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200 Cards in this Set
- Front
- Back
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Commensal Skin Microbes
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Diphtheroids
Micrococci Yeasts |
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Diphtheroids
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Gram positive
Resemble C. diphtheriae, but usually not virulent Propionibacterium acnes |
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Micrococci
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Staphylococcus and Micrococcus
S. epidermidis – most well-adapted to life on human body |
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Yeasts
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Low numbers, can cause opportunistic disease
Candida albicans |
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Acne
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All follicle-associated lesions
If skin is prone to pimples and acne, it has Structure that traps the mass of sebum and dead cells, clogging the pores Exaggerated process of keratinization in and around the follicle, blocking the pore Overproduction of sebum when the sebaceous gland is stimulated by hormones Propionibacterium acnes in the follicle releases lipases to digest the oil, results in local inflammation that can burst the follicle Virulence factors include lipases, proteases, WBC attractant |
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Impetigo
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Superficial itchy bacterial infection
Not serious, but highly contagious Usually seen in children Caused by Staphylococcus aureus or Streptococcus pyogenes Looks like peeling skin, crusty and flaky scabs, or honey-colored crusts Lesions usually found around mouth, face, and extremities |
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Impetigo Caused by Staphylococcus aureus
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Causes a long list of diseases in humans, including impetigo
Facultative anaerobe Produces exfoliative toxins A & B that attack epithelial cell interactions -> blistering Produces coagulase which causes deposition of fibrin around bacteria & decreases phagocytosis Antibiotics Necrotizing fasciitis |
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Impetigo Caused by Streptococcus pyogenes
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Mainly a respiratory pathogen
Same symptoms as with S. aureus Has many virulence factors (Ch. 21) Binds host plasminogen, and turns it into plasmin with streptokinase turns bacteria into a tissue degrader! Transmitted through direct contact and by fomites Good hygiene is prevention |
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Cellulitis
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Caused by a fast-spreading infection in the dermis and the subcutaneous tissues
Causes pain, tenderness, swelling, and warmth Follows introduction of bacteria or fungi into the dermis (takes several days to develop) most commonly Staphylococcus aureus or Streptococcus pyogenes |
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Staphylococcal Scalded Skin Syndrome (SSSS)
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Caused by Staphylococcus aureus
Mostly in newborns and babies Transmitted by adults in newborn nursery (30% are carriers for S. aureus) Can be thought of as a systemic form of impetigo exfoliative toxins A & B enter bloodstream & travel to skin desquamation of the skin, making skin look burned Now protective keratinized layer is gone, making patient vulnerable to secondary infections |
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Gas Gangrene (Clostridial myonecrosis)
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Caused by Clostridium perfringens
Bacteria require anaerobic environment to cause disease Anaerobic cellulitis bacteria spread within damaged necrotic tissue, but does not spread into healthy tissue True myonecrosis toxins produced in necrotic tissue diffuse into healthy tissue and cause local necrosis this allows for continued clostridial growth |
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Clostridium perfringens Pathogenesis & Virulence Factors
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clostridia require anaerobic environment, so infection requires dying or dead tissue
alpha toxin causes RBC rupture, edema and tissue destruction also makes collagenase, hyaluronidase, and DNase produces gas from fermentation of muscle carbohydrates – destroys muscle structure |
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Transmission & Prevention of gas gangrene
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Person is predisposed to gangrene by surgical incisions, fractions, diabetic ulcers, gunshot wounds, and crushing injuries – anything that causes dying or dead tissue
Prevention is immediate and rigorous cleaning of wounds & debridement of diseased tissue Hyperbaric oxygen therapy Amputation |
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Chickenpox
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Caused by varicella zoster virus
Generally mild but can be life threatening in compromised patients Chickenpox parties Fever and abundant rash that begins on scalp, face, and trunk; radiates to the extremities Lesions fill with a clear fluid In several days, encrust and drop off Can experience secondary infections by streptococci or staphylococci |
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Shingles
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after clearance of chickenpox, virus enters the sensory endings of nerves and becomes latent
reemerge after reactivation as shingles inflammation of nerve pathways leads to pain, tenderness for weeks or months |
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Varicella Zoster Virus mode of infection
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Enters respiratory tract, attaches to repiratory mucosa, and enters bloodstream
Disseminates to skin where adjacent cells are made to fuse and lyse -> lesions virus enters sensory nerves and becomes latent (protection from immune system) |
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Transmission & Prevention chicken pox
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Humans only natural host
Harbored in respiratory tract but is communicable from respiratory droplets & fluid of skin lesions Contact with a person with shingles leads to chickenpox (cannot transmit shingles) Incredibly contagious, almost 100% transmission, but lifelong immunity Vaccine for chickenpox & shingles No treatment |
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Smallpox
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Naturally occurring smallpox no longer occurs, but may be a bioterrorism threat
Fever and malaise, then a rash in the pharynx Spreads to the face and progresses to the extremities within 24 h Two weeks for pustules to scab over contagious throughout because virus in crusts Survival leads to lifelong immunity |
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Pathogenesis & Virulence Factors of small pox
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Caused by Variola virus, small DNA virus
Infection begins in nasopharynx, invades mucosa and multiples in regional lymph node in WBCs Leads to viremia Lesions occur in dermis, which is why scars remain after lesions heal |
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Transmission & Prevention of small pox
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Before eradication in the 1970s, most people contracted disease (30% fatality)
Spread through droplets or contaminated bedding/clothing No treatment Vaccine: Edward Jenner, milkmaids, cowpox, & the vaccinia virus very high rate of side effects |
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Measles
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Sore throat, dry cough, headache, conjunctivitis, lymphadenitis, and fever
Koplik’s spots on head progresses to the trunk and extremities Complications can result Pneumonia Laryngitis Secondary bacterial infections Progressive degeneration of cerebral cortex & death |
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Pathogenesis & Virulence Factors of measles
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Caused by measles virus, single-stranded RNA
Virus implants in respiratory mucosa & infects tracheal & bronchial cells Travels to lymphatic system, multiples, enters bloodstream & is carried to various organs Virus induces fusion of adjacent cells to form syncytia, which inhibits cellular function Disables cell-mediated immunity, leaving patient vulnerable -> high incidence of secondary bacterial infections |
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Transmission & Prevention of measles
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One of the most contagious infectious diseases
Transmitted mostly through respiratory droplets Humans only reservoir MMR Vaccine No treatment |
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Rubella
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Also known as German measles
Usually relatively minor rash disease Two forms Postnatal infection multiplies in respiratory tract, enters lymph & bloodstream often accompanied with joint inflammation rather than rash Congenital (prenatal) infection Transmission of virus to a fetus in utero even if asymtomatic mom Fetal injury varies, from miscarriage to deafness (stops mitosis) Infection initiated through contact with respiratory secretions MMR vaccine |
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Fifth Disease
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Caused by parvovirus B19
5th of the diseases to cause childhood rashes “slapped-cheek” appearance Spreads on the body but is most prominent on arms, legs, and trunk Mild disease with low-grade fever and malaise Transmitted through respiratory droplets or through placenta to fetus No vaccine or treatment |
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Roseola
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Caused by herpes virus 6 (HHV-6)
Common in young children and babies 100% of US is infected by adulthood Most cases proceed without the rash stage Children get high fever that lasts for 3 days Fourth day, fever disappears, and rash can appear – at this point, disease is almost over Becomes latent & can become reactivated in adults to cause mononucleosis or other herpes symptoms No vaccine or treatment |
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Scarlet Fever
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Most often the result of a respiratory infection with Streptococcus pyogenes
Erythrogenic toxin |
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Warts
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Affect children more than adults
Gradual immunity Benign squamous epithelial growths All are caused by viruses, mostly the papilloma viruses (HPVs) (ch 23) Molluscum contagiosum (pox virus) |
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Molluscum contagiosum
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Smooth waxy nodules on the face, trunk, and limbs
May contain milky fluid Common in children Most often causes nodules on the face, arms, legs, and trunk in children; mostly in genital areas in adults Transmitted through direct contact or from towels, shower stall; autoinoculation to other parts of body Almost all nongenital warts are harmless & resolve over time (2-3 yrs) |
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Leishmaniasis
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Zoonosis transmitted by female sand flies
Infected fly injects protozoa into host while feeding multiplies in macrophage if macrophage remains fixed, infection stays localized in skin or mucous membranes Lesions can be extensive & disfiguring No vaccine; chemotherapy treatment |
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Cutaneous Anthrax
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Most common and least dangerous version of infection with Bacillus anthracis
Caused by endospores entering the skin through small cuts or abrasions Papule that becomes increasingly necrotic then ruptures to form a black eschar 20% fatal if untreated Vaccine but only for high-risk, military Antibiotics |
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Ringworm
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(Cutaneous Mycoses)
Fungal dermatophytes Confined to the nonliving epidermal tissues, hair, nails Different names all beginning with the word tinea |
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Tinea Capitis:
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Fungal invasion of scalp, head hair
Common in children Ringworm of the Scalp |
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Tinea Barbae:
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Ringworm of the Beard
Fungal infection of chin and beard of adult males “barber’s itch” because common aftereffect of unhygienic barbering Now contracted from animals |
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Tinea Corporis
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Ringworm of the Body
Can appear nearly anywhere on the body’s smooth, bare skin Usually appears as one or more scaly reddish rings on the trunk, hip, arm, neck, or face Transmitted by direct contact, clothing, bedding |
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Tinea Cruris
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Ringworm of the Groin
Also known as jock itch Thrives under conditions of moisture and humidity caused by sweating |
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Tinea pedis
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Ringworm of the Foot
Also known as athlete’s foot and jungle rot Connected to wearing shoes & keeping feet in a closed, warm, moist environment Begin with blisters between toes that burst, crust over, and spread to rest of foot & nails |
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Tinea Manuum
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Ringworm of the Hand
Almost always associated with concurrent infection of the foot Usually occur on the fingers and palms of one hand |
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Tinea Unguium
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Ringworm of the Nail
Masses of keratin in nails are sites for persistent fungus colonization Superficial white patches in the nail bed, or thickening, distortion, and darkening of the nail Artificial fingernails |
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Causative agents of the ringworm diseases
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Trichophyton, Microsporum, Epidermophyton
Can invade & digest keratin, present in the epithelial cells, but do not invade deeper tissues Spores can last for years on fomites Transmitted through direct contact or fomites Prevent by keeping susceptible skin areas dry Antifungal agent |
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Conjunctivitis or “pink eye”
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Infection of the conjunctiva
Fairly common & extremely contagious Inflammation and discharge Bacterial infections- milky discharge Viral infections- clear exudate Usually caused by staphylococci or streptococci in children or adults Adenoviruses Neonatal conjunctivitis (chlamydia, gonorrhea) |
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Trachoma
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Chronic Chlamydia trachomatis infection of the epithelial cells of the eye
Major cause of blindness in certain parts of the world First signs are mild discharge and slight inflammation Followed by marked infiltration of lymphocytes and macrophages Pebbled appearance to the upper eyelid Eventually, pseudomembrane forms over cornea Transmitted by contaminated fingers & fomites Recurrent infections may lead to scarring & blindness Antibiotics |
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Keratitis
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More serious infection than conjunctivitis
Invasion of deeper eye tissues occurs, can lead to complete corneal destruction Any microorganism can cause this condition more common causes is herpes simplex virus misdirected activation of oral herpes (travels through nerve to eye instead of mouth) Preliminary symptoms: gritty feeling in the eye, conjunctivitis, sharp pain, and sensitivity to light 25-50% of cases are recurrent and can lead to blindness (leading infectious cause of blindness in US) |
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River Blindness
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Chronic parasitic (helminthic) infection
Onchocerca volvulus transmitted by black flies larvae deposited into bite wound & develop into adults in subcutaneous tissues form nodules within 1-2 years migrate into the bloodstream & eventually invade the entire eye produce inflammation and permanent damage to the retina and optic nerve worms are often visible in eye Produces itchy rash that can last for 15+ years Avoid black fly (almost impossible in endemic areas) Treatment with antifilarial drug |
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Normal Biota of the Nervous System
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None!
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Meningitis
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Inflammation of the meninges
Many different microorganisms can cause an infection More serious forms caused by bacteria Lumbar puncture for CSF Typical symptoms: headache, painful or stiff neck, fever, and usually an increased number of white blood cells in the CSF |
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Neisseria meningitides
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Gram-negative diplococci
Meningococcus Causes the most serious form of acute meningitis Enters meninges, releases endotoxin into general circulation -> inflammation, vascular collapse, petechiae Leads to delirium, shock, coma, death |
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Pathogenesis & Virulence Factors of neiseria mengitides
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Pathogenesis
Portal of entry: nasopharynx Attach with pili Engulfed by mucosal epithelial cells -> pharyngitis Can infect meninges Carriage state (days to months) 30-50% Virulence factors IgA protease Capsule |
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Transmission & Prevention of neiseria mengitides
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Do not survive long in environment
Close contact with secretions or droplets Natural immunity during early years of life Antibiotic treatment immediately |
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Streptococcus pneumoniae
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Causes the majority of bacterial pneumonias, so referred to as the pneumococcus
Most frequent cause of community-acquired meningitis Mostly occurs in those with underlying susceptibilites (alcoholics, sickle-cell disease, absent or defective spleen function) Very severe Does not cause the petechiae associated with meningococcal meningitis- useful diagnostically Covered in more detail in Ch 21 (resp tract) |
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Haemophilus influenza
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Tiny gram-negative pleomorphic rods
Thought to be the causative agent of the flu Causes severe meningitis in sporadic outbreaks adult humans carriers are the reservoir Sensitive to drying, temperature extremes, and disinfectants Symptoms: fever, stiff neck, vomiting, and neurological impairment 33% of children who recover have damage Most common in children 3mo-5yrs now a vaccine available (Hib) |
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Listeria monocytogenes
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Gram-positive coccobacilli to long filaments
Intracellular bacteria--moves directly into adjacent uninfected cell Resistant to cold, heat, salt, pH extremes, bile Most cases from eating contaminated dairy products, poultry, meat found in 12% ground beef, 30% chicken/turkey carcasses, 10% lunch meat & cheese, hot dogs In normal adults- mild infection with nonspecific symptoms of fever, diarrhea, and sore throat In elderly or immunocompromised patients, fetuses, or neonates- affects the brain and meninges and results in septicemia (death rate 20%) Miscarriage |
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Cryptococcus neoformans
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Fungus
Spherical to ovoid shape and a large capsule Usually just lung infection—can lead to meningitis (both usually in immunocompromised individuals) Gradual onset of symptoms Headache- most common symptom; also nausea and stiff neck |
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Pathogenesis & Virulence Factors of cryptococcus neoformans
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Escape of yeasts from lung into the blood
Shows affinity for meninges & brain Forms tumor-like masses |
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Transmission & Prevention of cryptococcus neoformans
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Ecological niche is pigeons—grows in high nitrogen droppings
Portal of entry is respiratory tract Treatment with amphotericin B No prevention |
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Viral meningitis
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“Aseptic meningitis”
Majority of cases occur in children 90% caused by enteroviruses Herpes, CMV, HIV Generally milder than bacterial or fungal meningitis (<1% mortality) |
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Neonatal Meningitis
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Almost always a result of infection transmitted by the mother, either in utero or during passage through the birth canal
Two most common causes Streptococcus agalactiae (Group B strep, GBS) Escherichia coli review pg 18 chapter 19 |
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Meningoencephalitis
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Inflammation of the meninges and the brain
Caused by two microorganisms (both amoebas) Naegleria fowleri Acanthamoeba |
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Naegleria fowleri
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Small, flask-shaped amoeba
Forms a rounded, thick-walled, uninucleate cyst resistant to extreme temps & mild chlorination Infection begins when amoebas are forced into human nasal passages while swimming Amoeba burrows in to the nasal mucosa, multiplies, and migrates into the brain and surrounding structure Primary amoebic meningoencephalitis (PAM) destruction of tissue -> coma & death within one week Many children carry as normal biota Treatment usually futile |
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Acanthamoeba
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Large, amoeboid trophozoite with spiny pseudopods and a double-walled cyst
Portal of entry different from Naegleria invades broken skin, the conjunctiva, and occasionally the lungs and urogenital epithelia Granulomatous amoebic meningoencephalitis (GAM) traumatic eye injuries, contact lens wearers |
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Acute Encephalitis
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Encephalitis can present as acute or subacute
Always a serious condition Acute is almost always caused by viral infection Signs and symptoms vary but may include behavior changes, confusion, decreased consciousness, seizures |
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West Nile Encephalitis
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Arbovirus
Commonly found in Africa, Middle East, Asia First cases in US seen in 1999 By mid 2005, 1 million infections & 664 deaths Mosquitos become infected when feed on infected birds, then bite & transmit to humans Infection results in flu-like symptoms for few days, only 1% get encephalitis Transmission based on vector control Virus isolated in 200 bird species & cats, dogs, rodents, horses, alligators |
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Herpes Simplex Virus
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Can cause encephalitis in newborns born to HSV-positive mothers
Prognosis is poor |
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Subacute Encephalitis
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Diagnosed when symptoms take longer to show up and are less striking
Most common cause: Toxoplasma Also measles, prions |
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Toxoplasma gondii
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Flagellated parasite
Primary reservoir are cat family, but attacks over 200 species of birds & mammals Most cases go unnoticed Asymptomatic or marked by mild symptoms such as sore throat, lymph node enlargement, and low-grade fever In the fetus and immunodeficient people, severe and often fatal parasites does not cycle in cats alone is spread to rodents & birds protozoan changes brain of rodent! |
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Prions
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Neurodegenerative diseases with long incubation periods but rapid progression once they begin
Abnormal host protein converts normal host proteins Leads to plaques, holes in the brain, severe loss of brain function Transmission requires contact with brain or CSF Humans were getting from cattle, due to contaminating brain matter Human TSE Creutzfeldt-Jakob disease (CJD) Kuru |
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Rabies
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Slow, progressive zoonotic disease
Characterized by fatal encephalitis Average incubation time: 1-2 months or more Prodromal phase begins with fever, nausea, vomiting, headache, fatigue, and other nonspecific symptoms Furious rabies Periods of agitation, disorientation, seizures, and twitching Hydrophobia Dumb rabies Patient is paralyzed, disoriented Both forms progress to the coma phase, resulting in death |
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Pathogenesis & Virulence Factors of rabies
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Infected animal’s saliva enters puncture site
Multiplies for one week at inoculation site Enters nerve endings and advances toward brain Migrates toward eye, heart, oral cavity Cycle completes when replicates in salivary gland & is shed in saliva Envelope glycoprotein allows spread in CNS & invasion of neural cells |
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Transmission & Prevention of rabies
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Reservoirs are wild mammals that spread to domestic dogs & cats
Don’t get bitten by wild animal! |
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Poliomyelitis
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Acute enteroviral infection of the spinal cord
Can cause neuromuscular paralysis Most infections are contained as short-term, mild viremia Some develop mild nonspecific symptoms of fever, headache, nausea, sore throat, and myalgia Two types: Nonparalytic: invasion but not destruction of nervous tissue Paralytic: various degrees of flaccid paralysis |
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Transmission of poliomyelitis
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Ingested & carried to throat, intestinal mucosa
Multiplies in tonsils Cross into certain nerve cells of CNS Intestine actively sheds virus More pronounced during summer & fall Passed through food, water, objects contaminated with feces Often affects small children Increase during first half of 1900’s due to increased hygiene Vaccine Used to be contained until rise in anti-vaccine campaigns worldwide and in US |
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Tetanus
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Also known as lockjaw
Clostridium tetani: Gram-positive, spore-forming rod Tetanus toxin blocks the inhibition of muscle contraction spastic paralysis First symptoms : clenching of the jaw, followed in succession by extreme arching of the back, flexion of the arms, and extension of the legs Death due to paralysis of respiratory muscles & arrest |
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Pathogenesis & Virulence Factors of tetanus
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Spores enter through puncture wounds, burns, umbilical stumps, frostbite
Not sufficient for infection because C. tetani is a strict anaerobe likes necrotic wounds Muscle contractions are violent enough to break bones |
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Botulism
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Clostridium botulinum
Spore forming anaerobe Releases an exotoxin, botulinum toxin Intoxication associated with eating poorly preserved foods, but can also occur as a true infection Symptoms: double vision, difficulty in swallowing, dizziness; later symptoms include descending muscular paralysis and respiratory compromise Major forms Food-borne botulism: Ingestion of preformed toxin Infant botulism: Entrance of botulinum toxin into the bloodstream |
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Normal Biota of cardiovascular system
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None
Some microorganisms may be present transiently |
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Endocarditis
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Inflammation of the endocardium (usually heart valves)
Acute and subacute, with similar symptoms Fever, anemia, abnormal heartbeat, abdominal or side pain Sometimes symptoms similar to heart attack Petechiae review slide 9 on chapter 20 |
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Septicemias
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Actively multiplying organisms in the blood
Many different bacteria and a few fungi (10%) can cause this condition Fever- prominent symptom Patient appears very ill, altered mental state, shaking, chills, and gastrointestinal symptoms, increased breathing |
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Plague
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Killed 100 million people in 6th century
Late 1800s-early 1900s – through rat-infested ships Three possible manifestations Pneumonic plague: respiratory disease Bubonic plague: results in a swollen lesion called a bubo, usually in the groin or axilla Incubation period: 2 to 8 days, ending with the onset of fever, chills, headache, nausea, weakness, and tenderness of the bubo Septicemic plague: when the case progresses to massive bacterial growth in the blood |
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Yersinia pestis Pathogenesis & Virulence Factors
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Bubonic plague
3-50 cells infectious dose Yops – secretion system + toxins capsule, plasminogen activator clotting -> less phagocytosis similar to S. pyogenes |
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Transmission bubonic plague
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Plague bacillus occurs in 200+ mammals, esp rodents
Flea ingests blood meal from infected animal bacterial multiplication in gut esophagus blocked, flea jumps rapidly to multiple animals |
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Tularemia
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Pathogen of concern on the lists of bioterrorism agents
ID of 10-50 organisms Rabbit fever (mostly associated with wild rabbits) Tick bites no human-to-human transmission Incubation period of a few days to 3 weeks Symptoms: headache, backache, fever, chills, malaise, and weakness Further symptoms tied to the portal of entry: ulcerative skin lesions, swollen lymph glands, conjunctival inflammation, sore throat, intestinal disruption, pulmonary involvement |
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Lyme Disease
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Nonfatal
Progressive syndrome that mimics neuromuscular and rheumatoid conditions Early symptom: rash at the site of a tick bite Other early symptoms: fever, headache, stiff neck, and dizziness Second stage: cardiac and neurological symptoms develop Immune evasion by changing surface antigens Borrelia burgdorferi from deer to tick to man |
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Mononucleosis
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Majority caused by Epstein-Barr virus (EBV)
“kissing disease”— transmitted by saliva, teen disease Most of the remainder caused by cytomegalovirus (CMV) Sudden leukocytosis Fatigue Sore throat, high fever, may exhibit gray-white exudates in the throat, skin rash Long incubation period- 30 to 50 days |
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Yellow Fever
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Caused by an flavivirus
Found only in Africa & S. America Transmission mosquito Aedes aegypti (standing water) Leads to capillary fragility & disrupts the blood-clotting system Begins with fever, headache, and muscle pain Sometimes progresses to oral hemorrhage, nosebleed, vomiting, jaundice, and liver & kidney damage |
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Dengue Fever
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Caused by a flavivirus
Carried by Aedes mosquito Usually mild Sometimes it can progress to dengue hemorrhagic shock syndrome Causes severe pain in muscles and joints “breakbone fever” 600% increase in cases in Mexico since 2001 |
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Ebola and Marburg
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Filoviruses
Related viruses, cause similar symptoms Extreme manifestations of hemorrhagic events with extensive capillary fragility and disruption of clotting Patients bleed from their orifices, mucous membranes, and experience massive internal and external hemorrhage Often manifest a rash on the trunk in early stages No treatment... 25-100% mortality |
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Lassa Fever
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Arenavirus
Most cases asymptomatic In 20% of cases, a severe hemorrhagic syndrome develops Chest pain, hemorrhaging, sore throat, back pain, vomiting, diarrhea, and sometimes encephalitis Patients who recover often suffer from deafness Reservoir is the rat virus spread to humans through dropping, urine, etc. |
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hemorrahagic fevers
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yellow fever
dengue fever ebola and marburg lassa fever check slide 25 chapter 20 |
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Nonhemorrhagic Fever Diseases
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All caused by bacteria
Cause high fever but no capillary fragility |
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Brucellosis
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Bacteria enter through skin breaks or mucus membranes and are carried into the bloodstream by phagocytic cells
Brucella live inside phagocytic cells Create focal lesions in the liver, spleen, bone marrow, and kidney Fluctuating pattern of fever accompanied by chills, profuse sweating, headache, muscle pain and weakness, and weight loss Symptoms can continue for 1 year, even with treatment! |
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Cat-Scratch Disease
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Caused by Bartonella henselae (found in 40% of cats!)
Symptoms start after 1 to 2 weeks Cluster of small papules at the site of inoculation In a few weeks, lymph nodes swell and can become pus-filled Only about 1/3 of patients experience high fever |
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Rocky Mountain Spotted Fever (RMSF)
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Caused by Rickettsia rickettsii
Transmitted by tick bites Mostly found in Southeast & eastern seaboard 2 to 4 days incubation First symptoms: sustained fever, chills, headache, and muscular pain Distinctive spotted rash 2-4 days later In most severe untreated cases, enlarged lesions merge and become necrotic Other manifestations: restlessness, delirium, convulsions, tremor, and coma |
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Malaria
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Caused by Plasmodium falciparum
The world’s dominant protozoan disease 10- to 16-day incubation period First symptoms: malaise, fatigue, vague aches, and nausea with or without diarrhea Next symptoms: bouts of chills, fever, and sweating Symptoms occur at 48- or 72-hour intervals when RBCs are lysed Sporozoites enter capillary through feeding mosquito Invade liver cells, develop into merozoites Released from liver, enter RBCs Burst out of RBCs Feeding mosquito eats protozoa |
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Anthrax
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Caused by Bacillus anthracis
Cutaneous anthrax Pulmonary anthrax Usually transmitted by kicking up dust Air, soil, animal hides, food Virulence factors capsule hemolysins tripartite toxin inhibits cellular metabolism, results in massive inflammation, shock |
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HIV & AIDS
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Retrovirus: human immunodeficiency virus (HIV)
Hybrid virus from two separate monkey SIVs Acquired immunodeficiency syndrome (AIDS) Spectrum of clinical disease associated with HIV infection Symptoms directly tied to two things: the level of virus in the blood and the level of T cells in the blood see slides 36 and 37 chapter 20 |
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Symptoms of HIV and AIDS
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Initial infection: mononucleosis-like symptoms that soon disappear (initial high levels of virus)
Within days, about 50% of the T helper cells with memory for the virus are destroyed Period of asymptomatic infection that varies in length from 2 to 15 years number of T cells steadily decreases Once T cells reach low enough levels, symptoms of AIDS ensue Initial symptoms of AIDS: fatigue, diarrhea, weight loss, and neurological changes Opportunistic infections Severe immune deregulation, hormone imbalances, metabolic disturbances Pronounced wasting of body mass Protracted fever, fatigue, sore throat, and night sweats Lesions in the brain, meninges, spinal column, and peripheral nerves |
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Defenses of the Respiratory Tract
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Nasal hair
Cilia Mucus Involuntary responses (coughing, sneezing, swallowing) Macrophages/tonsils Secretory IgA |
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Normal Biota of the Respiratory Tract
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Generally limited to the upper respiratory tract
Gram-positive bacteria (streptococci and staphylococci) Candida in mouth Disease-causing bacteria are present as normal biota can cause disease if host becomes immunocompromised Streptococcus pyogenes, Haemophilus influenza, Streptococcus pneumoniae, Neisseria meningitides, Staphylococcus aureus |
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Respiratory Tract Diseases Caused by Microorganisms
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Upper Respiratory Tract
Rhinitis Sinusitis Acute Otitis Media Pharyngitis Diptheria Both Whooping Cough RSV Influenza Lower Respiratory Tract Tuberculosis Pneumonia |
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Rhinitis (the common cold)
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Caused by one of over 200 different viruses!
usually rhinovirus or coronavirus Symptoms: sneezing, scratchy throat, runny nose Symptoms begin 2-3 days after infection Generally not accompanied by fever May get secondary bacterial infection |
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Pathogenesis & Virulence Factors of rhinitis
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Penetrate mucus in respiratory tract & attach
Use host cells to reproduce Symptoms are host immune response Not many virulence factors |
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Transmission & Prevention of rhinitis
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Droplet contact
Indirectly through fomite contamination Because there are over 200 different viruses, no vaccine & easy to get another cold Most colds as child, least colds middle-aged |
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Sinusitis
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Sinus infection
Caused by allergy or by infections (normal biota) Generally follows the common cold NOT communicable Symptoms: nasal congestion, pressure above the nose or in the forehead, feeling of headache or toothache Discharge opaque green or yellow (often bacterial) clear with itchy, watery eyes (often allergy) |
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Acute Otitis Media (Ear Infection)
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Also can follow cold
Upper respiratory viral infections can lead to the buildup of fluid in the middle ear (child vs adult anatomy) bacterial growth Streptococcus pneumoniae Haemophilis influenza Chronic otitis media when fluid remains in the middle ear for indefinite periods of time may be caused by biofilm bacteria Symptoms: sensation of fullness or pain in the ear, loss of hearing Untreated or severe infections can lead to eardrum rupture |
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Pharyngitis
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Inflammation of the throat
Pain and swelling, reddened mucosa, swollen tonsils, white pus nodules Mucous membranes may swell, affecting speech and swallowing Often results in foul-smelling breath Incubation period: 2-5 days |
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Streptococcus pyogenes
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Pharyngitis usually caused by same viruses as cause cold
Most serious cause is S. pyogenes Gram-positive bacteria Untreated infections can result in serious complications |
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Complicating diseases of pharyngitis
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Scarlet fever
erythrogenic toxin manifests as sandpaper rash & high fever 95% fatal but treatable with antibiotics Rheumatic fever immunologic cross-reaction with heart muscle occurs 3 weeks after pharyngitis has subsided results in permanent damage to heart valves, arthritis preventable if original pharyngitis treated Glomerulonephritis results from antigen-antibody complexes in kidney can result in permanent kidney damage |
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Virulence factors strep pyogenes
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M protein—assists in adherence & resists phagocytosis
Hyaluronic acid capsule—adhesiveness (same as human tissue) Streptolysins—cause lysis of WBCs, liver & heart muscle cells Erythrogenic toxin—responsible for bright red rash of scarlet fever; induces fever by acting on brain Both toxins are superantigens |
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Transmission & Prevention of pharyngitis
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30% of sore throats caused by S. pyogenes
transmits through respiratory droplets or direct contact with mucus membranes humans only reservoir 80 serotypes so multiple infections possible Sore throat doctor! |
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Diphtheria
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Corynebacterium diphtheriae
Symptoms initially experienced in the upper respiratory tract Sore throat, lack of appetite, low-grade fever Pseudomembrane forms on the tonsils or pharynx contains bacteria, fibrin, lymphocytes, dead tissue may eventually block respiration |
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Pathogenesis & Virulence Factors of diptheria
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A-B exotoxin
A (active) toxin B (binding) toxin adds an ADP-ribose to EF-2 inhibits protein synthesis |
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Prevention & Treatment of diptheria
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Mixed vaccination: DTaP
Antitoxin derived from horses Antibiotics against bacteria |
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Whooping Cough
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Caused by Bordetella pertussis
Two distinct symptom phases Catarrhal stage Incubation of 3 to 21 days Cold symptoms (runny nose) Lasts 1 to 2 weeks Paroxysmal stage Severe and uncontrollable coughing Violent coughing spasms can result in burst blood vessels in the eyes or vomiting Followed by convalescent phase Complete recovery requires weeks or even months Other microorganisms can more easily cause secondary infection |
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Pathogenesis & Virulence Factors of whooping cough
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Causes localized inflammation/mucus production
Filamentous hemagglutinin (FHA) to attach to epithelial cells of mouth/throat Secretes two exotoxins that damage respiratory epithelial cells & phagocytic cells pertussis toxin—excess mucus tracheal toxin—direct ciliated cell destruction |
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Transmission & Prevention of whooping cough
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Transmitted via respiratory droplets
300,000-500,000 deaths worldwide yearly Only 85% of US children are vaccinated Part of DTaP vaccine Antibiotics |
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Respiratory Syncytial Virus (RSV)
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Produces giant multinucleated cells (syncytia) in the respiratory tract
Most prevalent respiratory infection in newborns First symptoms: fever that lasts approximately 3 days, rhinitis, pharyngitis, and otitis More serious infections give rise to symptoms of croup: coughing, wheezing, difficulty breathing Adult infections manifest like a cold No vaccine; supportive care immediately in children |
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Influenza
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Begins in the upper respiratory tract; serious cases may also affect the lower respiratory tract
1- to 4-day incubation period Symptoms begin very quickly: headache, chills, dry cough, body aches, fever, stuffy nose, and sore throat Extreme fatigue can last a few days or a few weeks |
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Influenza Pathogenesis & Virulence Factors
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Antigenic drift
ssRNA genome is subject to constant variability Antigenic shift swapping of genes with those from another influenza virus 1918 flu pandemic H1N1 makes vaccine difficult Virus binds to ciliated cells of respiratory mucosa Causes rapid shedding of those cells + virus Eliminates protective ciliary clearance & leads to inflammation & irritation Symptoms subside when ciliated epithelium is restored (~1 week) Glycoprotein spikes on envelope (e.g. H1N1) hemagglutinin (H) – binds host receptors on respiratory mucosa neuraminidase (N) – breaks down mucus coating in respiratory tract, viral budding & release |
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Transmission & Prevention of influenza
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Aerosols & droplets containing virus
Fomites ~36,000 US death yearly Vaccine is combination of 3 most likely variants for upcoming flu season educated guess ~9 months in advance |
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Tuberculosis
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Humans are easily infected with Mycobacterium tuberculosis but are resistant to the disease
Only ~5% of infected people actually develop a clinical case of TB Untreated TB progresses slowly Clinical TB is divided into primary tuberculosis, secondary tuberculosis, and disseminated tuberculosis |
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Primary Tuberculosis
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Asymptomatic or accompanied by mild fever
After 3 to 4 weeks, large influx of mononuclear cells into lungs Tubercles form central core of TB in macrophages & outer wall of fibroblasts, lymphocytes, neutrophils Centers of tubercles break down into necrotic caseous lesions |
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Secondary (Reactivation) Tuberculosis
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Live bacteria can reactive weeks-years later
Chronic tuberculosis -- tubercles filled with bacteria expand and drain into bronchial tubes and upper respiratory tract Severe symptoms: violent coughing, greenish or bloody sputum, low-grade fever, anorexia, weight loss, extreme fatigue, night sweats, chest pain Consumption |
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Extrapulmonary Tuberculosis
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Outside of the lungs
More common in immunosuppressed patients and young children Regional lymph nodes, kidneys, long bones, genital tract, brain, and meninges Complications are usually severe |
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Mycobacterium tuberculosis
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acid-fast rod bacteria
15-20h generation time Waxy surface – survival in environment & within macrophages strong cell-mediated immunity |
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Transmission & Prevention of tuberculosis
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Droplets of respiratory mucus
small particles inhaled directly into lower respiratory tract easier in crowded settings Can survive for 8 months in fine aerosol particles Limit exposure to airborne particles Antibiotics for 9 months (many are MDR due to patient non-compliance) |
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Pneumonia
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Anatomical diagnosis -- inflammatory condition of the lung in which fluid fills the alveoli
Can be caused by a wide variety of different microorganisms Viral pneumonias are usually milder than bacterial Community-acquired vs. nosocomial pneumonias Begin with upper respiratory tract symptoms Runny nose and congestion Headache & fever common Onset of lung symptoms follows chest pain, fever, cough, discolored sputum Causative agents: S. pneumoniae, L. pneumophila, hantavirus, SARS-associated coronavirus, Pneumocystis |
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Streptococcus pneumoniae
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Causes 2/3 of community-acquired pneumonia
Normal biota in upper respiratory tract; infection occurs when inhaled into lower regions or by transfer via mucus droplets Host defenses prevent pneumonia in healthy people Pneumonia occurs when mucus containing bacteria passes into sterile bronchi & alveoli induces inflammatory response infection spreads down through lung until person drowns Pneumococcal vaccine for the elderly |
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Legionella pneumophila
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Gram-negative bacteria
Legionnaire’s disease—1976 Philadelphia Found in water, water, water (tap water to showers to vegetable sprayers) Mostly opportunistic disease |
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Hantavirus
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Doesn’t just cause hemorrhagic fever
Sporadic disease, but 33% mortality New Mexico outbreak in 1993 Lung symptoms due to large amounts of hantavirus antigen becomes disseminated through bloodstream, including in lung inflammatory response -> breathing difficulties |
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SARS
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Coronavirus
concentrated in Asia 9% death rate No treatment |
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Pneumocystis jiroveci
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Fungal infection
Organism commonly found in majority of population by age of 3 or 4 Very rare until HIV/AIDS Usually held in check by lung WBCs Lung epithelial cells slough off, cause inflammation Life cycle is unknown |
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Nosocomial Pneumonia
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see slide 41 chapter 21
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Defenses of the GI Tract
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Mucus
Secretory IgA Peristalsis Fluids with antimicrobial properties saliva, stomach fluid, bile Host defense tissues: tonsils, adenoids, Peyer’s patches Microbial antagonism |
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Dental Caries (Tooth Decay)
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Most common infectious disease of human beings
Symptoms: range from minor disruption in the enamel to complete destruction of the enamel and deeper layers Deeper lesions can result in infection to soft tissue and lead to a toothache |
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Periodontal Disease
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97% to 100% of the population has some manifestation by age 45
Most are due to bacterial colonization and inflammation Gingivitis (reversible) swelling, loss of normal contour, patches of redness, and increased bleeding Periodontitis (irreversible) Extension of gingivitis into the periodontal membrane and cementum Bone resorption Tooth may fall out |
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Mumps
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Incubation period 2 to 3 weeks
Initial symptoms: fever, nasal discharge, muscle pain, and malaise Followed by multiplication/inflammation of the salivary glands, producing gopher-like swelling of the cheeks Followed by invasion of testes, ovaries, thyroid gland, pancreas, meninges, heart, and kidneys Transmission through droplets Prognosis is usually complete recovery with permanent immunity |
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Causative Agent of mumps
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Mumps virus
Enveloped single-stranded RNA virus genus Paramyxovirus Induce fusion of adjacent cells —multinucleated cells |
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Pathogenesis & Virulence Factors of mumps
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HN spikes in cell membrane
Bind uninfected neighboring cell fusion Allows direct passage of viruses from infected to uninfected cells Virus evades antibodies |
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Gastritis and Gastric Ulcers
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Barry Marshall’s experiment
Heliobacter pylori thrives in the acidic environment of the stomach Gastritis: sharp or burning pain emanating from the abdomen Gastric ulcers: lesions in the mucosa of the stomach Severe ulcers can be accompanied by bloody stools, vomiting, or both Long-term infection with H. pylori might be a contributing factor to stomach cancer |
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Pathogenesis & Virulence Factors of H. Pylori
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Bores through mucus layer lining stomach
Attaches to specific receptors on cell one receptor is O blood type Urease converts urea into compounds that neutralize stomach acid WBCs attach pathogen, damage epithelium by accident ulcer |
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Salmonella
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10 years ago, 33% of chickens were contaminated; now 10%
Peanut butter, sprouts, spinach, etc. Classified by H (flagella), K (capsule), O (cell wall) salmonellosis (S. typhimurium) can be severe (elevated body temperature and septicemia) or mild (vomiting, diarrhea, and mucosal irritation) symptoms usually spontaneously subide after 2 to 5 days |
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Pathogenesis & Virulence Factors of salmonella
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Adheres particularly well to gut mucosa
endotoxin |
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Transmission/Prevention of salmonella
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Meat & milk contamination during slaughter, collection, processing
Uncooked meat Unpasteurized milk, cheese Avoid contact! |
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Shigella
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Causes the most severe form of dysentery
Uncommon in the U.S Frequent, watery stools, fever, and intense abdominal pain Nausea and vomiting are common Often bloody stools |
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Pathogenesis & Virulence Factors of shigella
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Invades villus cells of large intestine
Enters intestinal mucosa by lymphoid cells in Peyer’s patches Starts inflammatory response causing extensive tissue destruction Shiga toxin—more serious intestinal damage, including systemic nerve damage interrupts protein synthesis in host cell |
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Transmission & Prevention of shigella
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Oral route like Salmonella
Can be acquired from person to person because low ID (10-200 bacteria) Acquired in crowded settings (daycares, prisons, nursing homes, military camps) Good hygiene and avoidance of infected persons |
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Acute Diarrhea Caused by E.coli
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Enterohemorrhagic E. coli
Most virulent strain of E. coli Symptoms range from mild gastroenteritis with fever to bloody diarrhea About 10% of patients develop hemolytic uremic syndrome Can cause kidney damage and failure Neurological symptoms such as blindness, seizure, and stroke |
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Pathogenesis & Virulence Factors of e.coli
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Shiga toxin (identical to Shigella)
destroys gut epithelial cells secretion system to inject toxins lesions in large intestine |
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Transmission & Prevention of acute diarrhea caused by e.coli
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Ingestion of contaminated or undercooked beef (esp ground beef)
Lettuce, vegetables, apples ID of 10 bacteria! Cook, cook, cook that hamburger! denatures Shiga toxin |
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Acute Diarrhea Caused by Campylobacter
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Frequent watery stools, fever, vomiting, headaches, and severe abdominal pain
Symptoms may last beyond 2 weeks Symptoms may subside then recur over a period of weeks In a small number of cases, can lead to a serious neuromuscular paralysis called Guillain-Barré syndrome (GBS) |
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Acute Diarrhea Caused by Clostridium difficile
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Causes pseudomembranous colitis
Most common cause of diarrhea in US Able to superinfect the large intestine when drugs have disrupted the normal biota Produces two enterotoxins (toxins A and B) that cause areas of necrosis in the wall of the intestine Severe cases exhibit abdominal cramps, fever, and leukocytosis |
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Acute Diarrhea Caused by Vibrio cholera
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Incubation period of a few hours to a few days
Symptoms begin abruptly with vomiting Followed by copious watery feces called secretory diarrhea Can lose up to 1 liter of fluid an hour in severe cases (special tables with holes and buckets) Cholera toxin mechanism |
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Acute Diarrhea Caused by Rotavirus
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dsRNA genome
primary viral cause of death from diarrhea (50%) transmitted by fecal-oral route Effects of infection vary with age, nutritional state, general health, and living conditions of the patient |
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Acute Diarrhea Caused by Other Viruses than rotavirus
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Many other viruses can cause gastroenteritis
For example adenoviruses, noroviruses, and astroviruses Common in the U.S. and around the world Cruise ships Profuse, water diarrhea of 3 to 5 days duration |
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Acute Diarrhea with Vomiting (Food Poisoning)
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Symptoms in the gut that are caused by a preformed toxin, not bacterial growth
Toxins do not noticeably alter the food’s taste or smell Heating the food after toxin production may not prevent disease If the symptoms are violent and the incubation period is very short (1-6h), intoxication rather than infection should be considered |
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Food Poisoning by Staphylococus aureus Exotoxin
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Associated with food such as custards, sauces, cream pastries, processed meats, chicken salad, or ham that have been contaminated and then left unrefrigerated for a few hours
July 4th picnics Symptoms: cramping, nausea, vomiting, and diarrhea Rapid recovery- usually within 24 hours |
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Food Poisoning by Bacillus cereus Exotoxin
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Two exotoxins: one causes diarrhea, the other causes vomiting
Emetic form frequently linked to fried rice, especially when cooked and kept warm for long periods of time Diarrheal form associated with cook mats or vegetables that are held at a warm temperature for long periods of time |
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Chronic Diarrhea by Giardia
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Protozoa, first seen by Leeuwenhoek
Cysts enter duodenum, germinate, multiply in jejunum Leads to maladsorption, esp of fat -> weight loss Diarrhea of long duration, abdominal pain, and flatulence Stools have a greasy, malodorous quality Fever usually not present |
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Chronic Diarrhea by Entamoeba
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Clinical amoebiasis exists in intestinal and extraintestinal forms
Intestinal targets: cecum, appendix, colon, and rectum Secretes enzymes that dissolve tissues Leaves erosive ulcerations as it penetrates deper layer of mucosa Dysentery, abdominal pain, fever, diarrhea, weight loss Extraintestinal: common target is the liver Amoebic hepatitis Rarer complication- pulmonary amoebiasis |
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Helminthic Intestinal Infections
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Usually provoke an increase in granular leukocytes called eosinophils (eosinophilia)
Most spend part of their life cycle in the intestinal tract Diagnosis based on Differential blood count showing eosinophilia Serological tests indicating sensitivity to helminthic antigens Discovery of eggs, larvae, or adult worms in stools or other tissues |
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Pathogenesis and Virulence Factors
of helminthic intestinal infectino |
Most do not have sophisticated virulence factors
Have numerous adaptations that allow them to survive in their hosts Specialized mouthparts Enzymes to liquify, penetrate tissues Cutical or other covering for protection against host defenses Damage caused to host is usually the result of the host’s response to the presence of the worm Many have more than one host- the host in which the adult worm is found is the definitive host |
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Prevention and Treatment of helminths
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Prevention - minimizing human contact with parasite or interrupting its life cycle
Treatment - worm/larvae removal or antihelminthic drugs paralysis block metabolism inhibit ATP formation |
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Enterobius vermicularis (pinworm)
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Common of children in temperate zones
Also cycle A type Worms ingested from contaminated food, drink or self-inoculation from fingers Pronounced anal itching when the mature female emerges from the anus and lays eggs Freshly deposited eggs are sticky—remain on fomites, under nails (transmission) Can also suffer from disrupted sleep, nausea, abdominal discomfort, and diarrhea |
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Taenia solium (tapeworm)
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Where humans and pigs are in close proximity
Cysts live in pig muscles Cycle C: humans eat worm cysts in meat Adults are 16 feet long! Few symptoms however Occasionally proglottids in the stool Sometimes vague abdominal pain and nausea |
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Intestinal Distress Accompanied by Migratory Symptoms
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Larvae penetrate intestinal wall, enter the lymphatic and circulatory systems, move into the heart, arrive at the capillaries of the lungs
Then larvae migrate up the respiratory tract to the glottis Worms are swallowed and returned to the small intestine, reach adulthood, and reproduce Inflammatory reactions along migratory routes inside the human Can result in eosinophilia and pneumonia |
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Ascaris lumbricoides
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Cycle A
Larvae and adult stages in humans Releases eggs in feces which are then spread to other humans Ingested eggs hatch in intestine, migrate up, are swallowed, and return to intestine Can also invade biliary channels of the liver and gallbladder, and sometime emerge from the nose and mouth Severe inflammatory reactions mark the migratory route |
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Strongyloides stercoralis
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Threadworm
Can complete its life cycle either inside or outside the human body Cycle B Larvae penetrate the skin Worm enters the circulation, carried to the respiratory tract and swallowed, enters the small intestine to complete development Eggs are laid in the gut, eggs hatch into larvae in the colon Itchy skin rash at infection site |
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Defenses of the Genitourinary Tract
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Flushing action of urine
Desquamation of the epithelial cells Acidity of urine Antibacterial proteins in urine lysozyme lactoferrin Secretory IgA Female-specific Childhood and after menopause: mucus + secretory IgA antibodies During reproductive years: changes in pH |
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Normal Biota of the Urinary Tract
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Outer region of the urethra
streptococci, staphylocci, corynebacteria, lactobacilli Normal Biota of the Male Genital Tract Same as described for urethra Normal Biota of the Female Genital Tract Vagina contains Lactobacillus & Candida albicans at low levels |
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Cystitis
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Infection of the bladder
Pain in the pubic area Frequent urges to urinate even when the bladder is empty Burning pain accompanying urination Cloudy urine Orange tinge to the urine Fever and nausea Back pain indicates kidneys may also be involved Causative agents 95% are normal biota in GI tract E. coli is most common Staphylococcus saprophyticus, Proteus mirabilis |
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Pathogenesis & Virulence Factors of e. coli in cystitis
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E. coli use specific adhesins on long fimbrae to attach to epithelial lining of urinary tract
Induces an inflammatory response since area normally sterile May result in scarring |
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Transmission & Prevention of cystitis
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Transmitted from organ to organ, not person to person
GI tract to urinary tract especially women because of short urethra & nearness to anus Vaccine in development based on adhesin Antibiotics Prevention: “front-to-back” cranberry juice to prevent epithelial attachment? |
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Vaginitis and Vaginosis
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Inflammation of the vagina
Vaginal itching to some degree Burning and sometimes a discharge occurs Symptoms depend on the etiologic agent Candida albicans Gardnerella vaginalis |
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Candida albicans
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Normal biota living in low numbers
Opportunistic infection disruptions in normal biota tight pants antibiotics Fungus grows in thick, curd-like colonies on vaginal wall Colony debris leads to white vaginal discharge Treated with fungicide |
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Gardnerella vaginalis
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Infection called vaginosis rather than vaginitis
NO vaginal inflammation Results of shift from “good” bacteria (lactobacilli) to “bad” bacteria Itching & vaginal discharge with a very fishy odor metabolic byproducts of anaerobic metabolism Can result in infertility, ectopic pregnancies Antibiotics |
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Discharge Diseases
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Increase in fluid discharge in male and female reproductive tracts
Includes HIV, gonorrhea, and Chlamydia infection |
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Gonorrhea
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Neisseria gonorrhoeae - also known as the gonococcus
Gram-negative bacteria |
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Symptoms in the Female of gonorrhea
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Both urinary and genital tracts are infected
Bloody vaginal discharge Painful urination if urethra is affected Major complications occur when the infection ascends from the vagina and cervix to higher reproductive structures Salpingitis (fallopian tubes |
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Symptoms in the male of gonorrhea
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Urethritis
painful urination and a yellowish discharge Can occasionally spread from the urethra to the prostate gland and epididymis Scar tissue in the spermatic ducts during healing can render a man infertile (rare) |
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Pathogenesis & Virulence Factors gonorrhea
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Specific chemicals on fimbriae tips used to anchor to mucosal epithelial cells
Invades the cell & multiplies on basement membrane Phase variation Fimbrae rapidly change antigens, making immunity difficult IgA protease ` |
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what causes blindness in newborns
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gonorrhea
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Transmission & Prevention of gonorrhea
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Most infectious when transmitted to mucous membrane
does not survive longer than 1-2 hrs on fomites Spreads through sexual contact One of most common STD worldwide 10-50% have no symptomsspread unknowingly (Huge increase after 1960’s pill introduction) No vaccine Antibiotics |
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Chlamydia
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Most common reportable infectious disease in the U.S.
Majority of cases are asymptomatic Symptoms in males Inflammation of the urethra Symptoms mimicking gonorrhea Symptoms in females Cervicitis Discharge Salpingitis |
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Pathogenesis & Virulence Factors of chlamydia
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Intracellular pathogen – evades immune system
Cell wall prevents fusion of lysosome with vacuole in phagocyte Inflammation leads to scarring -> infertility |
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Transmission & Prevention of chlamydia
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Reservoir is human body
Transmitted through sexual contact and mother/baby Annual screening, since no symptoms (during PAP smear) No vaccine Antibiotic treatment |
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Genital Ulcer Diseases
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Three common infectious conditions resulting in lesions on a person’s genitals
Having one of these diseases increases the chances of HIV infection Syphilis, chancroid, and genital herpes |
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Syphilis
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Three distinct clinical stages: primary, secondary, and tertiary
Caused by Treponema pallidum thin, coiled spirochete |
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Primary Syphilis
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Appearance of a hard chancre at the site of entry of the pathogen (after an incubation period of 9 days to 3 months)
Chancre filled with spirochetes Chancre heals spontaneously in 3 to 6 weeks spirochete has moved into the circulation |
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Secondary Syphilis
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3 weeks to 6 months after the chancre heals
Many systems have been invaded Fever, headache, sore throat, followed by a red or brown rash Lesions contain viable spirochetes and disappear spontaneously in a few weeks Major complications occur in bones, hair follicles, joints, liver, eyes, and brain |
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Latency and Tertiary Syphilis
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Highly varied latent period, can last for 20 years or longer
Tertiary syphilis is rare because of the use of antibiotics Major complications occur by this stage Cardiovascular syphilis- weakens the arteries in the aortic wall Gummas develop in tissues such as the liver, skin, bone, and cartilage |
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Congenital Syphilis
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From a pregnant woman’s circulation into the placenta and fetal tissues
Inhibits fetal growth Disrupts critical periods of development |
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Transmission & Prevention of syphilis
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Reservoir is human body
Extremely sensitive – survives only a few minutes to hours in body secretions, 36 h in blood 12-30% risk of transmission per sexual encounter Antibiotics 1918, O’Leary & malaria cure |
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Chancroid
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Caused by Haemophilus ducreyi
No systemwide effects Infection usually begins as a soft papule at the point of contact Develops into a soft chancre (painful in men, but may be unnoticed in women) Spread through direct sexual contact Antibiotics |
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Genital Herpes
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Caused by herpes simplex viruses (HSVs)
Multiple presentations No symptoms, or Single or multiple vesicles on the genitalia, perineum, thigh, and buttocks Lesions from initial infection can be accompanied by malaise, anorexia, fever, and swelling and tenderness Occasionally meningitis or encephalitis can develop After recovery from initial infection, may have recurrent episodes of lesions; generally less severe |
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Herpes of the newborn
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In the neonate and fetus, HSV infections can be fatal
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Herpes Simplex Virus I & II
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Enveloped DNA viruses with icosahedral capsids & glycoprotein spikes
HSV I causes oral herpes (cold sores) HSV II causes genital herpes |
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Pathogenesis & Virulence Factors of herpes
|
Latency
Reactivation caused by stress, sunlight, injury, etc. New lesions form |
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Transmission & Prevention of herpes
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Occurs globally in all seasons & all age groups
Direct exposure to viral secretions Gential herpes can be transmitted even without lesions 20% of Americans have genital herpes (reported) Treatment to reduce viral shedding & lesion occurance (Acyclovir) |
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Wart Diseases
|
Molluscum Contagiosum (ch 18)
Human papillomavirus (HPV) |
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Human papillomavirus (HPV
|
Causative agent is DNA virus, 90 types
Genital warts Silent or cellular changes in the cervix cervical cancers Contain oncogenes that result in uncontrolled growth of cervical cells Direct contact, auto-innoculation Incurable PAP smear Vaccine developed at U of L |
