses
    • Communication
    • Supplies
      • Antibiotics
      • Antitoxins
      • Vaccines
    • Initiate PROACTIVE strategies and appropriate countermeasures
slide45
Collaboration at all levels
    • Local
    • State
    • Federal
    • Global
weapons of mass destruction or distraction
Weapons of Mass Destruction? ………….or Distraction?
  • The purpose of bioterrorism it to bring society to its knees by shutting down government, media, commerce and industry.
  • We must continually assess the evolving threat from biological weapons – the threat will change with time.
  • Proactive medical countermeasures may be effective deterrents.
slide49
Bacterial Vaginosis
    • Disease is sexually transmitted with polymicrobic etiology
      • Gardnerella vaginalis (image, previous slide)
      • Mobiluncus spp.
      • Mycoplasma hominis
      • Other anaerobic bacteria
    • Autoinfection in women from the rectum, which is inhabited by these organisms
    • Disease is mild but is a risk factor for obstetric infections, various adverse outcomes of pregnancy, and pelvic inflammatory disease
slide50
Diagnosis is based on fishy odor and microscopic observation of clue cells (sloughed-off vaginal epithelial cells covered with bacteria) in the discharge
  • Treatment is with metronidazole to kill the anaerobes necessary for continuation of the disease
cat scratch disease

Cat Scratch Disease

Bartonella henselae

slide52
Cat Scratch Disease (CSD)
    • Probably caused by Bartonella henselae
    • Diagnosis is based on the clinical history of a cat scratch or bite and subsequent swelling of the regional lymph nodes and by PCR amplification of appropriate gene sequences
    • It is typically self-limiting with abatement of symptoms over a period of days to weeks
chancroid

Chancroid

Haemophilus ducreyi

slide54
Chancroid-genital ulcer disease
    • It is sexually transmitted, caused by the Gram-negative bacillus, Haemophilus ducreyi
    • The bacterium enters the skin through a break in the epithelium
    • After 4 to 7 days a papular lesion develops with swelling and white blood cell infiltration
slide55
 A pustule forms and ruptures leading to a painful ulcer on the penis or vagina
    • It is a cofactor in the transmission of AIDS
    • Diagnosis is by isolating the bacterium
    • Treatment is with erythromycin or ceftriaxone
    • Prevention is by use of condoms or abstinence
gas gangrene

Gas gangrene

Clostridium perfringens

slide57
Gas gangrene or clostridial myonecrosis - Clostridium perfringens
    • Gram positive, sporing, rod
    • “Histotoxic” clostridia
    • Found in soil and intestinal tract microbiota
      • Contamination of wounds with soild or bowel flora
    • Obligate anaerobe; problem in deep puncture wound where organism can grow readily and produce toxin
      • Muscle affected – degraded  tissue death
    • Tissue necrosis (gangrene) occurs because of the toxin; growth of the organism leads to production of carbon dioxide and hydrogen gas
slide58
Commonly associated with wounds involving:
    • Frostbite
    • Abortions
    • Automobile accidents
    • Military combat
slide59
Virulence
    • Collagenase – dissemination
    • Alpha toxin
  • Treatment
    • Antitoxin
    • Antibiotics
    • Hyperbaric oxygen: increase oxygen concentration under pressure
    • Debridement: surgically remove dead tissue (may be extensive)
  • Amputation may be necessary to prevent spread
gonorrhea

Gonorrhea

Neisseria gonorrhoeae

neisseria gonorrhoeae
Neisseria gonorrhoeae
  • Gonococcus
    • Gram negative, diplococcus, difficult to grow in the lab
      • Requires enriched growth medium
      • Chocolate blood agar + 10% CO2
    • Disease of the mucous membranes of genitourinary tract, eye, rectum and throat
slide62
Males:
    • Urethral inflammation, pus, painful voiding 3-9 days after infection
    • May involve prostate and epididymis
    • Fibrosis may lead to urethral stricture
  • Females:
    • Usually asymptomatic or there may be a minor discharge (may go unnoticed)
    • Organisms may infect urethra, vagina, cervix and fallopian tubes
    • May lead to pelvic inflammatory disease (PID)
      • ~10-20% of infected females develop PID
        • Sterility
        • Ectopic pregnancy due to scar tissue
slide63
Infection, if disseminated through the bloodstream can involve other organs
    • Dissemination most often during menstruation and pregnancy
    • Bacteremia, increase in free iron
    • May affect:
      • Joints (gonococcal arthritis)
      • Heart (gonococcal endocarditis)
      • Pharynx (gonococcal pharyngitis)
      • Eyes (gonococcal lesions)
      • Meninges (gonococcal meningitis)
slide64
Birth through infected vagina can result in neonatal eye infections (ophthalmia neonatorum, or conjunctivitis of the newborn) leading to possible blindness
    • In the past newborns were given silver nitrate drops in eyes to prevent this
      • More recently: tetracycline/erythromycin or povidone/iodine
  • Diagnosis is by culture of the organism and/or use of a DNA probe
slide65
Treatment - several combination antibiotic treatment regimens have been found to be effective
    • Mid 1930’s: sulfonamide – but resistance has developed
    • Up to mid 1970’s – Penicillin, bu then penicillinase producing strains arose (PPNG) – now ~40% of clinical isolates are penicillin resistant
      • Strains must be tested
    • Tetracycline + erythromycin for those allergic to penicillin
    • Spectinomycin or cefoxitin may also be used
slide66
Control by public education, diagnosis, treatment of symptomatic and asymptomatic individuals, and use of condoms
  • Vaccine development hindered because bacteria express multiple antigenic types of fimbriae and outer membrane proteins
    • Recombination of gene fragments (rearrangemnts)
leprosy hansen s disease
Leprosy (Hansen’s Disease)
  • Mycobacterium leprae
slide68
General features
    • 13 million cases worldwide
    • 200 new cases annually in USA
    • 4000 cases total in USA
    • Cannot grow in lab medium, but will grow if injected into animals
      • Obligate intracellular parasite
      • Found in Schwann cells and monocytes
    • Acid fast
slide69
Pathogenicity

Spread via respiratory route (nasal secretions)

Usually requires prolonged exposure to nasal secretion of heavy bacteria shedders

Children are especially susceptible; males>females (2x)

Incubation period 3-5 years or longer

Source = humans and nine-banded Mexican armadillos

Skin lesions are prominent

Sensory loss

75% of infections heal after cell-mediated immunity is induced

MHC-dependent clearance

slide71
Lepramatous disease

Hypersensitivity not developed

Malignant, relentlessly progressive disease

Very high mortality if not treated

Systemic infection  organs, skin, nerves, testes, eyes (blindness), nodules, no eyebrows

Severely disfiguring

Defect in TH1 activation to M. leprae antigens; however humoral IR is fine

TH1 unable to produce IL-2 or gamma interferon

No DTH response to lepromin skin test (lepromin purfied from infected armadillo tissues)

slide72
Tuberculoid disease

Less severe, non-progressive  self-limiting

Cell-mediated IRs lead to inflammation in nerves

Hypersensitivity

Damage to nerves

Skin lesions

Sensory loss

Skin test positive for lepromin (DTH)

slide73
Clinical management and control
    • Dapsone
      • Anti-metabolite
      • Long-term treatment
      • Blocks metabolism of PABA (part of folic acid)
        • Similar to sulfa drug activity)
        • Lepramatous – drug must be taken for remainder of life
        • Resistant strains are developing
    • Rifampin also effective, but MUCH more expensive
      • Also must be taken long-term
      • Often combined with dapsone + clofazimine
slide74
Children of contagious parents should be given prophylactic drug therapy until their parents are treated and have become noninfectious
slide75
Experimental vaccines in endemic areas
    • Spleens and livers of armadillos  cells killed  injected
    • Killed M. leprae and viable BCG
    • M. leprae – recombinant proteins made in other bacteria  new vaccine trends
slide76
Diagnosis
    • Loss of feeling (anaesthesia) and acid fast rods  non-culturable
    • ELISA – serodiagnosis
    • Fluorescent antibodies
    • Biopsy  acid fast
    • PCR
peptic ulcer disease
Peptic ulcer disease
  • Helicobacter pylori
slide78
Peptic ulcer disease and gastritis - Helicobacter pylori
    • The evidence of pathogenicity of this organism is now very strong, if not overwhelming
      • Chronic gastritis and duodenal ulcers
      • By age 60, 50-60% are infected
    • Alters gastric pH to favor its own growth near the mucosal cells
      • Urease positive  enables survival in stomach
    • Colonizes gastric mucus-secreting cells
      • Adhesins attach to intestinal epithelium
slide79
Releases cytotoxins and proteolytic enzymes that damage epithelial mucosal cells
  • Transmission is probably propagated, but common source has not been definitively ruled out
  • Diagnosis is by culture of gastric biopsy specimens and serological testing
  • Treatment includes antibiotics and bismuth subsalicylate (Pepto-Bismol)
slide81
Staphylococcal diseases
    • Staphylococci are facultative anaerobes and are usually catalase positive
    • S. aureus
      • Coagulase positive (clots blood plasma, form a fibrin clot around themselves and avoid host’s attack))
        • Pathogenic
        • Causes severe chronic infections
      • Most pathogenic strains of staph also produce DNAase (decreases viscosity  dissemination)
slide82
S. epidermidis
    • Coagulase negative
    • Less invasive
    • Opportunistic pathogens associated with nosocomial infections
slide83
Many of the pathogenic strains are slime producers (SP);
    • Slime is a viscous extracellular glycoconjugate that allows the bacterium to adhere to smooth surfaces such as medical prostheses and catheters
    • Slime producers form biofilms on prosthetic devices
    • Slime also inhibits neutrophil chemotaxis, phagocytosis and the antimicrobial agents vancomycin and teicoplanin
slide84
Disease can be produced in any organ of the body but is most likely to occur in individuals whose defenses have been compromised
    • Newborns
    • Surgical or burn patients
    • Immunosuppressed patients
    • CGD
    • Lower respiratory tract infection (flu)
    • Measles
    • Diabetes
  • Exotoxins
    • SEA, B, C, D and E = Enterotoxins  cause diarrhea annd vomiting
slide85
Production of substances that promote invasiveness

Coagulase

DNAse

Hemolysins (a,b,c and d)

Leukocidin

Exfoliatin toxin

Scalded skin syndrome, exfoliative dermatitis, most often in newborns

Penicillinase

Hyaluronidase

Lipase

Staphylokinase

Staphlococcal decomplementation antigen (suppresses opsonization with C3b)

……… See Table

slide86
Can cause food poisoning, localized abscesses, impetigo contagiosum, toxic shock syndrome, and staphylococcal scalded skin syndrome
slide87
Diagnosis is by culture identification, catalase and coagulase tests, serology, DNA fingerprinting, and phage typing
  • Several antibiotics can be used for treatment but isolates should be tested for sensitivity because of the existence of many drug-resistant strains
slide88
20-40% carriers
    • Reservoirs
    • Often spread by hands
slide89
Toxic shock syndrome (1978)
    • Abrupt onset
    • Fever, erythematous rash
    • TSST-1
      • Superantigen
        • TNF-alpha, IL-1 by T cells
      • Hypotension
        • Often leading to irreversible shock!
    • 5-12% mortality rate
syphillis
Syphillis
  • Treponema pallidum
slide91
Syphilis - Treponema pallidum
    • Sexually transmitted or congenitally acquired in utero
    • Believed to have spread through Europe after Columbus’ sailors returened from Haiti ~1493
    • Viewed by darkfield microscopy (spirochetes – axial filaments)
    • Gram negative-type cell wall (+OM)
slide92
Primary stage:
    • Produce localized ulcer (chancre) in 1-4 weeks
      • Can make immediate diagnosis by examining fluid from chancre using darfield microscopy
    • Healing occurs weeks later  disease appears quiescent
      • But organisms have invaded the bloodstream and invade multiple body organs
slide93
Secondary Stage
    • Widespread lesions over entire body appear = Secondary syphilis – swarming with treponemes
      • Skin
      • Mucous membranes
      • Eyes
      • Bones CNS
    • Direct contact with secondary lesions can cause non-sexually acquired syphillis
slide94
Healing again occurs after a few monts to a few years
    • ~1/4 of cases retain latent infection for life
    • ~1/4 recover
    • ~1/2 reactivate as tertiary syphilis
slide95
Tertiary syphilis
    • May occur 5-40 years after initial infection
    • Lesions called gummata may occur in
      • CNS causing paresis (insanity)
        • ~1/3 of patient in mental institutes in first quarter of 20th century were attributed to earlier syphilic infection
      • Cardiovascular system causing aortic aneurysm (ballooning out of the aortic artery)
      • Eyes, skin, bones or viscera
slide96
Congenital syphilis
    • T. pallidum can cross placenta to infect fetus
    • Often fatal in utero
    • Newborn born with manifestations of disease may have early death or latent syphilis with death at a later date
    • Survivors – have notched incisors (Hutchison’s teeth)
    • Latency followed by tertiary syphilis (blindness, deafness, neurosyphilis, bone deformities)
slide97
Diagnosed by clinical history, microscopic examination, and serology
    • Complement fixation = Wassermann test
      • Antibody to cardiolipin
    • VDRL test
      • Venereal disease research lab test
        • Agglutination test (cardiolipin, lecithin, cholesterol and serum)
  • Treatment - penicillin in early stages, tertiary stage is highly resistant to treatment
  • Immunity is incomplete
  • Control is by public education, treatment, follow-up on sources and contacts, sexual hygiene, and prophylaxis (use of condoms)
tetanus
Tetanus
  • Clostridium tetani
slide99
Tetanus - Clostridium tetani
    • Large, Gram positive, endospore-forming, rod
    • Anerobic
    • Terminal spores (drumsticks)
    • Found in soil, dust, hospital environments, and mammalian feces
    • Low invasiveness, but in deep tissues with low oxygen tension, the spores germinate
      • When the vegetative cells lyse, they release tetanospasmin (an exotoxin)
        • Toxin causes prolonged muscle spasms by destroying acetylcholinesterase
        • Neurotoxin blocks release of neurotransmitters for inhibitory synapses
slide100
A hemolysin (tetanolysin) is also produced
  • Prevention is important and involves:
    • Active immunization with toxoid (DPT)
  • Debridement of wounds
  • Prophylactic use of antitoxin
  • Administration of penicillin
tularemia
Tularemia
  • Francisella tularensis
slide102
Tularemia - Francisella tularensis
    • Extremely small, pleomorphic, Gram negative rods, facultative anaerobe
    • Among the most virulent organisms that infect humans
    • Antiphagocytic capsule
    • Other virulence factors still under investigation
    • Grows and survives in monocytes protecting them from humoral Ab and complement
    • Is spread from animal reservoirs by a variety of mechanisms
    • A vaccine is available for high-risk laboratory workers
slide103
Three major manifestations of tularemia
    • 1. Ulceroglandular tularemia
      • From direct contact with infected animals or from the bite of an infected arthropod
        • Primary lesions at entry site
        • Open ulcer after 7 days
        • May reach lymph nodes and then spread systemically to other organs (~10% to lungs)
slide104
2. Pneumonic tularemia
    • Affects lungs following systemic spread or via respiratory route (e.g. skinning an infected rabbit)
      • Person-to-person spread via respiratory route
      • High mortality rate
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3. Typhoidal tularemia
    • From contaminated food or water
    • High fever and GI symptoms associated with typhoid fever