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531 Cards in this Set
- Front
- Back
most common cause of ascending UTI
|
E. Coli
|
|
enterobacteria associated w/ urinary stones
|
proteus mirabelis (produces potent urease to produce ammonia and make urine alkaline)
|
|
gram + causes of UTI
|
staph saprophyticus, staph epidermis, and enterococcus
|
|
causes UTI in young sexually active women
|
staph saprophyticus
|
|
causes UTI in hospitalized pts
|
Staph. epidermis and Enterococcus
|
|
viral UTI common?
|
no
|
|
viral UTI causes?
|
human polyomavirus, adenovirus, hantavirus
|
|
How does humanpolyoma infect?
|
enters via respiratory tract and spreads to tubular epithel cells in kidneys and ureters. establishes latency
|
|
35% of healthy individs have infx with ____________ but it remains latent
|
polyomavirus
|
|
fungal causes of UTI
|
candida and histoplasma capsulatum
|
|
parasitic causes of UTI
|
Trichomonas vaginalis, Schistosoma haematobium
|
|
which causes urethitis in males/vaginitis in females
|
T. vaginalis
|
|
which causes allergic response to worm’s egg leading to scarring in area where bladder/ureters meet and ureters get blocked- results in bladder inflammation
|
S. haematobium
|
|
mechanical factors that predispose to UTI
|
1. shorter female urethra
2. sexual intercourse 3. uncircumcised boys |
|
obstructions to complete bladder emptying
|
1.residual urine
2. loss of neurologic control 3. vesicoureteral reflux 4. diabetes mellitus 5. catheterization |
|
causes of loss of neurological control:
|
spina bifida, paraplegia, multiple sclerosis
|
|
who is vesicoureteral reflux common with
|
children w/ anatomic abnormalities of the urinary tract
|
|
diabetes mellitus may lead to...
|
pyelonephritis
|
|
where do most urinary tract pathogens originate
|
fecal flora
|
|
which can colonize/infect the urinary tract
|
aerobic and facultative species such as E. coli
|
|
what structural feature helps E. coli adhere to epithelium
|
fimbriae
|
|
what does E. coli produce that causes kidney damage
|
hemolysin
|
|
is healthy urinary tract resistant to bacterial colonization?
|
yes- eliminates microorganisms rapidly/efficiently
|
|
how
|
via pH, chemical content, and flushing mechanism
|
|
3 clinical features of acute lower UTIs (bladder infxs)
|
dysuria, urgency, frequency
|
|
urine sample shows:
|
cloudiness due to pyuria and bacteriuria, hematuria
|
|
what may result from an ascending infx?
|
acute bacterial prostatis
|
|
sx?
|
fever, low back pain, dysuria, and frequency
|
|
upper UTI spreads to
|
kids
|
|
what is pyelonephritis
|
kidney infx
|
|
sn/sx
|
lower UTI sx of dysuria, urgency, frequency but also FEVER
|
|
common cause of upper UTIs
|
staphylococci
|
|
what can repeated episodes lead to
|
loss of fx of renal tissue, and HTN
|
|
how is infx distinguished
|
quantitative culture methods
|
|
definition of bacteriuria
|
over 10^5 organisms/mL
|
|
T/F usually are several bacterial species
|
F- only one
|
|
do a significant proportion of lower UTI pt's have recurrent infxs?
|
yes- either by same organism or by different one
|
|
does upper or lower cause renal abcesses
|
upper
|
|
methods of urine collection
|
1. sterile container by pt
2. "bag urine" for babies/infants 3. catheter- collected from tube with syringe and needle |
|
Tx of UTI
|
antibiotics- ie augmentin
|
|
prevention of UTI
|
empty bladder often (esp after intercourse), prophylactic anti-biotic use, good catheter care
|
|
host factors that influence risk of acquiring an STD
|
genital lesions or ulcers, uncircumcised men, multiple infx
|
|
What causes syphilis
|
the spirochete Treponema pallidum
|
|
how does it enter body
|
minute abrasions on skin or mucous m'branes
|
|
why does transmission require close contact
|
b/c doesn't survive well out side body, sensitive to drying, heating, disinfectants
|
|
spread?
|
horizontally thru sexual contact or vertically via transplacental infx of fetus
|
|
5 stages of syphilis pathogenesis?
|
1. initial contact 2. primary syphilis 3. secondary 4. latent 5. tertiary
|
|
what occurs w/ initial contact
|
2-10 wks: treponemes multiply at infx site, develop a primary painless chancre
|
|
primary?
|
1-3 months; treponemes proliferate, enlarged inguinal nodes and spontaneous healing
|
|
secondary?
|
2-6 weeks: treponeme multiplication,flu-like illness, headache, fever, mucocutaneous rash and spontaneous healing, lesions in lymph nodes, liver, joints, muscles, skin and mucous m'branes
|
|
latent
|
3-30 years: treponemes are dormant in liver or spleen, no sign of illness
|
|
tertiary
|
re-awakening, multiplication, dissemination, and invasion of trepes; neurosyphilis (general paralysis), and cardiosyphilis (aortic lesions, heart failure; progressive and destructive
|
|
does T. pallidum respond to vigorous immune response
|
no
|
|
how does it evade recognition and elimination by the host
|
maintains a cell surface rich in lipid that is antigenically unreactive
|
|
when is congenital syphilis acquired
|
first 3 mos of pregnancy
|
|
results in:
|
1. serious infx--> intrauterine death
2. congenital abnormalities 3. silent infx (at 2 y.o) |
|
tx
|
penicillin
|
|
prevention
|
early diagnosis (for 2ndary and tert), early screening and penicillin treatment (congenital)
|
|
what causes gonorrhea
|
gram pos diplococcus Neisseria gonorrheae
|
|
resevoir:
|
humans
|
|
transmission:
|
sexual contact or vertically from mother to baby during childbirth (ophthalmia neonatorum)
|
|
does it survive outside the body?
|
no- sensitive to drying
|
|
men or women more?
|
women
|
|
sx?
|
asymptomatic
|
|
4 special mechanisms of N. gonorrhea to allow mucosal attachment:
|
1. fimbriae (attachment and antigenic diversity
2. LPS (endotoxin activity) 3. IgA protease (destroys IgA1) 4. capsule (resists phagocytosis) |
|
how do they infect?
|
invade non-ciliated epithelial cells that internalize the bacteria, allowing them to multiply in intracellular vacuoles protected from phagos and Abs
|
|
how does it damage host
|
by inflammatory response elicited by organism
|
|
sn/sx in males
|
discharge/pain
-complications rare |
|
sn/sx in females
|
discharge- no pain, assymptomatic therefore don't seek treatment
|
|
female complications of gonor:
|
PID, chronic pelvic pain, infertility
|
|
ophthalmia neonatorum:
|
gon in infants, characterized by sticky discharge
|
|
other parts infected by gon:
|
throat, rectum (purulent discharge)
|
|
Tx
|
penicillin, ceftriazone, ciprofloxacin, spectinomycin
|
|
prevention
|
condoms
|
|
Cause of chlamydial infxs:
|
Chlamydia trachomatis serotypes D-K
|
|
2 forms:
|
elementary body (EB):extracellular survival
reticulate body (RB): intracellular multiplication |
|
how does it invade/infect?
|
-enter host thru small mucosal abrasions
-bind specific receptors on host and enter by endocytosis -lysosome fusion is inhibited and EB begins development -after 9-10 hrs become active RBs -new EBs produced |
|
pathogenesis in men:
|
urethritis, epidymitis, proctitis, conjunctivitis
|
|
pathogenesis in women:
|
urethritis, cervicitis, salpingitis, conjunctivitis
|
|
tx
|
doxycycline, tetracycline (beta lactam antibios dont work); tx for babies is erythromycin
|
|
causes of inguinal lymphadenopathy:
|
genital infxs, LGV, chancroid, donovanosis
|
|
cause of LGV:
|
C. trachomatis serotypes L1, L2, and L3
|
|
pathogenesis of LGV:
|
-after 1-4 wks primary lesion develops at site of inoculation
-fever/headache accompany -lesion heals rapidly and draining lymph nodes are infected causing inguinal buboes |
|
complications
|
proctitis, fever, hepatitis, pneumonitis, meningo-encephalitis
|
|
tx:
|
tetracycline/doxycycline
|
|
cause of chancroid (soft chancre):
|
H. ducreyi
|
|
characteristics:
|
painful genital ulcer and local lymphadenitis
|
|
tx:
|
erythromycin, caftraixone, otrimoxazole
|
|
cause of donovanosis:
|
Calymmatobacterium granulomatis
|
|
characteristics:
|
genital nodules that erode to form granulomatous ulcers; bleed readily on contact
|
|
tx:
|
tetracycline
|
|
which is most common form of genital ulcers in africa and asia
|
chancroid
|
|
which is common in caribbean, new guinea, india, and central australia
|
donovanosis
|
|
What causes mycoplasmas and non-gonococcal urethritis?
|
mycoplasma hominis and ureaplasma urealyticum
|
|
where do they colonize?
|
genital tracts of healthy sexually active people
|
|
what are they also associated with
|
PID, postabortal and postpartum fevers
|
|
tx
|
tetracycline
|
|
what are other causes of vaginitis and urethritis
|
candida albicans, trichomonas vaginalis, gardnerella vaginalis
|
|
characteristics of candida
|
-irritant vaginitis
-cheesy discharge -UTI with it maybe |
|
Tx
|
fluconazole or nystatin
|
|
chars of trichomonas infx
|
-protozoan parasite inhabits vagina/urethra
-transmit during sex -women: copious foul-smelling discharge, increased pH with actively motile trophozoites -men: assymptomatic |
|
tx
|
metronidazole
|
|
what causes bacterial vaginosis
|
gardnerella vaginalis plus anaerobic infx of bacteroides that disrupt normal acidity of vagina
|
|
sx in women:
|
-excessive fish-odored discharge
-pH >4.5 -clue cells (vaginal epithelial cells coated w/ bacteria) |
|
tx
|
metronidazole
|
|
cause of genital herpes
|
HSV2
|
|
when is primary lesion seen
|
3-7 days after infx
|
|
sn/sx
|
-vesicles that form shallow ulcers
-local lymph nodes swollen -fever -headache -malaise |
|
pathogenicity:
|
healing up to 2 weeks, but virus travels up sensory nerve and establishes latent infx in dorsal root ganglion neurons where it can reactivate and cause a recurrent lesion
|
|
spread from mom to infant?
|
yes, during delivery and can give rise to disseminated herpes or encephalitis
|
|
tx
|
acyclovir
|
|
cause of genital warts
|
HPV- papillomavirus 6,11,12,16,18,and 31
|
|
where/when do warts appear
|
on penis, vulva, and perianal regions after 1-6 mos incubation
|
|
cervical lesion description:
|
a flat area of dysplasia visible by colposcopy as a white plaque after local application of 5% acetic acid
|
|
which are associated with cervical cancer
|
16 and 18
|
|
tx
|
podophyllin
|
|
HIV infects which cells
|
TH, monocytes and dendritics
|
|
pathogenesis
|
-CH4 mc binds GP120 protein
-virus specific CD8+ Tc cells are formed and reduce viremia -neutralizing antibodies appear -immune system starts suffering and CD4+ T cells decrease -delayed type hypersensitivity is absent, NK cell activity and Tc cell activity is dec'd and polyclonal activation of B cell is reduced |
|
mechanisms of immunosuppression:
|
1. Th cells are directly killed by virus
2. Th cells undergo apoptosis 3. Th cells are attacked by Tc cells 4. T cell replenishment is impaired by thymus/lymph node damage and stem cell infx 5. defects in antigen presentation (infx of dendritics) 6. antigenic variation in hypervariable region of gp120 |
|
how does viral invasion of CNS occur
|
independently of AIDS
|
|
which are the infected cells in CNS
|
microglia or infiltrating macrophages which express CD4
|
|
this is seen in about 21% of homosexual/bisexual males and is associated with human herpes virus 8 (HHV8)
|
kaposis sarcoma
|
|
what is a major source of transmitted virus
|
peripheral blood mononuclear cells
|
|
what are sn of initial infx
|
mild mononucleosis type illness including fever and malaise
|
|
are antibodies detectable right away
|
no- may take many months; also many mos for t-cells to form
|
|
what happens to viral replication after initial infx
|
it's reduced and individual remains well
|
|
sn/sx in later years
|
weight loss, fever, persistent lymphadenopathy, oral candidiasis, diarrhea, ARC-AIDS related complex
|
|
what occurs with ARC
|
-less than 10% may be well
-may develop AIDS (opportunistic infxs_ -may develop subacute encephalitis and dementia |
|
AIDS dementia=
|
opportunistic CNS infxs like HSV, CMV, and toxoplasmosis
|
|
lab tests for HIV
|
-ELISA
-western blot, radioimmunoassay, or immunofluorescence testing to confirm |
|
odds of getting HIV after needle stick
|
<1%
|
|
what types of HIV vaccinations are being developed
|
various subunit envelope glycoproteins and a whole virus vaccine
|
|
whats the problem?
|
a vaccine that will induce abs against gp120 may combine w/ the virus w/o neutralizing it.....it then attaches to the Fc receptors on monocytes and the whole complex is ingested and monocyte is now infected
|
|
tx
|
-AZT
-PIs -individual tx of opportunistic infxs |
|
cause of pubic or crab lice
|
phthirus pubis
|
|
pathogenesis
|
-clings tight to hairs, takes up to 10 blood feedings/day causing itching
-eggs attached to hairs, lice are visible at base of hair -infestation is common |
|
tx
|
application of malathion
|
|
cause of genital scabies
|
Sarcoptes scabei
|
|
characteristics:
|
local lesions on genitalia, can spread as STD; pts may have scabies elswhere on body
|
|
tx
|
10% benzyl benzoate or 1% benzene hexachloride
|
|
whats the most common outcome of GI tract infxs
|
diarrhea
|
|
gastroenteritis:
|
nausea, vomiting, diarrhea, abdominal discomfort
|
|
diarrhea:
|
abnormal fecal discharge- frequent fluid stool; disease of sm intestine
|
|
dysentery:
|
inflammatory disorder of GI tract associated w/ blood and pus in feces; accompanied by fever, pain, abdominal cramps; disease of lg intestine
|
|
enterocolitis:
|
inflammation involving mucosa of both small and large intestine
|
|
Bacterial causes of diarrhea:
|
E. coli, Salmonella, campylobacter jejuni, helicobacter pylori, vibrio cholerae, shigella dysenteriae, shigella sonei, vibrio parahemolyticus, yersinia enterolytica, c. perfringens, b. cereus, staph aureus, c. botulism
|
|
What are the 4 types of E. coli:
|
1. Enterotoxigenic (ETEC)
2. Enteroinvasive (EIEC) 3. Enterohemoerrhagic (EHEC) 4. Enteropathogenic (EPEC) |
|
which is the most imp bacterial cause of diarrhea in children in developing countries and the most common cause of travelers diarrhea
|
ETEC
|
|
most important in developed countries but outbreaks an sporadic cases occur worldwide:
|
EHEC
|
|
important cause of diarrhea in areas of poor hygiene, usually food borne infxs:
|
EIEC
|
|
spread via water contaminated by human or animal sewage:
|
ETEC
|
|
causes sporadic cases of infx in babies and young children:
|
EPEC
|
|
caused by verotoxin-producing serotype 0157 that has direct affect on intestinal epithelium:
|
EHEC
|
|
produces powerful enterotoxins (LT and ST):
|
ETEC
|
|
which of these toxins is heat labile
|
LT
|
|
heat stable
|
ST
|
|
has a mechanism of adhesion to enterocytes that appears to destroy microvilli
|
EIEC
|
|
caused by food and unpasteurized milk:
|
EHEC
|
|
Tx
|
specific antibios not indicated; fluid replacement if necessary
|
|
prevention:
|
clean water, adequate sewage disposal, food/milk pasteurization
|
|
what is the most common case of food-associated diarrhea in developed countries
|
salmonellae
|
|
salmonella and e. coli are both:
|
enterobacteria
|
|
salmonella transmission:
|
animal resevoir- transmitted via contaminated poultry and dairy
|
|
frequent waterborne transmission?
|
no
|
|
where do they invade?
|
epithelial cells of terminal portion of small intestine
|
|
which species are responsible
|
s. enteritidis, s. cholera suis
|
|
tx:
|
usually self-limiting (vomiting rare); fluid/electrolyte replacement if necessary
|
|
which bacteria are S-shaped curved rods
|
campylobacter
|
|
how acquired?
|
via contaminated milk, poultry, H20
|
|
tx:
|
erythromycin for severe cases
|
|
which bacteria is associated with over 90% of duodenal ulcers and 70-80% of gastric ulcers
|
helicobacter pylori
|
|
what does it produce that helps it survive acid environments
|
urease
|
|
tx:
|
proton pump inhibitor with 2 antibiotics; eradication heals ulcers
|
|
acute infx of GI tract caused by comma-shaped gram-negative bacteria
|
cholera
|
|
species?
|
vibrio cholerae
|
|
reservoir and spread?
|
-a free living inhabitant of fresh water
-assymptomatic humans major resevoir -spread via contaminated food (fresh water shellfish) |
|
sn/sx
|
severy watery diarrhea, marked dehydration, loss of carbonates and loss of potassium ions, shock resulting in cardiac failure
|
|
tx:
|
rapid fluid/electrolyte replacement; abs not necessary
|
|
prevention:
|
clean drinking water supply/ adequate sewage disposal
|
|
which condition is also known as bacillary dissentery?
|
shigellosis
|
|
its most severe form is characterized by:
|
-invasion of the mucosa of lg intestine
-inflammation of intestines -blood/pus in diarrhea -lower abdomen cramps |
|
which species causes mild infxs?
|
shigella sonnei
|
|
severe?
|
shigella dysenteriae
|
|
spread?
|
poor sanitation and personal hygiene
|
|
a halophilic organism that contaminates seafood and fish; causes diarrhea if eaten uncooked:
|
Vibrio parahemolyticus
|
|
primarily a pediatric disease:
|
shigellosis
|
|
rice water stool:
|
cholera
|
|
causes infx in colder parts of the world:
|
Yersinia enterolytica
|
|
Tx includes omeprazole with amoxicillin and metronidazole:
|
H. pylori
|
|
enterotoxin producing type A strain and beta-toxin producing type C strains:
|
C. perfringens
|
|
which are more common and caused by spores that contaminate food?
|
A strains
|
|
characteristics of type c strains:
|
-acute necrotizing disease of sm. intestine
-more rare -abdominal pain/diarrhea |
|
prevention?
|
thoroughly re-heating food
|
|
which disease has a long standing history of epidemics and pandemics
|
cholera
|
|
most common cause of diarrhea:
|
Campylobacter jejuni
|
|
clinically, which other bacteria is indistinguishable from c. jejuni?
|
salmonella
|
|
caused by eating contaminated meat in people who are unaccustomed to high protein diets:
|
C. perfringens
|
|
why?
|
lack sufficient intestinal trypsin to destroy the toxin
|
|
a heat stable enterotoxin thats resistant to degradation by enzymes in stomach/ sm. intestine:
|
staph aureus
|
|
spores and vegetative cells contaminate food:
|
B. cereus
|
|
2 forms of B. cereus:
|
1. ingestion of enterotoxin in food (rice and potatoes)
2. production of enterotoxin in gut |
|
which causes rapid onset vomiting and which causes diarrhea?
|
vomiting= ingestion
diarrhea= production in gut |
|
found in rabbits, pigs, sheep, cattle, horses, domestic pets:
|
yersinia enterolytica
|
|
an acute but self-limiting diarrhea that's resolved without tx:
|
salmonella
|
|
diarrhea not a feature, vomiting occurs 3-6 hrs after consumption and recovery w/in 24 hrs:
|
staph aureus
|
|
spores are found widespread in the environment and can be isolated from soil samples, animals, and fish:
|
clostridium botulinum
|
|
is botulin an exotoxin or endotoxin?
|
exotoxin
|
|
how does it invade?
|
toxins are ingested in food (canned or reheated) or are produced in the gut after ingesting the organisms
|
|
pathogenesis:
|
-toxins are absorbed by the blood stream
-reach peripheral nerve synapses and block neurotransmission -leads to flaccid paralysis, progressive muscle weakness, and respiratory distress |
|
3 types:
|
1. foodborne (toxin released in food, then ingested)
2. infant (organism ingested) 3. woulnd (organism implanted in wound) |
|
tx
|
antibacterial agents not helpful; polyvalent antitoxin recommmended
|
|
Causes antibiotic associated diarrhea- broad spectrum antibios that inhibit normal flora:
|
Clostridium difficile
|
|
pathogenesis:
|
produces 2 exotoxins that produce diarrhea and lead to colitis
|
|
tx:
|
if severe, anti-anaerobic agents (metronidazole)
|
|
how is viral diarrhea distinguised from bacterial?
|
clinically indistinguishable
|
|
transmission:
|
fecal-oral route
|
|
viruses:
|
Rotavirus and Calcivirus
|
|
which includes the Norwalk virus?
|
Calcivirus
|
|
sn/sx
|
fever, chills, headaceh, nausea, vomiting, diarrhea
|
|
transmission:
|
eating sewage contaminated shellfish or mussels
|
|
Who does rotavirus mostly infect
|
children under 2
|
|
incubation period:
|
1-4 days
|
|
where does viral replication occur?
|
intestinal epithelial cells
|
|
sn/sx
|
acute onset of projectile vomiting and diarrhea
|
|
tx:
|
rehydration/salt replacement; no anti-virals
|
|
Protozoa that cause diarrhea:
|
Entamoeba histolytica, Giardia lamblia, and Cryptosporidium parvum
|
|
how does infx occur with E. histolytica
|
food/drink is contaminated with cysts that pass thru the stomach and excyst in the sm. intestine where they multiply
|
|
sn/sx
|
-small ulcers in mucosa that lead to mild diarrhea
-more sever leads to amebic dysentery |
|
chars. of amebic dysentery:
|
mucus, pus and blood in stool
|
|
difference between amebic dysentery and bacillary dysentery:
|
amebic can perforate small intestine (peritonitis) and invade extra-intestinally when trophozoites spread via blood to the liver and form an abcess
|
|
tx:
|
metronidazole
|
|
Which protozoa causes infx when cysts are swallowed in contaminated drinking water from rivers/streams?
|
Giardia lamblia
|
|
animal host?
|
beaver
|
|
characteristics:
|
-assymptomatic infxs (mild)
-self-limiting diarrhea 7-10 days -immunocompromised may develop chronic infx |
|
tx:
|
metronidazole
|
|
prevention:
|
chlorination and water filtration
|
|
Pathogenesis of Cryptosporidium parvum:
|
-fecally contaminated material is ingested
-cysts release infective trophozoites which invade epithelial cells in sm. intestine -parasite found in many animals |
|
sn/sx
|
ranges from moderate diarrhea to severe lasting 20 days in immunocompromised
|
|
cryptosporidiosis:
|
common infx in AIDS; diarrhea can be irreversible and life threatening
|
|
tx:
|
spiramycin (immunocompromised only)
|
|
which protozoa is common in subtropical and tropical countries
|
Entamoeba histolytica
|
|
What are the most important intestinal worms?
|
soil transmitted nematodes
|
|
2 groups of them:
|
1. Ascaris lumbricoides/Trichuris trichiura
2. Anchylostoma duodenale/Necator americanus/Strongyloides stercoralis |
|
large roundworm:
|
ascaris lumbridcoides
|
|
whipworm:
|
Trichuris trichiura
|
|
hookworm:
|
Necator americanus
|
|
which occur by swallowing infective eggs which hatch in intestine and release larvae
|
Ascaris and Trichuris
|
|
which can cause abdominal pain and nausea
|
Ascaris
|
|
what happens if there's large numbers of ascaris
|
can cause intestinal blockage and perforations of wall
|
|
What can Tricuris infx lead to?
|
chronic diarrhea and impaired nutrition/retarded growth (since children mostly affected)
|
|
How do Ancylostoma, Necator, and Stronglyoides infect?
|
-active skin penetration by infective larvae
-then migration via blood to lungs -then swallowed where, in intestine, adult worms attach to intestinal mucosa where they rupture capillaries and suck blood |
|
Hookworm disease can lead to:
|
iron deficiency anemia due to blood feeding
|
|
Strongyloidiasis:
|
profuse diarrhea with dehydration and electrolyte imbalance; fatal if immunosuppressed
|
|
pinworm:
|
Enterobium vermicularis
|
|
What is the most common intestinal nematode in developed countries?
|
pinworm (Enterobius)
|
|
how do they infect?
|
females live in the lg. bowel and release infective eggs in the perianal skin
|
|
sn/sx
|
itching and mild diarrhea
|
|
transmission
|
contaminated fingers
|
|
tx
|
anti-heminitic drugs;
piperazine for Ascaris hookworms and pinworms |
|
what are the systemic infxs initiated at intestinal tract?
|
typhoid fever, paratyphoid fever (enteric fevers), listeriosis, and hepatitis
|
|
What causes the enteric fevers?
|
Salmonella typhi and S. paratyphi types A and C
|
|
transmission:
|
contaminated food/water; spread person to person and they can cary it for months or years
|
|
pathogenesis:
|
-after ingestion they penetrate the gut mucosa and reach intestinal lymph nodes
-survive and multiply within macrophages -released into bloodstream and seed other organs (spleen, bone marrow, liver, Peyer's patch) -gallbladder infected via blood or liver (carrier) |
|
incubation period:
|
10-14 days
|
|
sn/sx
|
fever, aches, repiratory problems, resembles flu-like illness, diarrhea, or constipation, transient rose spots in the upper abdomen (may disappear)
|
|
complications:
|
-GI lesions that hemorrhage and perforate
-myocarditis, bone marrow damage -meningitis, osteomyelitis, or endocarditis due to multiplication on other body sites |
|
what are chronic carriers?
|
1-3% of pt's who excrete S. typhi in feces or urine for up to 1 yr. after infx
|
|
Tx:
|
chloramphenicol, ampicillin, ciprofloxacin
|
|
prevention:
|
good hygiene, exclude carriers from food handling, gallbladder removal in carriers
|
|
vaccination:
|
killed vaccine of S. typhi and S. paratyphi recommended for travelers
|
|
Who is listeriosis associated with
|
pregnancy (risk or abortion or stillbirth)and reduced immunity
|
|
Cause (species):
|
Listeria monocytogenes
|
|
transmission:
|
uncooked foods= pate, milk, soft cheese, coleslaw
|
|
Hepatitis=
|
inflammation and damage to the liver
|
|
causes:
|
Virus (A, E, B, C) or bacteria (less common)
|
|
sn/sx
|
malaise, anorexia, nausea or if severe acute liver failure (rare)
|
|
can liver be repaired?
|
yes, regeneration of liver cells is rapid
|
|
if infx persists, what can result?
|
cirrhosis
|
|
what type of virus is Hep A (HAV)
|
enterovirus
|
|
transmission:
|
fecal-oral route (excreted in lg. amounts in feces)
|
|
incubation period:
|
2-4 weeks
|
|
pathogenesis:
|
after infection, it enters blood from unknown sites in the GI tract where it can replicate and then infect liver cells
|
|
what is a sign in adults?
|
jaundice
|
|
vaccine?
|
yes
|
|
Hep E spread?
|
fecal oral
|
|
where common?
|
undeveloped countries and India (waterborne)
|
|
incubation period:
|
6-8 weeks
|
|
mild or severe?
|
usually mild, but severe in pregnant women (high mortality)
|
|
Hep B (HBV) transmission:
|
in blood: between IV users, male homosexuals, or heterosexuals with ulcers, mother/child, earpiercing, actupuncture
|
|
pathogenesis:
|
enters body and replicates in the lymphoid tissue then reaches the blood and then liver. Then, immune-mediated attack of infected liver cells by T-cells, leading to inflammation and necrosis. IR slowly works and virus replication stops
|
|
Do all individuals eliminate it?
|
10% don't and become carriers; blood remains infectious for life but liver damage is mild
|
|
Predisposition to becoming a carrier:
|
-immunodeficiency
-age (infants) -males more than females |
|
complications of HBV
|
-cirrhosis
-hepatocellular carcinoma |
|
How likely are hep B carriers to develop liver cancer
|
200 times more likely than non carriers
|
|
detection:
|
HBsAg (antigen) remains in carriers and is detected
|
|
Tx:
|
interferon alpha, vaccine
|
|
What is Hep C most common with
|
transfusion
|
|
spread?
|
same as HBV-blood
|
|
differences betw. C and B:
|
-more aggressive
-higher degree of carriers -also causes liver cancer -same transmission |
|
disease progression:
|
50% get chronic active hepatits and 20% get cirrhosis
|
|
tx:
|
interferon alpha and ribavirin; no vaccine
|
|
Congenital infxs:
|
congenital rubella, CMV, syphillis, toxoplasmosis, HIV, listeriosis
|
|
when is fetus susceptible to rubella?
|
in 1st 3 mos. of pregnancy
|
|
abnormalities:
|
development of heart, brain, eyes, ears; low birth weight and eye and heart lesions
|
|
25% develop what
|
IDDM
|
|
where does virus replicate
|
pancreas
|
|
prevention:
|
totally- vaccine before pregnancy
|
|
how many fetuses are infected after primary maternal infx with CMV?
|
40%; 5% show signs at birth
|
|
abnormalities:
|
mental retardation, spasticity, eye abnormalities, hearing defects, hepatosplenomegaly, anemia
|
|
vaccine:
|
in clinical trials
|
|
where's con. syphillis common
|
developing countries
|
|
abnormalities:
|
rhinitis, skin/mucosal lesions, hepatosplenomegaly, and bone, teeth, and cartilage abnormal
|
|
prevention:
|
treat mom before 4th month
|
|
cause of toxoplasmosis:
|
Toxoplasmosis gondii
|
|
abnormalities:
|
microcephaly, convulsions, chorioretinitis, hepatosplenomegaly, jaundice, mental retardation, defective vision
|
|
prevention:
|
women avoid contact w/ cat feces or lightly cooked meat
|
|
HIV abnormalities:
|
poor weight gain, sepsis, developmental delays, oral thrush, pneumonitis, diarrhea, AIDS
|
|
prevention:
|
mom take AZT
|
|
Listeriosis sn/sx in mother:
|
flu-like sx or asymptomatic
|
|
abnormalities:
|
abortion, premature delivery, neonata septicemia and neurological damage
|
|
tx:
|
penicillin, ampicillin
|
|
vaccine:
|
no
|
|
What are the main routes of infx in the CNS?
|
blood vessels and nerves that transverse the walls of the skull and vertebral column
|
|
what type of invasion is most common
|
bloodborne
|
|
encephalitis:
|
invasion across the blood-brain barrier
|
|
meningitis:
|
invasion across the blood-cerebrospinal fluid
|
|
is invasion via peripheral nerves common?
|
no
|
|
how does body respond to invading viruses in CNS?
|
increased lymphocytes (mostly T cells) and monocytes in CSF
|
|
response to pyogenic bacterial invasion:
|
rapid increase in PMNs
|
|
clear CSF, "aseptic":
|
viral
|
|
turbid CSF, "septic":
|
pyogenic bacteria
|
|
which is more severe
|
bacterial
|
|
which is more common
|
viral
|
|
bacterial agents:
|
Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae
|
|
cause of meningococcal meningitis:
|
Neisseria meningitidis
|
|
transmission:
|
person to person by droplets
|
|
who's mostly infected:
|
children whove lost abs acquired by their mother, adolescents who've not previously encountered the infecting serotype
|
|
blood/meninges invasion rare?
|
yes, and poorly understood
|
|
incubation period:
|
1-3 days
|
|
sn/sx:
|
sore throat, headaceh, drowsiness, fever, irritability, neck stiffness, hemorrhagic skin rash with petechiae (Due to septicemia)
|
|
severe complications:
|
35%; intravascular coagulation, shock, renal failure, bleeding into the brain and adrenal glands
|
|
Mortality:
|
100% if untreated, 10% if treated; serious/lasting complications not common
|
|
Tx
|
penicillin, ampicillin ASAP! if suspected
|
|
Prophylaxis:
|
chemoprophylaxis of rifampicin for close contacts for 2-3 days to clear carriage of bacteria in nasopharynx
|
|
who does haemophilus meningitis infect?
|
infants from 3-4 mo to 2-3 y.o.
|
|
incubation period:
|
5-6 days
|
|
mortality:
|
less frequently fatal but 10% higher incidence of lasting complications
|
|
complications:
|
hearing loss, delayed language development, mental retardation, seizures
|
|
vaccine:
|
yes- children 6 mos. and older
|
|
prophylaxis:
|
rifampicin to close contacts
|
|
cause of pneumococcal meningitis:
|
Streptococcus pneumoniae
|
|
where is it carried?
|
in the throats of healthy people
|
|
mortality:
|
20-30% in treated cases
|
|
complications:
|
sequela such as deafness in 15-20% of treated cases
|
|
Tx:
|
penicillin
|
|
vaccine:
|
polyvalent (23 serotype) vaccine
|
|
which is an important cause of miningitis in immunocompromised adults, esp, renal transplant and cancer pts.
|
Listeria mnoncytogenes
|
|
Tx:
|
ampicillin and gentamicin
|
|
causes of neonatal meningitis:
|
E. coli and group B hemolytic streptococci
|
|
mortality:
|
fatal in 35%
|
|
complications:
|
permanent neurological sequela such as cerebral or cranial nerve palsy, epilepsy, mental retardation, or hydrocephalus
|
|
why is clinical diagnosis of neonatal meningitis rare?
|
b/c common sn/sx of fever, poor feeding, vomiting, respiratory distress, or diarrhea
|
|
tx:
|
gentamicin and ampicillin
|
|
Tuberculous meningitis:
|
-associated w/ acute miliary TB
-gradual onset of malaise, apathy, and anorexia and proceeds to photophobia, neck stiffness, and altered consciousness |
|
Tx:
|
isoniazin, rifampicin, and pyraminamide
- BCG vaccine and isoniazind prophylaxis |
|
Fungal meningitis:
|
-Cryptococcus neoformans
-Coccidioides immitis -invade blood from primary infx in lungs then infect brain |
|
C. neoformans:
|
-AIDS pts (depressed T cell immunity)
|
|
C. immitis:
|
southwest US, Mexico, S. America
|
|
Tx:
|
amphotericin B
|
|
Protozoan meningitis:
|
-Naegleria and Harmanella
-multiply in stagnant water in warm countries -high mortality |
|
pathogenesis:
|
inhaled or swallowed and reach meninges via the olfactory tract
|
|
Most common type of meningitis:
|
viral
|
|
sn/sx
|
-headache, fever, general illness but less neck stiffness
|
|
viral causes:
|
HSV, mumps, poliovirus, coxsackievirus, echovirus, Japanese encephalitis virus, Eastern/western equine encephalatis virus, and HIV
|
|
recovery from viral?
|
no antivirals (except HSV) but usually complete recovery
|
|
Primary cause of encephalitis:
|
viruses: HSV, poliovirus, mumps, rabies
|
|
sn/sx
|
cerebral dysfunction: abnormal behavior, seizures, altered consciousness, nausea, vomiting, fever
|
|
most common severe sporadic encephalitis:
|
HSV, 2 forms:
1. primary and generalized in infancy 2. adults due to reactivation in trigeminal ganglie |
|
Tx
|
acyclovir
|
|
Poliovirus sn/sx
|
1-4 days of fever initially, sore throat, malaise, meningeal sn/sx, paralysis, motor neuron problems
|
|
common?
|
used to be- CNS disease in less than 1% of those infected now
|
|
vaccine?
|
yes= completely preventable with it
|
|
common cause of mild encephalitis:
|
mumps virus- assymptomatic
|
|
transmission of rabies encephalitis:
|
saliva of infected dogs, foxes, jackals, wolves, skunks, raccoons, and vampire bats and transmitted via a bite or salivary contamination of a wound/abrasion
|
|
pathogenesis:
|
virus travels up peripheral nerves to CNS; once in brain it spreads cell to cell until many neurons are infected; invades limbic system
|
|
incubation:
|
4-13 weeks (the further the bite from the CNS, the longer the period)
|
|
sn/sx
|
sore throat, headache, fever, discomfort at site of bite, muscle spasms, convulsions, diff swallowing, hydrophobia
|
|
immediate preventative action:
|
1. clean wound
2. confirm if animal is infected (if dog appears healthy after 10 day, infx is unlikely) 3. adiminister human rabies Immunoglobulin (passive immunization) 4. if risk is definite, active immunization with killed virus |
|
Causes of togavirus meningitis and encephalitis:
|
arthropod-borne togaviruses
|
|
which are transmitted via the mosquito Culex tarsalis?
|
western equine encephalomyelitis and St. Louis encephalitis virus
|
|
What is transmitted via other Culex species?
|
west nile enephalitis virus
|
|
where is japanese encephalitis virus prevalent?
|
india - 50% mortality; vaccine available
|
|
Retrovirus meningits and encephalitis:
|
-HIV invades CNS after initial infx
-later, subacute encephalitis may develop, associated w/ dementia |
|
cause of brain abcesses:
|
-follow surgery/trauma, chronic osteomyelitis, septic embolism, or chronic cerebral anoxia
-various bacteria of oropharynx origin -rare b/c of antibiotics |
|
Tx:
|
surgical drainage and antibios
|
|
Scrape-Type Agent features:
|
-slow replication occurs by the conversion of host prion protein into abnormal form
-not a virus -prion protein is host encoded but slightly altered -resistant to heat, chemicals and irradiation -no test tube cultivation -spongiform appearance -little or no inflammatory response -infectious agent restricted to CNS and lymphoid tissues -No tx, no vaccine, lethal -originated in sheep/goats in Europe 200-300 yrs ago |
|
CJD transmission:
|
-eating bovine spongiform encephalopathy (BSE) contaminated food
-person to person by: 1. neurological steriotactic electrodes 2. corneal grafts 3. injections of growth hormone |
|
genetic disposition:
|
10% of CJD occurs in families where affected people have mutation in the gene encoding for the prion protein; easily and spontaneously converted to pathogenic form
|
|
a fatal neurologic disease with cerebellar signs exclusive to Fore tribes in Papua New Guinea
|
Kuru
|
|
transmission
|
person to person via cannibalism
|
|
incubation period:
|
4-20 years
|
|
Tetanus and botulism affects on CNS:
|
toxins have effect, but bacteria themselves dont invade
|
|
cause of tetanus:
|
Clostridium tetani
|
|
pathogenesis:
|
-spores are in soil and animal feces
-spores enter wound and if tissue is necrotized it allows anaerobic growth of the organism -toxin is carried in peripheral nerve axons and in the blood to CNS where it binds to neurons and blocks release of inhibatory mediators in the synapses causes overactivity of the motor neurons leading to spastic paralysis |
|
sn/sx
|
after 3-21 days: exaggerated reflexes, muscle rigidity, uncontrolled muscle spasms, lockjaw, neck stiffness, dysphagia; spasms can lead to injury/respiratory failure
|
|
immunization:
|
toxoid, lasts 10 years; tetanus immunoglobulin in severe cases
|
|
pathogenesis of botulism:
|
-spores in soil contaminate veggies, meat, and fish
-can survive in improperly canned food -ingested then enters blood where it acts on peripheral nerve synapses by blocking acetylcholine |
|
sn/sx
|
after 2-72 hrs., descending weakness, flaccid paralysis, dysphagia, vomiting, vertigo, respiratory muscle failure
|
|
tx:
|
antibodies against toxins
|
|
Most commmon cause of skin infections such as boils, abcesses, or postoperative wound infxs:
|
Staph aureus
|
|
how acquired?
|
either from self-innoculation froma carrier state (nose) or from contact with another person
|
|
This begins w/in 2-4 days of innoculation as a superficial infection of a follicle (foliculitis)
|
boil
|
|
this typically contains abundant yellow creamy pus formed by organisms and dead WBCs:
|
abcess
|
|
what can inward drainage of an abcess lead to?
|
peritonits, empyema, or meningitis
|
|
Tx
|
drainage, antibiotics if severe/fever: enzyme stable penicillins (cloaxicillin and flucoloxacillin)
|
|
What causes staphylococcal scalded skin syndrome, seen in infants and older children
|
Staph aureus that produces exfoliatin or scalded skin syndrom toxin
|
|
pathogenesis:
|
minor lesion initally but toxin causes destruction of intercellular connections and separates epidermis from dermis
|
|
sn/sx
|
-large blisters with clear fluid
-entire skin lost -irritable, uncomfortable -rarely severely ill |
|
Tx:
|
fluid replacement and cloxacillin
|
|
What causes TSS?
|
TSS-toxin prodcucing Staph aureus
|
|
sn/sx
|
skin manifestations, rash followed by desquamation of skin in soles and palms
|
|
cause of streptococcal skin infxs:
|
Strep. pyogenes (diff strain than sore throat)
|
|
This occurs independently of upper respiratory tract infx and is limited to the epidermis
|
streptococcal impetigo
|
|
sn/sx
|
crusted yellow papules that develop 24-48 hrs. after infx
|
|
This may infect deeper in the dermis causing erysipelas and involves blocking of dermal lymphatics
|
strep pyogenes
|
|
sn/sx
|
well defined spreading erythromatous inflammation on face, legs or feet; fever, pain
|
|
tx:
|
penicillin per os or IM
|
|
If infx with strep pyogenes is deeper than erysipelas, it may infect subcutaneous fat causing:
|
Cellulitis
|
|
sn/sx
|
hot red swollen lesion, regional lymph nodes enlarged; malaise, fever, chills
|
|
cause of cellulitis:
|
staph aureus or strep pyogenes
|
|
where does anaerobic cellulits develop
|
in areas of traumatized or devitalized tissue:
surgical or trauma wounds, diabetic pts are prone |
|
sn/sx (anaerobic cellulitis)
|
foul smelling discharge, swelling and gas in tissues
|
|
tx:
|
antibiotics, surgical debridement
|
|
This resembles bacterial gangrene but is more acute and highly toxic causing widespread necrosis:
|
Necrotizing fascitis (flesh eating bacteria)
|
|
Tx
|
radical excision, local and systemic antibios
|
|
cause of gas gangrene:
|
clostridium perfringens
|
|
pathogenesis:
|
-organisms invade deep muscle and cause necrosis and produce gas bubbles
-in poor circulation areas -proceeds rapidly -lecithinase (alpha toxin) hydrolyzes lipids in cells membranes resulting in cell lysis and death -dead tissue further allows multiplication and more toxin |
|
if toxin gets in blood stream?
|
massive hemolysis, renal failure , death
|
|
tx:
|
excision, amputation, anit-alpha toxin, hyperbaric oxygen chamber, penicillin, metronidazole
|
|
Pathogenesis of Proprionibacterium acnes:
|
increase in androgenic hormones leads to in'd sebum production and blockage of ducts leads to sac where they can multiply
|
|
what causes inflammation:
|
p. acnes acts on sebum to form fatty acids and acts with polymorphs
|
|
comedones (black heads):
|
greasy plugs composed of keratin, sebum and bacteria capped by melanin
|
|
tx
|
tetracycline, erythromycin, vitamin A derivates (isoretinoin)
|
|
cause of leprosy:
|
mycobacterium leprae
|
|
are there more organisms in nasal secretion or skin lesions
|
nasal secretions
|
|
transmission:
|
possibly arthropod vecotors; not highly contagious- need prolonged exposure
|
|
where concentrated on the body?
|
in the skin and superficial nerves (within macrophages and Schwann cells of peripheral nerves)b/c grow under 37 degrees
|
|
2 manifestations (partly genetically determined):
|
1. Tuberculoid (TT)- blotchy red lesions with anesthetic areas of face, trunk, and extremeties- good prognosis
2. lepromatous (LL)- due to weak CMI- extensive skin involvement- loss of eyebrows, thickening nostrils, ears, and cheeks, typical lion-like appearance |
|
tx:
|
LL- triple therapy- dapsone, rifampicin, clofazimine for 2 years
TT- dapsone and rifampcin for 6 mos. -dapsone prophylaxis for close contacts |
|
what are the most common infxs in humans
|
dermatophytes- superficial mycoses (tinea or ringworm)
|
|
what are they
|
keratin-loving fungi that invade, skin, hair, and nails
|
|
capitis-
|
affects hair and scalp
|
|
corporis-
|
affects body
|
|
pedis-
|
feet
|
|
sx
|
thickening, dry , scaly skin, cracks between toes, hair loss
|
|
tx:
|
topical antifungals (miconazole) and ketatolytic agents (salicylic acid, benzoic acid); or griseofulyin orally
|
|
response time:
|
scalp -6-12 weeks
fingernails- up to 6 mos. toenails- one year or more |
|
When can candida colonize skin
|
when damaged b/c its moist
|
|
viral mucotaneous lesions:
|
Papillomavirus, HSV, VZV, Varicella, Zoster, or HHV
|
|
what does papilloma cause
|
skin warts
|
|
of the 70 types, which infgect genitals:
|
6, 11, 16, 18, and 32
|
|
sn/sx
|
cauliflower like
|
|
what do HPV1 and 4 cause
|
plantar warts: flat
|
|
what causes common warts
|
HPV 2, 3, 10
|
|
pathogenesis
|
-after entering body via surface abrasions, virus infects cells in basal layers of skin or mucosa
-no spread to deep tissue -infected cells are stimulated to divide, after 6 months start protruding -wart regresses and teh viral DNA remains latent in basal cell layer -immune compromised reactives |
|
tx
|
apply karyolytic agents- salicyclic acid, freezing, liquid nitrogen
|
|
HSV-1 pathogenesis:
|
-basic lesion is intraepithelial vescicle where virus sheds
-virus rich vesicles ulcerate and become coated with whitish gray liquid, then scab over and heal in a week -virus enters sensory nerve endings in the lesion and goes to tirgeminal ganglia and initiate latent infx -virus remains for life and can cause cold sore |
|
transmission:
|
from saliva or cold sores
|
|
primary infx can occur in:
|
1. eye- conjunctivitis
2. finger 3. other skin sites (rubbing) 4. genital tract |
|
reactivation provoked by:
|
1. common cold, pneumonia
2. direct sunlight 3. stress 4. menstruation 5. immunocompromised |
|
txL:
|
acyclovir
|
|
what does VZV cause
|
chicken pox (varicella) and zoster (shingles
|
|
what group does VZV belong to
|
herpesvirus
|
|
transmission:
|
inhalation from respiratory secretions and saliva or by direct contact of lesions
|
|
Primary infx with VZV causes:
|
chicken pox
|
|
reactivation causes:
|
shingles
|
|
pathogenesis of varicella:
|
-after primary infx virus passes across surface epithelium in respiratory tract to lymphoid tissues
-no sx or lesions yet -replicates and seeds to epithelial celss and produces varicella vesicles -vesicles appear as crops, develop into pustules and scab over, scarring |
|
adult complications:
|
interstitial pneumonia, CNS involvement
|
|
where is latent infx with zoster established?
|
dorsal root ganglia
|
|
sn/sx
|
erythromatous rash in thoracic region, severe pain
|
|
predispostion to zoster if:
|
-increasing age
-leukemia, lymphoma, AIDS, renal transplant (ImunoComp) -fractures/tumors |
|
tx:
|
famciclovir
|
|
vaccine:
|
live attenuated
|
|
HHV 6 sn/sx
|
-affects most before age 5
-roseola infantum rash -2 weeks incubation, then fever and rash |
|
how many serotypes of mumps exist
|
1
|
|
spread?
|
intimate contact-airborne droplets, salivary secretions and possibly urine
|
|
pathogenesis:
|
-enters respiratory tract, spreads systemically to lymphoid tissues
-after 7-10 days enters the blood and localizes in salivary and other glands -cells lining ducts degenerate causing inflammation, lymphocyte infiltration, and edema resulting in disease - |
|
sn/sx
|
painful tender and swollen parotid gland: classic 30-40% of cases
|
|
recovery:
|
1 week, life long resistance
|
|
tx
|
none, live attenuated vaccine
|
|
how many serotypes of rubella?
|
1
|
|
transmission:
|
droplet infx
|
|
more or less contagious than measles
|
less
|
|
pathogenesis:
|
-enters respiratory tract and grows in local lymphoid tissue
-spreads to spleen and lymph nodes elswhere -after 1 week, multiplication in placenta, joints, and kidneys |
|
sn/sx
|
after 14-21 days, milde disease, fever, malaise, and maculopapular rash lasting 3 days
|
|
tx
|
live attenuated vaccine
|
|
what is the lgst human herpes virus
|
CMV
|
|
how many serotypes
|
1
|
|
transmission
|
saliva "salivary gland virus", urine, semen, cervical secretions, blood transfusions, organ transplant
|
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pathogenesis
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-starts as silent infx in URT, then spreads locally to lymphoid tissues and systmeically in circulaing monocytes and lymphocytes
-then localizes in epithelial cells of salivary glands and kidney tubules and in the cervix, epididymis and testes where virus sheds |
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sn/sx
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assymptomatic; mabye fever in young adults
|
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may lead to:
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1. fetal malformations
2. interstitial pneumonia |
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tx
|
ganciclovir; no vaccine
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EBV transmission
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saliva, kissing
|
|
pathogenesis:
|
-replicates in B lymphocytes binding to Cd3 receptors
-T lymphos respond to infected B's -remains latent in some B's |
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what are sn/sx attributed to?
|
immunologic response--cytokines released
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sn/sx
|
-infants/children: none or weak
- mono, fever, sore throat, petechiae on hard palate, lymphadenopathy, splenomegaly, anorexia, lethargia |
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Immunodeficiency can lead to:
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reactivation with no symptoms
|
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tx;
|
no antivirals; acyclovir useful; no vaccine
|
|
EBV is closely related to
|
Burkitts lymphoma; co-carcinogen is marlaria (weakens t cells)
|
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where is it restricted to
|
Africa and papua new guinea
|
|
Smallpox (variola) caused by:
|
poxvirus
|
|
spread
|
person to person via contact with skin lesions and via respiratory tract
|
|
sn/sx
|
generalized rash
|
|
global eradication of smallpox in 1980 b/c :
|
1. no subclinical infxs
2. no carriers 3. no animal resevoir 4. effective vaccine available (live attenuated vaccinia) |
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what are the arbovirus infxs
|
yellow fever and dengue fever
|
|
how are they transmitted
|
arthropod borne- via ticks, mosquitoes, and sandflies
|
|
arbovirus pathogenesis in vector:
|
enters the arthropod as it takes a bloodmeal from infeced animal, passes to the gut and reaches salivary gland where it multiplies and can now transmit (1-2 weeks)
|
|
Who spreads urban yellow fever
|
person to person by Aedes aegypti
|
|
jungle yellow fever:
|
monkey to human by Haemoagogus
|
|
where?
|
Africa, central/south america, and caribean
|
|
pathogenesis:
|
-virus enters blood vessel
-spreads to vascular epithelium and liver -2-6 days incubation |
|
sn/sx
|
fever, headache, muscle ache; severe- shock, severe liver damage
|
|
tx
|
prevention via live attenuated vaccine; vector control w/ insecticides, repellants
|
|
Where does dengue fever occur
|
SE asia, pacific area, india, and caribbean
|
|
principal vector
|
A. aegypti
|
|
pathogenesis:
|
-virus replicates in monocytes and in vascular epithelium
-incubation 4-8 days -increased cytokine release into circulation |
|
sn/sx
|
malaise, fever, nausea, vomiting, maculopapular rash
|
|
SEVERE:
|
dengue hemorrhagic fever syndrome- children endemic 10% mortality
|
|
what does incre'd cytokine release cause
|
vascular damage, shock, hemorhging into GI tract and skin
|
|
tx:
|
none
|