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characteristics of clostridium tetani
motile, gram + rod
where is clostridium tetani found
soil, dust, GI tract
fatality of clostridium tetani
18%, but 0% if vaccines are current
how does clostridium tetani infect
spore enters skin though membranes or puncture wound and germinates producing tetanus toxin.
what does tetanus toxin do
blocks the release of inhibitory neurotransmitter which results in muscle contraction with no relaxation
signs/symptoms of clostridium tetani
incubates few days-1 weeks
- tightening of neck and jaw
- perspiration, drooling, grouchiness, back spasm, irregular heartbeat
- patients dies because they cant exhale
treatment for clostridium tetani
penicillin/metronidazole
characteristics of clostridium botulinum
gram +, anaerobic bacteria
serotypes of clostridium botulinum
seven types affect different species
how infectious is clostridium botulinum and how does it work
only a few nanograms cause illness, it binds neuromuscular junctions and blocks the release of acetylcholine so there is no muscle contraction
what are the three forms of clostridium botulinum
food-borne, infant, wound
describe foodborne botulism and symptoms
-pre-formed toxins are ingested from contaminated food
- common from home canned food
- nausea, vomiting, diarrhea, double vision, difficulty speaking, descending weakness
describe infant botulism
spore ingestion, germination, toxin production
- insufficient competition from normal flora
- from honey, dust, corn syrup
- constipation, lack of expression, weak suckling, drooling, floppiness, poor head control, non-reactive pupils
describe wound botulism
- gets into would and develops anaerobically
- from ground in dirt or travel
- will not penetrate intact skin
- recently associated with black-tar heroin users
treatment of clostridium botulinum
repeated washing of GI tract, antibodies against toxin, NO antibiotics
what special thing is clostridium botulinum used for?
botox, keeps muscles from contraction
characteristics of clostridium difficile
gram + rod, motile via flagella
toxins of clostridium difficile
A & B toxins - cause water secretions and damage to mucosa, explosive diarrhea (self-limiting), life threatening pseudomembranous colitis
epidemiology of clostridium difficile
- leading cause of hospital acquired diarrhea
- opportunistic pathogen - antibiotic treatment suppresses normal flora
- number of cases increasing
- affects many elderly
- resistant to many antibiotics
pseudomembraneous colitis
life threatening, sections of colon wall become removed, perforation of colon, infection with fecal bateria
diagnosis of clostridium difficile
- patients undergoing antibiotic treatment
- culture - isolation from feces
- immunological detection of toxins
- just recovering organism from feces does not mean it caused it
treatment of clostridium difficile
stop antibiotics
- fecal transplant
- vancomycin/metronidazole/fidaxomicin(dificid)
characteristics of clostridia perfingens
gram + rod, anaerobic, non-motile
where is clostridia perfingens found
soil, water, sewage, GI tract of humans and animals
describe infection of clostridia perfingens
- 8-22 hrs after consumption, intense abdominal cramps and diarrhea
- usually over in 24 hrs
- disease from ingesting organism followed by growth and toxin release
toxins of clostridia perfingens
-alpha toxin= degrades cell membrane and kills WBCs
- perfringolysin O (PLO) - pore forming toxin
- enterotoxin - affects epithelial cells in GI tract
what does clostridia perfingens (food) result from
temperature abuse of food, spores survive cooking and food is improperly stored, meats, gravy
what are the diseases associated with clostridia perfingens
food poisoning and gas gangrene
describe food poisoning with clostridia perfingens
- intense abdominal cramps 8-22 hrs after consumption
- over within 24 hrs
- bacteria produce enterotoxins
complication of food poisoning with clostridia perfingens
very few deaths reported from dehydration or other complications
describe gas gangrene from clostridia perfingens
- non-invasive, but spores gain entry through wound and grow anaerobically
- alpha toxin and PLO induce swelling and tissue death
- foul smelling gaseous metabolic products
- shock, kidney failure, and death within 1 week
diagnosis for gas gangrene
lesions, presence of large gram + bacilli, naglar test
treatment of gas gangrene
remove dead tissues, large doses of anti-toxin, penicillin, apply oxygen
what is the mortality rate of gas gangrene
40%
what disease does treponema palindum cause
syphilis
epidemiology of treponema palindum (syphilis)
3rd most common bacterial STD in USA
- humans are only reservoirs
- 30% transmission rate from single sexual contact
- labile organism
describe the primary stage of syphilis
- lesion occurs 2-10 days post infection
- small-hard-painless chancre, ulcerated papule, very infectious
- regional swollen lymph node
- 3-8 wks chancre erodes and no further symptoms for 2-10 wks
describe the secondary stage of syphilis
- 2-12 wks after infection
- skin rash in90% of pts (macular, papular, pustular)
- mucus patches in patients mouth/throat
- fever, malaise, joint pain, hair loss, weight gain
-CNS involvement - headache, ocular disease
- lasts several weeks and subsides
- wart like lesions in moist sites
describe tertiary syphilis
- occurs in less than 1/2 untreated pts
- may begin 10-30 yrs after latent period
- inflammation due to pathogen components
- gummas (rubbery) of bones, organs, skin
- necrotic/perforated palate
- few lesions, not highly contagious
- CNS - dementia, ataxia, sensory defects
describe congenital syphilis
- mother to fetus transmission though placenta or birth canal
- pregnancies during primary and secondary stages result in still birth
- most common when pregnancies are in latent phase
- child has no symptoms at birth
- rash develops, multi-organ malformations, cardio problems
- bone destruction and mental problems
epidemiology of congenital syphilis
350-1000 cases per year
diagnosis of syphillis
- culture is not possible
- dark field microscopy of fresh skin lesion
treatment of syphillis
penicillins
tetracyclines if allergic
facts to know about leptospira
- acquired from rodent/animal urine contaminated water
- rowers and tri-athletes at risk
- flu like symptoms and failure of liver
what disease does borrelia burgodorferi cause
lyme disease
describe stage 1 of lyme disease
3-14 days after tick bite, bulls eye rash forms, fever, muscle pain, joint pain
- resolves in weeks
describe stage 2 of lyme disease
- weeks to months after infection
- disseminated infection - joint and muscle pain, multiple tissues and organs affected
- irregular heartbeat, facial paralysis, neurological conditions, conjuctivitis
describe stage 3 of lyme disease
may develop months or years after infection
- arthritis, immune disorders, high antibodies to borrelia
- disabling fatigue, memory loss, dementia, paralysis
what are the 3 spirochetes
leptospira
borrelia burgodorferi
treponema pallidum
diagnosis of borrelia burgodorferi
clinical signs - bull's eye rash
prevalence of ticks
culture from skin lesions
serological tests or PCR
treatment of borrelia burgodorferi - lyme disease
tetracycline, erythromycin = 10-3- days
- pts with arthritis = >1 month
epidemiology of borrelia burgodorferi
tick borne disease
- tick eggs not infected
- reservoir = deer and rodents
- takes ~6 hrs for bacteria to adapt to humans
- no human to human spread
- most common vector born disease in US
what disease is caused by bartonella henselae
cat scratch disease
characteristics of bartonella henselae
gram - bacilli
fastidious growth - needs enriched BAP, CO2, and time
facultative intracellular bacterium
transmission and epidemiology of bartonella henselae
cats and cat fleas
- 22,000 cases per year
-80-90% pts are
symptoms of bartonella henselae
papule/pustule
- regional adenopathy
- bacillary angiomatosis
- lesions in liver
- endocarditis
diagnosis of bartonella henselae
history of cat contact, positive skin test response, no evidence of other infection, histopathology of nodes
treatment of bartonella henselae
90% infection resolve on own
azithromycin
what disease does ehrlichia chaffeensis cause
ehrlichiosis - monocytic disease
characteristics of ehrlichia chaffeensis
obligate intracellular
gram - cocci
- grows in vacuole and replicated in phagosome in leukocyes
- cytoplasmic morulae
epidemiology of ehrlichia chaffeensis
-tick borne disease
- humans are dead end/accidental host
- reservoir= deer and ticks
- eggs are uninfected
- cases increasing
symptoms of ehrlichiosis
- may be asymptomatic
- clinical signs resemble RMSF = fever, headache, malaise, muscle ache
- rash develops in
diagnosis of ehrlichiosis
very difficult
- low WBC count
- immunoflurescence assay
- PCR
-isolation, which is difficult and time consuming
characteristics of rickettsia richettsiae
rod-shaped coccobacillus
gram -
obligate intracellular pathogen
no flagella based motility
free in cytosol
like endothelial cells and trick them into taking them up
what disease does rickettsia richettsiae cause
rocky mountain spotted tick fever
symptoms of rocky mountain spotted fever
5-10 days after bite = fever, chills, muscle pain, headache, nausea/vomiting, lack of appetite
2-5 days after fever = rash on extremities that spreads to trunk (35-60% pts)
pathenogenesis of rickettsia richettsiae
replication in endothelial cells
leakage of blood vessels
complications = GI tract probs, respiratory failure, hear probs
- 20% fatality if untreated
diagnosis of rickettsia richettsiae
culture is useless
look for antibodies via immunofluorescence
treatment of rocky mountain fever
tetracyclines (doxycycline)
chloramphenicol
epidemiology of rocky mountain spotted fever
vector= tick
reservoir - ticks, rodents, humans
no human to human
eggs of ticks are infected
what does chlamydophila psittaci cause
atypical pneumonia
characteristics of chlamydophila psittaci
zoonosis
gram - coccobacillus
epidemiology of chlamydophila psittaci
-seldom transmitted from human to human
-transmitted by contact/inhalation of infected bird droppings
-can be fatal in elderly if untreated
symptoms of chlamydophila psittaci
non-productive cough
10 incubation then sudden onset of headache and fever
what does chlamydophila pneumoniae cause
mild pneumonia
epidemiology of chlamydophila pneumoniae
humans are only known host
human to human transmission
symptoms of chlamydophila pneumoniae
may be asymptomatic or mild cough and malaise
correlation with atherosclerosis
what does mycoplasma pneumoniae cause
primary atypical pneumonia
mild upper respiratory disease 2-3 weeks after
characteristics of mycoplasma pneumoniae
- fried egg look
- extracellular pathogen- targets respiratory epithelial cells
-
symptoms of mycoplasma pneumoniae
non-productive cough
pathogenesis of mycoplasma pneumoniae
- adhere by specialized tip structure
-
diagnosis of mycoplasma pneumoniae
grows on serum containing media (slow)
cold-agglutination test
serological and DNA based tests
treatment of mycoplasma pneumoniae
ribosome inhibitors - tetracycline, erythromycin
penicillins DO not work
what does ureaplasma urealytieum cause
causes STD of human genital tract
- 80% individuals had >3 partnters
-50% non chlamydial, NGU in men and women
symptoms of ureaplasma urealytieum
inflammation of chorion and amnion, post partum fever, PID
characteristics of ureaplasma urealytieum
mycoplasma that produces urease > NH3 causes inflammation
chlamydia trachomatis causes
trachoma, inclusion conjunctivitis, non-gonococcal urethritis, lymphogranuloma venerum
different serotypes of chlamydia trachomatis
cause different disease
epidemiology of trachoma caused by chlamydia trachomatis
-leading cause of preventable blindness in the world
- limited to native americans in the US
transmission of trachoma caused by chlamydia trachomatis
typically eye to hand to eye, contaminated clothing, flies
- children are at greatest risk- largest reservoir
- overcrowding, poor hygiene, lack of water
describe trachoma symptoms
starts w/ tears, ocular discharge, inflammation of conjunctiva, follick formation, vasceularization of cornea, eyelid deformities (inversion)
- blindness results from long term scarring of cornea (10-20yrs)
epidemiology of inclusion conjunctivitis cause by chlamydia trachomatis
very common in infants - birth canal (44%)
- 17% adults get w/ genital tract infection
-50% conjunctivitis pts have genital tract infection
symptoms of inclusion conjunctivitis caused by chlamydia trachomatis
- mucopurulent yellow discharge
- inflammation of conjunctiva and swelling of eyelid
-heals spontaneously- rarely leads to scarring of cornea
epidemiology of non-gonococcal urethritis caused by chlamydia trachomatis
most common bacterial STD in the US
-10% of sexually active 15-35 yr olds infected
-1.6 million cases and increasing
-6x greater risk of cervical cancer
-3x greater risk of infection of HIV pts
symptoms of non-gonococcal urethritis caused by chlamydia trachomatis
-infection may be asymptomatic
- 40% untreated women will develop PID
-20% of those will be infertile
-18% will experience chronic pelvic pain
-9% will have life threatening tubal pregnancies
- manifests as genital discharge
describe lymphogranuloma venerum cause by chlamydia trachomatis
-more virulent & invasive STD
- most common in men
- enters via breaks in skin and primary lesion is ulcer
- 10-30 days= lymph buboes
~30% rupture if untreated, then obstruction
characteristics of candida albicans
dimporphic fungus that resides in GI tracts
- grown at
clinical presentation of candida albicans
mucocutaneous-skin & mucosal surfaces
- oral thrush, esophageal candidiasis, vulvovaginits, diaper rash
what is the treatment for candida albicans
topical antifungals and keeping skin dry
epidemiology of histoplasma capsulatum
arkansas, illinois, kentucky, missouri, ohio, tenessee