Microbiology

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stephie6390
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48780
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Microbiology
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2010-11-11 18:15:28
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3rd exam diseases by organ system
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overview,skin,nervous,cardiac/lymph
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  1. presence of microorganism
    infection
  2. can be from microorganism
    disease
  3. microorganism cause of disease
    pathogen
  4. capacity of microorganism
    pathogenicity
  5. mechanism of pathogen
    pathogenesis
  6. measure of pathogen
    virulence
  7. toxin capsule receptors pili flagella
    virulence factors
  8. mouth eye nose genitals wounds
    how pathogens enter host
  9. specific to host cells part of how pathogen cause disease
    adhere to host cell
  10. inter-cellular spaces
    bodily fluids
    intracellular
    ways for pathogen to cause disease
    invade or colonize
  11. cells die induce host immune response
    ways for pathogen to cause disease
    inflict damage
  12. maintain a ______________ in nature
    reservoir
  13. no apparent symptoms carrier
    in-apparent sub-clinical
  14. can transmit disease to others
    dormant latent
  15. zoonosis, inadvertent
    accidental
  16. caused by normal flora or transient bacteria
    host immune system is compromised
    opportunistic
  17. obvious infection or disease
    primary
  18. infection subsequent to primary infection
    secondary
  19. two or more microbes infecting the same tissue
    mixes
  20. rapid onset brief duration
    acute
  21. last for long duration
    chronic
  22. affecting many organ systems
    generalized
  23. pus forming
    pyogenic
  24. microbes ascend in a duct or tube against the flow of secretions
    retrograde
  25. occur suddenly and intensely
    fulminant
  26. fingers
    body fluids
    fomites
    food
    flies
    feces
    six ways to spread pathogens
  27. hygiene
    *personal hygiene
    *water treatment
    *sewage
    *antimicrobial
    Vaccination
    *live-dead-toxoid-recombinant
    prevention of disease
  28. antibiotics antivirals
    supportive
    *treat symptoms
    treatment
  29. *symptoms
    blisters
    itchy
    virus becomes latent in spinal ganglia
    Reyes syndrome in children
    chicken poxs
  30. varicella zoster virus
    herpes virus family
    chicken pox
  31. respiratory
    skin to skin contact
    chicken pox
  32. cell mediated immunity (t cells)
    host defense chicken pox
  33. clinical presentation
    chicken pox diagnosis
  34. avoid exposure to virus
    vaccination
    chicken pox prevention and treatment
  35. zoster
    reactivation of latent virus
    virus travels down nerves and produces blisters
    appear in band
    can be life threatening in immunocompromised
    shingles
  36. *symptoms
    – Raised overlapping rash over the entire body
    – Pustules arise deep in the skin
    – Pustules form a crust and scab over
    – Scabs fall off
    smallpox
  37. Variola major
    • Severe form• Very high fever
    • 30% fatality rate– Blindness–
    Variola minor
    • Less rash
    • Lower fever
    • 1% fatality rate
    smallpox
  38. Transmission
    – Direct contact (inhalation
    – Bodily fluids
    – Fomites
    smallpox
  39. Host Defense:
    – Interferon
    – Humoral and cellular immunity
    smallpox
  40. Diagnosis:
    – Clinical presentation
    – Isolation of virus
    smallpox
  41. Prevention & Treatment
    – Vaccine (Jenner)
    smallpox
  42. Current interest:
    – Last US case 1949, Last case in the world, Somalia 1977
    – Cultures at CDC and Russia– Fear of bio-terrorism
    smallpox
  43. • Symptoms
    – Fever, cough, runny nose
    – Koplik spots
    – Rash begins on face and spreads through out the body
    – Complications:
    • Brain damage from encephalitis
    • Could have secondary bacterial infection
    – Death from bacterial pneumonia
    measles
  44. Cause
    – virus
    – Enveloped, RNA virus
    – Only human host
    measles
  45. Transmission
    – Inhalation
    – Highly contagious
    measles
  46. Host Defense
    – Cell mediated immunity
    measles
  47. Diagnosis
    – Presence of giant cells (formed by virus fusing together human cells and RBC)
    – Koplik spots
    measles
  48. Prevention & Treatment
    – Live attenuated vaccine
    measles
  49. German measles/ three day measles
    rubella
  50. Symptoms
    – Rash
    - Fever
    – Enlarged lymph nodes
    - stiff joints
    rubella
  51. Cause– Rubella virus
    rubella
  52. Transmission
    – Respiratory droplet
    – Virus multiplies in respiratory tract and spread throughout the body
    – Mother to fetus: teratogen
    rubella
  53. Host Defense
    – Life long immunity
    – Cellular and humoral
    rubella
  54. Diagnosis
    – Symptoms
    – Serology
    rubella
  55. Prevention & Treatment
    – Live attenuated virus vaccine
    – Antiserum for pregnant women exposed to virus
    rubella
  56. HSV-1
    Herpes Simplex Virus
  57. Symptoms
    – Cold sores/ fever blister
    – Sub-clinical
    hsv
  58. Transmission
    – Oral
    – Respiratory
    – Contact
    hsv
  59. Latency
    – Latent in trigeminal nerve ganglion
    hsv
  60. Occurrence
    – 90% of people infected
    hsv
  61. Treatment
    – None
    hsv
  62. Impetigo:• Superficial, skin wound• Oozes a clear fluid• Forms a crust• Most common in children• Glomerulonephritis
    Streptococcus pyogenes
  63. Erysipelas:• Infection of the dermis• Spreads rapidly through lymph• Enter blood stream, could be fatal
    Streptococcus pyogene
  64. Streptococcal gangrene• Deep tissue infection• Intense inflammation destroys blood vessels & tissue• Bacteria enter blood, could be fatal
    Streptococcus pyogenes
  65. Transmission– Contact with wound secretions
    Streptococcus pyogenes
  66. Host Defense– Antibodies to surface proteins & toxins
    Streptococcus pyogenes
  67. Diagnosis– Isolation of bacteria
    Streptococcus pyogenes
  68. Prevention & Treatment– Antibiotics
    Streptococcus pyogenes
  69. Impetigo• Superficial skin layers
    Staphylococcus aureus
  70. Folliculitis & Cellulitis• Pus filled lesions within hair follicles• Diffuse skin infection
    Staphylococcus aureus
  71. Scalded skin syndrome• Exfoliating toxin• Skin peels off
    Staphylococcus aureus
  72. Transmission– Contact with wound or fomites
    Staphylococcus aureus
  73. Host Defense– Antibodies
    Staphylococcus aureus
  74. Diagnosis– Isolate bacteria from the wound
    Staphylococcus aureus
  75. Prevention & Treatment– Clean all wounds– Good hygiene– Antibiotics
    Staphylococcus aureus
  76. Causative agent Strains of Staphylococcus aureus
    toxic shock syndrome
  77. Symptoms– High fever with chills– Nausea Vomiting– Diarrhea Headache– Red rash followed by peeling of the skin(especially palms & soles of feet)– Confusion Seizures– Hypotension– Organ failure (kidneys and liver)
    Toxic Shock Syndrome
  78. Risk factors– Barrier contraceptives– Tampons– Surgery– Open wounds– S. aureus infection
    Toxic Shock Syndrome
  79. • Toxin– Toxic shock syndrome toxin (TSST
    )– Toxic shock-like syndrome toxin by Streptococcus spp.
    Toxic Shock Syndrome
  80. Treatment– Antibiotics– Supportive– Eliminate predisposing factors
    Toxic Shock Syndrome
  81. Symptoms– Infects deep wounds– Produces alpha-toxin and gas– Skin turns black, renal failure & death
    Clostridium perfringens
  82. Cause– Clostridium perfringens– Gram positive anaerobic rod– Grows in soil
    Clostridium perfringens
  83. Transmission– Contamination of wounds with soil
    Clostridium perfringens
  84. Host Defense:– Antibodies
    Diagnosis:– Gas under the skin– Isolation of bacteria
    Clostridium perfringens
  85. Prevention & Treatment– Antibiotics– Antitoxin– Hyperbaric chamber– Remove dead tissue (amputation
    Clostridium perfringens
  86. Mostly in men, rarely women
    • Symptoms– Infection of the skin– Skin is locally red, may oozefluid– Tinea pedis, capitis, cruris,unguinum, corporis
    ringworm
  87. Cause– Trichophyton– Microsporum– Epidermophyton
    Ringworm
  88. Transmission– Soil
    Clothes
    Fomites
    ringworm
  89. *Host Defense– Cell mediated immunity– Local inflammation
    • Diagnosis– Symptoms
    • Prevention & Treatment– Topical antifungals: miconazole– Oral: griseofulvin
    ringworm
  90. • Symptoms
    – Thrush: white plaques on mucous membranes
    – Diaper rash: red raised rash
    – Vaginitis: Women susceptible following antibiotics,contraceptives, hormonal changes
    – Systemic: immunocompromised, fatal
    candidiasis
  91. Cause
    –Candida albicans
    – Opportunistic pathogen
    candidiasis
  92. • Prevention & Treatment
    – Antifungals: miconazole or nystatin
    – Keep skin dry
    candidiasis
  93. • Symptoms
    – Mite lives in the epidermis
    – Severe itch
    • Cause
    – Sarcoptes scabiei
    -mite
    scabies
  94. • Transmission
    – Close contact
    – Fomites
    – Found worldwide, epidemicsevery 15 years and last 15 years
    scabies
  95. *Host Defense:– none
    • Diagnosis– Identifying mites and eggs undermicroscope
    • Prevention & Treatment– Medication kills mites– Itching stops only after the infectedskin layer is shed
    scabies
  96. Allows very few compounds to pass throughinto the brain
    blood brain barrier
  97. cerebrospinal fluid
    fluid contained within spinal column
  98. Organisms (Bacterial meningitis)
    – Neisseria meningitidis• meningococcal
    – Haemophilus influenzae
    – Streptococcus pneumoniae• pneumococcal
    – E. coli (oppirtunistic)
    meningitis
  99. spinal tap
    diagnosis of meningitis
  100. Pathogenesis
    – inflammation of the meninges membrane
    • brain and spinal cord
    – sudden fever, severe headache, neck rigidity
    meningitis
  101. Occurs mostly in children (6 months to 4years)
    • Gram-negative aerobic bacteria,• normal throat microbiota
    • Capsule antigen type b
    • Prevented by Hib vaccine
    Haemophilus influenzae Meningitis
  102. • N. meningitidis
    • Gram-negative aerobic cocci, capsule
    • 10% of people are healthynasopharyngeal carriers
    • Begins as throat infection, rash• Serotype B is most common in the UnitedStates
    • Vaccination recommended for collegestudents.
    Neisseria Meningitis,Meningococcal Meningitis
  103. • Gram-positive diplococci
    • 70% of people are healthynasopharyngeal carriers• Most common in children (1 month to 4years)
    • Mortality: 30% in children, 80% in elderly
    • Prevented by vaccination
    Streptococcus pneumoniae Meningitis,Pneumococcal Meningitis
  104. – viral origin
    – Most common type of meningitis
    – No treatment
    Aseptic meningitis
  105. – Cryptococcus neoformans
    – occurs with underlying condition (surgery,immunocompromised
    Cryptococcal meningitis (fungal)
  106. *Treatment
    – Antibiotics for bacterial infections
    • Prevention
    – Vaccine against meningococcal meningitis, Hib
    meningitis
  107. • Organism– Clostridium tetani– Spore former– Anaerobic growth• deep wounds• decaying tissue
    tetnaus
  108. • Pathogenesis– tetanospasmin• neurotoxin• ink dot enough for 30 deaths– contraction of muscles• spastic paralysis• lockjaw• respiratory distress
    tetnaus
  109. • Treatment– before clinical symptoms• antitoxin• blocks toxin– after clinical symptoms• no treatment
    • Prevention:– vaccine every 5-10 years– toxoid• develop antibodies against toxin, not organism
    tetanus
  110. • Organism– Clostridium botulinum• spores• growth inhibited by low pH
    • Pathogenesis– blocks release of acetylcholine– interferes with nerve impulse– Flaccid paralysis– paralysis of respiratory muscles– mortality 35%
    botulism
  111. • Different types of toxin– produced by different strains of C. botulinum
    – Type A
    • most potent
    • west of Mississippi River
    botulism
  112. • Age associated
    – infant botulism
    • differences in normal biota
    – adult botulism
    • food poisoning
    • heat-labile toxin
    botulism
  113. Symptoms
    – Skin rash Chronic infection
    – Peripheral nerve damage
    – Loss of sensation
    leprosy
  114. • Indeterminate: skin lesions, early stage• Tuberculoid– Cell mediated response– Infection is contained– Positive skin test– Loss of sensation in discrete spots
    • Lepromatous– Poor immune response– Skin damage– Negative skin test (no T-cell response)– Loss of fingers, toes, nose
    leprosy
  115. • Cause– Mycobacterium leprae– Hansen’s disease (Gerhard Hansen)– Bacteria grow slowly– Grows in peripheral nerves and skin cells
    • Transmission– Direct contact– Nasal secretions
    leprosy
  116. • Host Defense– Effective cell mediated response– Antibodies are present but not protective
    • Diagnosis– Positive skin test– Bacteria in nasal secretions
    • Prevention & Treatment– Multidrug therapy– Killed M. leprae vaccine
    leprosy
  117. • Cause– virus
    – Bullet-shaped
    • Epidemiology– reservoir: all mammals– humans: end of infectious cycle
    rabies
  118. • Symptoms– Flu-like initially– Excitation phase:
    • Neurological symptoms, loss of muscle control, speechimpaired, hydrophobia– Paralytic phase• muscles weaken, loss of consciousness and death
    rabies
  119. • Prevention– reduce exposure of virus in animals• wild mammals--uncontrollable reservoir• bats--dormant for long periods• domestic—vaccine
    rabies
  120. • Diagnosis– Clinical symptoms– Identifying virus in nerve tissue– brain tissue (negri body)• Treatment– Vaccine– Immune globulin immediately following infection
    rabies
  121. • Cause– virus– Picornavirus
    polio
  122. • Pathogenesis– alimentary phase--primarymultiplication– lymphatic phase--tonsils,lymph nodes– viremic phase--spread inblood– neurological phase--CNS,extraneural tissue
    • requires persistent viremia
    • low levels of antibodiesprevent spread
    • >l% of infections lead to severe paralytic infection
    poliomyelitis
  123. • Prevention &treatment– two vaccines• oral (OPV)--attenuated--Sabin
    • injected (IPV)--inactivated—Salk
    – WHO eradicationeffort
    polio
  124. • Encephalitis– Inflammation of the brain
    • Symptoms– Fever - headache - stiff neck– Confusion - paralysis - convulsions– Sleepiness - Coma
    Arbovirus Encephalitis
  125. • Eastern Equine Encephalitis (EEE)– severe
    • Western Equine Encephalitis (WEE)
    • California Encephalitis (CE)
    • St. Louis Encephalitis (SLE)
    • Japanese B encephalitis– endemic areas of Asia
    • • Arthropod borne viruses
    • arbovirus encephalitis
  126. • Diagnosis– Based on symptoms & case history– Easier during epidemics
    • Transmission– Mosquitoes (Culex, Aedes)– Birds are the carriers– Small mammals, birds and horses are reservoirs
    arbovirus encephalitis
  127. • Treatment & Prevention– Supportive care– Japanese encephalitis has a vaccine– Control mosquito population
    arbovirus encephalitis
  128. • Diseases– Bovine spongiform encephalitis– Sheep scrapie– Creutzfeldt-Jakob disease– Kuru
    • Cause– Prions– Aberrant proteins
    Spongiform encephalitis
  129. Transmission– Consumption of infected animal products– Transfusion of infected blood
    spongiform encephalitis
  130. • Prevention– Screen blood– Screen animal products
    • Treatment– None– Chronic, fatal
    prion diseases
  131. bacteria in blood
    bateremia
  132. bacteria persist in blood and is fatal
    septicemia
  133. • Dr. Carlos Juan Finlay & Dr. Walter Reed
    • Disease– Mosquito bite introduces virus into host– Virus travels to lymph node and blood– Multiplies in the liver– Fever, headache, weakness– Severe fever, chills, headache, jaundice, uncontrolledbleeding– 15 - >50% mortality in severe cases
    yellow fever
  134. • Cause– Yellow fever virus– Small RNA virus
    • Transmission– Mosquito, Aedes aegypti– Non-human primates-mosquitoes-humans
    • Host Defense– Immune after infection
    yellow fever
  135. • Diagnosis– Symptoms
    • Prevention & Treatment– Restrict mosquito population– Treat standing water– Live attenuated vaccine for people in regions with disease andtravelers (strain 17D)
    yellow fever
  136. • Disease– Ebola hemorrhagic fever– Extensive bleeding– Destruction of internal organs– >90% fatality rate (25-90%)
    ebola
  137. • Symptoms– Fever, headache, joint & muscleache, sore throat, weakness– Diarrhea, vomiting, stomachpain– Rash, red eyes, internal & external bleeding– Death in those who do notdevelop an immune response
    ebola
  138. • Cause– Ebola virus– Enveloped RNA virus
    ebola
  139. • Transmission– Maintained in animals– Index case: contact with infectedanimal– Person to person: Direct contact withinfected blood or bodily fluids– Fomites
    ebola
  140. • Prevention & Treatment– Supportive care– Isolation of patients and properdisposal of infected items to preventspread
    ebola
  141. • Disease– Infectious mononucleosis– Fever, fatigue, sore throat, swollenlymph nodes– Enlarged atypical lymphocytes– Enlarged spleen (could rupture)
    epstein barr virus
  142. • Cause– Epstein Barr Virus (EBV)– Enveloped DNA virus– Latent in B lymphocytes
    EBV
  143. • Transmission– EBV is secreted into the saliva– Saliva containing fomites
    • Diagnosis– Clinical diagnosis– Serological: increased number of lymphocytes/WBC– Presence of enlarged suppressor T cells (which stopproliferation of infected B cells)
    • Prevention & Treatment– Present in >90% of adults– Reactivates periodically and is present in saliva
    EBV
  144. • Lower respiratory tract infection
    • Symptoms– Fever– Muscle aches– Respiratory distress, fluid in airspaces– Death by catastrophic lung failure
    hantavirus
  145. • Cause– virus: Sin nombre– Known to cause kidney disease as well– Known to Native Americans before the 1993 incidence
    • Transmission– Mouse droppings aerosolized
    hantavirus
  146. • Occurrence– In small clusters, rural– Places with known large rodentpopulations– Four corners region
    • Host defense– None
    hantavirus
  147. • Prevention & Treatment– Avoid contact with rodents– Keep areas free of rodents– Treatment is supportive care
    hantavirus
  148. • Disease Symptoms– Fever; Severe muscle and joint pain ‘Breakbone fever’; Rash– Severe form: dengue hemorrhagic fever (DHF)
    • Occurs during subsequent infections
    • Antibodies from a previous infection combine with the virus.
    • Rash on face and extremities from skin hemorrhages
    • Drop in blood pressure, shock, death.
    • >90% in children with multiple infections
    dengue virus
  149. • Causative agent– virus (grows in white blood cells)– RNA virus
    • Transmission– Aedes aegypti– Aedes albopictus
    • Transovarian in the mosquito
    • Person to person via mosquito– No known animal reservoir
    dengue virus
  150. • Occurrence– Endemic in the Caribbean and tropics– United States sees mostly imported cases– Vector is present along the Gulf coast
    • Host defense– Interferon– Antibodies
    dengue fever
  151. • Diagnosis– Serology– Virus isolation and culture– Epidemiology
    • Treatment & Prevention– Mosquito control– Prevent mosquito bites-no vaccine
    dengue fever
  152. – Fleas bite humans and transfer thebacteria– Bacteria enter lymph and concentrate inlymph node– High fever– Swollen lymph node (bubo)– Bacteria grow within phagocytes– Bacteria spread to the blood– Black spots from destroyed blood vessels death
    bubonic plague
  153. – Lungs infected by inhaling bacterial cells– Symptoms within 2 days– >99 mortality within 24 hours
    penumonic plague
  154. • Cause– Yersinia pestis– Gram negative coccobacillus• Transmission– Infected fleas
    • Bacteria clogs the fleas digestive tract, flea regurgitates bacteriainto host during blood meal• Bites more often because it can not feed completely– Carried by many mammals
    plauge
  155. • Diagnosis– Culturing bacteria from bubo or sputum
    • Prevention & Treatment– Antibiotics– Eliminate rodents from homes– Vaccine for scientists
    plague
  156. • Disease– Small sore at site of infection– Swollen lymph node– Bacteria multiply in phagocytes & enter blood– Persistent fever, chills, headache
    • Cause– Francisella tularensis– Gram negative coccobacillus
    tularemia
  157. • Transmission– Carried in small mammals & ticks– Humans infected accidentally through open wounds– Through infected tick bite
    • Diagnosis– Based on patient history
    • Prevention & Treatment– antibiotics
    tularemia
  158. • Disease– Bacteria survive within phagocytes, pass intolymph & blood.– Acute stage: headache, chills, fever, malaise– Undulant fever (rises and falls): spikes everyevening (104°F, 40°C)
    brucellosis
  159. • Cause
    – Brucella abortus & B. canis (mild)
    – B. suis & B. melitensis (severe to fatal)
    – Gram negative coccobacilli
    burcellosis
  160. • Transmission
    – Direct contact with infected animals & secretions
    – Inhalation, broken skin, conjunctiva
    – Infected milk (unpasteurized)/ cheese
    • Diagnosis– Culturing bacteria– Rising antibody titer
    burcellosis
  161. • Prevention & Treatment– Antibiotics– Avoid unpasteurized diary product
    brucellosis
  162. – Bacteria enter through wound– Blister at site of infection, black crater ulcer– Septicemia possible– Treated with antibiotics
    cutaneous anthrax
  163. – Caused by inhaled spores– Respiratory distress– Septicemia and death
    respiratory anthrax
  164. – Caused by eating contaminated meat
    gastrointestinal anthrax
  165. • Cause– Bacillus anthracis– Gram positive, spore forming, rod
    • Host Defense– Antibodies to toxin
    • Diagnosis– PCR using specific primers
    • Prevention & Treatment– Antibiotics immediately following infection(Ciprofloxacin)
    anthrax
  166. *First stage• Red bulls eye rash at site of tick bite– *Second stage• Headache, stiff neck, muscle aches, fatigue
    *Third stage• Bacteria spread to lymph, blood & majororgans• Meningitis or myocardial damage– *Fourth stage• Chronic arthritis• Swelling of joints
    lyme disease
  167. • Cause– Borrelia burgdorferi– Spirochete
    lyme disease
  168. *Transmission– Deer tick Ixodes scapularis, Ixodes damini– Tick must have a blood meal from a large mammal(deer or humans)
    • Diagnosis– Rash, history
    • Prevention & Treatment– Antibiotics– Avoid tick bites
    lyme disease
  169. • Symptoms– Fever– Spotted rash– Abnormal blood clotting, death
    • Cause– Rickettsia rickettsii– Small gram negative rod, obligate intracellularpathogen– Bacteria multiply in the inner lining of bloodvessels causing them to burst and forming thered rash
    rocky moutian spotted fever
  170. • Transmission– Transovarian from tick to tick– Tick to human
    • Diagnosis– Clinical and epidemiological information
    • Prevention & Treatment– Tetracycline & chloramphenicol
    rocky mountian spotted fever
  171. • Disease– Cyclical chills-fever-sweating
    • Cause– Plasmodium vivax, P. falciparum, P. malariae, P. ovale
    • Transmission– Female anopheles mosquito
    malaria
  172. • Diagnosis– Presence of plasmodium in blood smears
    • Prevention & Treatment– Mosquito nets (insecticides)– Control mosquito population
    malaria
  173. • Disease– Infection of blood and lymph– Mosquitoes introduce the worm larvaeinto humans during blood meal– Larvae travel to lymph nodes in groin orextremities– Mature into adults, mate and producemicrofilariae that enter the circulation– Worms block circulation of lymph,lymph accumulates causing elephantiasis
    filariasis
  174. • Cause– Wuchereria bancrofti– Brugia malayi
    filariasis
  175. • Transmission– Mosquitoes: Anopheles, Aedes, Culex
    • Diagnosis– Presence of microfilariae in blood– Symptoms: Elephantiasis
    • Prevention & Treatment– Control mosquito population– Treat with antihelminths before elephantiasis stage
    filaraisis
  176. • Symptoms– Fever, fatigue– Pain in infected organ– Hypersensitivity reaction to masked worms– Blood in urine
    • Cause– Flatworm– Schistosoma mansoni (colon), S. japonicum (small intestine), S.haematobium (bladder)
    schistosomiasis
  177. • Transmission– Contaminated water– Infected snails
    • Diagnosis– Eggs in the stool or urine
    Schistosomiasis
  178. • Disease– Often asymptomatic– Fever, muscle ache, headache and swollen lymphnodes– Congenitally infected children: impaired vision, mentalretardation– Immunocompromised: encephalitis
    toxoplasmosis
  179. • Cause– Toxoplasma gondii– Protozoan– Cats are carriers and definitive hosts
    • Transmission– Contact with cat feces– Eating undercooked meat containing cysts
    toxoplasmosis
  180. • Host defense– Cell mediated immune response– Protects from reinfection
    • Diagnosis– Serology– Examination of tissue
    • Treatment and prevention– Cooking meat– Management of cats– Antimicrobials for acute cases
    toxoplasmosis
  181. • Disease & symptoms– Parasite replicates in red blood cells– Prolonged Fever, chills, night sweats– Often mistaken for malaria– Serious/ fatal in immunocompromised– Hemolytic anemia
    babesiosis
  182. • Cause– Babesia microti– Protozoan– Known in animals before it was recognized inhumans
    babesiosis
  183. • Transmission– Rodents are wild reservoir– Ixodes spp– Northeast and Midwest US have high incidence
    • Diagnosis– Known in animals for a long time– Blood smear to look for B. microti in RBCs
    babesiosis
  184. • Treatment and prevention– Combination antimicrobials– Supportive care (blood transfusion, fevercontrol)– Tick and rodent control– Check for ticks– Screen blood supply
    babesiosis

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