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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?
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
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...
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
what does E. coli produce that causes kidney damage
is healthy urinary tract resistant to bacterial colonization?
yes- eliminates microorganisms rapidly/efficiently
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
fever, low back pain, dysuria, and frequency
upper UTI spreads to
what is pyelonephritis
kidney infx
lower UTI sx of dysuria, urgency, frequency but also FEVER
common cause of upper UTIs
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
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
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
1-3 months; treponemes proliferate, enlarged inguinal nodes and spontaneous healing
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
3-30 years: treponemes are dormant in liver or spleen, no sign of illness
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
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)
early diagnosis (for 2ndary and tert), early screening and penicillin treatment (congenital)
what causes gonorrhea
gram pos diplococcus Neisseria gonorrheae
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?
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
-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)
penicillin, ceftriazone, ciprofloxacin, spectinomycin
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
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
proctitis, fever, hepatitis, pneumonitis, meningo-encephalitis
cause of chancroid (soft chancre):
H. ducreyi
painful genital ulcer and local lymphadenitis
erythromycin, caftraixone, otrimoxazole
cause of donovanosis:
Calymmatobacterium granulomatis
genital nodules that erode to form granulomatous ulcers; bleed readily on contact
which is most common form of genital ulcers in africa and asia
which is common in caribbean, new guinea, india, and central australia
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
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
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
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)
cause of genital herpes
when is primary lesion seen
3-7 days after infx
-vesicles that form shallow ulcers
-local lymph nodes swollen
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
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
HIV infects which cells
TH, monocytes and dendritics
-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
-western blot, radioimmunoassay, or immunofluorescence testing to confirm
odds of getting HIV after needle stick
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 then attaches to the Fc receptors on monocytes and the whole complex is ingested and monocyte is now infected
-individual tx of opportunistic infxs
cause of pubic or crab lice
phthirus pubis
-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
application of malathion
cause of genital scabies
Sarcoptes scabei
local lesions on genitalia, can spread as STD; pts may have scabies elswhere on body
10% benzyl benzoate or 1% benzene hexachloride
whats the most common outcome of GI tract infxs
nausea, vomiting, diarrhea, abdominal discomfort
abnormal fecal discharge- frequent fluid stool; disease of sm intestine
inflammatory disorder of GI tract associated w/ blood and pus in feces; accompanied by fever, pain, abdominal cramps; disease of lg intestine
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
most important in developed countries but outbreaks an sporadic cases occur worldwide:
important cause of diarrhea in areas of poor hygiene, usually food borne infxs:
spread via water contaminated by human or animal sewage:
causes sporadic cases of infx in babies and young children:
caused by verotoxin-producing serotype 0157 that has direct affect on intestinal epithelium:
produces powerful enterotoxins (LT and ST):
which of these toxins is heat labile
heat stable
has a mechanism of adhesion to enterocytes that appears to destroy microvilli
caused by food and unpasteurized milk:
specific antibios not indicated; fluid replacement if necessary
clean water, adequate sewage disposal, food/milk pasteurization
what is the most common case of food-associated diarrhea in developed countries
salmonella and e. coli are both:
salmonella transmission:
animal resevoir- transmitted via contaminated poultry and dairy
frequent waterborne transmission?
where do they invade?
epithelial cells of terminal portion of small intestine
which species are responsible
s. enteritidis, s. cholera suis
usually self-limiting (vomiting rare); fluid/electrolyte replacement if necessary
which bacteria are S-shaped curved rods
how acquired?
via contaminated milk, poultry, H20
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
proton pump inhibitor with 2 antibiotics; eradication heals ulcers
acute infx of GI tract caused by comma-shaped gram-negative bacteria
vibrio cholerae
reservoir and spread?
-a free living inhabitant of fresh water
-assymptomatic humans major resevoir
-spread via contaminated food (fresh water shellfish)
severy watery diarrhea, marked dehydration, loss of carbonates and loss of potassium ions, shock resulting in cardiac failure
rapid fluid/electrolyte replacement; abs not necessary
clean drinking water supply/ adequate sewage disposal
which condition is also known as bacillary dissentery?
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
shigella dysenteriae
poor sanitation and personal hygiene
a halophilic organism that contaminates seafood and fish; causes diarrhea if eaten uncooked:
Vibrio parahemolyticus
primarily a pediatric disease:
rice water stool:
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
thoroughly re-heating food
which disease has a long standing history of epidemics and pandemics
most common cause of diarrhea:
Campylobacter jejuni
clinically, which other bacteria is indistinguishable from c. jejuni?
caused by eating contaminated meat in people who are unaccustomed to high protein diets:
C. perfringens
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:
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?
how does it invade?
toxins are ingested in food (canned or reheated) or are produced in the gut after ingesting the organisms
-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)
antibacterial agents not helpful; polyvalent antitoxin recommmended
Causes antibiotic associated diarrhea- broad spectrum antibios that inhibit normal flora:
Clostridium difficile
produces 2 exotoxins that produce diarrhea and lead to colitis
if severe, anti-anaerobic agents (metronidazole)
how is viral diarrhea distinguised from bacterial?
clinically indistinguishable
fecal-oral route
Rotavirus and Calcivirus
which includes the Norwalk virus?
fever, chills, headaceh, nausea, vomiting, diarrhea
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
acute onset of projectile vomiting and diarrhea
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
-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
Which protozoa causes infx when cysts are swallowed in contaminated drinking water from rivers/streams?
Giardia lamblia
animal host?
-assymptomatic infxs (mild)
-self-limiting diarrhea 7-10 days
-immunocompromised may develop chronic infx
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
ranges from moderate diarrhea to severe lasting 20 days in immunocompromised
common infx in AIDS; diarrhea can be irreversible and life threatening
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
Trichuris trichiura
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
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
profuse diarrhea with dehydration and electrolyte imbalance; fatal if immunosuppressed
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
itching and mild diarrhea
contaminated fingers
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
contaminated food/water; spread person to person and they can cary it for months or years
-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
fever, aches, repiratory problems, resembles flu-like illness, diarrhea, or constipation, transient rose spots in the upper abdomen (may disappear)
-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
chloramphenicol, ampicillin, ciprofloxacin
good hygiene, exclude carriers from food handling, gallbladder removal in carriers
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
uncooked foods= pate, milk, soft cheese, coleslaw
inflammation and damage to the liver
Virus (A, E, B, C) or bacteria (less common)
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?
what type of virus is Hep A (HAV)
fecal-oral route (excreted in lg. amounts in feces)
incubation period:
2-4 weeks
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?
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
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:
-age (infants)
-males more than females
complications of HBV
-hepatocellular carcinoma
How likely are hep B carriers to develop liver cancer
200 times more likely than non carriers
HBsAg (antigen) remains in carriers and is detected
interferon alpha, vaccine
What is Hep C most common with
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
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
development of heart, brain, eyes, ears; low birth weight and eye and heart lesions
25% develop what
where does virus replicate
totally- vaccine before pregnancy
how many fetuses are infected after primary maternal infx with CMV?
40%; 5% show signs at birth
mental retardation, spasticity, eye abnormalities, hearing defects, hepatosplenomegaly, anemia
in clinical trials
where's con. syphillis common
developing countries
rhinitis, skin/mucosal lesions, hepatosplenomegaly, and bone, teeth, and cartilage abnormal
treat mom before 4th month
cause of toxoplasmosis:
Toxoplasmosis gondii
microcephaly, convulsions, chorioretinitis, hepatosplenomegaly, jaundice, mental retardation, defective vision
women avoid contact w/ cat feces or lightly cooked meat
HIV abnormalities:
poor weight gain, sepsis, developmental delays, oral thrush, pneumonitis, diarrhea, AIDS
mom take AZT
Listeriosis sn/sx in mother:
flu-like sx or asymptomatic
abortion, premature delivery, neonata septicemia and neurological damage
penicillin, ampicillin
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
invasion across the blood-brain barrier
invasion across the blood-cerebrospinal fluid
is invasion via peripheral nerves common?
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":
turbid CSF, "septic":
pyogenic bacteria
which is more severe
which is more common
bacterial agents:
Neisseria meningitidis, Haemophilus influenzae, and Streptococcus pneumoniae
cause of meningococcal meningitis:
Neisseria meningitidis
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
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
100% if untreated, 10% if treated; serious/lasting complications not common
penicillin, ampicillin ASAP! if suspected
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
less frequently fatal but 10% higher incidence of lasting complications
hearing loss, delayed language development, mental retardation, seizures
yes- children 6 mos. and older
rifampicin to close contacts
cause of pneumococcal meningitis:
Streptococcus pneumoniae
where is it carried?
in the throats of healthy people
20-30% in treated cases
sequela such as deafness in 15-20% of treated cases
polyvalent (23 serotype) vaccine
which is an important cause of miningitis in immunocompromised adults, esp, renal transplant and cancer pts.
Listeria mnoncytogenes
ampicillin and gentamicin
causes of neonatal meningitis:
E. coli and group B hemolytic streptococci
fatal in 35%
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
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
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
amphotericin B
Protozoan meningitis:
-Naegleria and Harmanella
-multiply in stagnant water in warm countries
-high mortality
inhaled or swallowed and reach meninges via the olfactory tract
Most common type of meningitis:
-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
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
Poliovirus sn/sx
1-4 days of fever initially, sore throat, malaise, meningeal sn/sx, paralysis, motor neuron problems
used to be- CNS disease in less than 1% of those infected now
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
virus travels up peripheral nerves to CNS; once in brain it spreads cell to cell until many neurons are infected; invades limbic system
4-13 weeks (the further the bite from the CNS, the longer the period)
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
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
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
-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
after 3-21 days: exaggerated reflexes, muscle rigidity, uncontrolled muscle spasms, lockjaw, neck stiffness, dysphagia; spasms can lead to injury/respiratory failure
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
after 2-72 hrs., descending weakness, flaccid paralysis, dysphagia, vomiting, vertigo, respiratory muscle failure
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)
this typically contains abundant yellow creamy pus formed by organisms and dead WBCs:
what can inward drainage of an abcess lead to?
peritonits, empyema, or meningitis
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
minor lesion initally but toxin causes destruction of intercellular connections and separates epidermis from dermis
-large blisters with clear fluid
-entire skin lost
-irritable, uncomfortable
-rarely severely ill
fluid replacement and cloxacillin
What causes TSS?
TSS-toxin prodcucing Staph aureus
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
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
well defined spreading erythromatous inflammation on face, legs or feet; fever, pain
penicillin per os or IM
If infx with strep pyogenes is deeper than erysipelas, it may infect subcutaneous fat causing:
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
antibiotics, surgical debridement
This resembles bacterial gangrene but is more acute and highly toxic causing widespread necrosis:
Necrotizing fascitis (flesh eating bacteria)
radical excision, local and systemic antibios
cause of gas gangrene:
clostridium perfringens
-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
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
tetracycline, erythromycin, vitamin A derivates (isoretinoin)
cause of leprosy:
mycobacterium leprae
are there more organisms in nasal secretion or skin lesions
nasal secretions
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
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
affects hair and scalp
affects body
thickening, dry , scaly skin, cracks between toes, hair loss
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
cauliflower like
what do HPV1 and 4 cause
plantar warts: flat
what causes common warts
HPV 2, 3, 10
-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
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
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
what does VZV cause
chicken pox (varicella) and zoster (shingles
what group does VZV belong to
inhalation from respiratory secretions and saliva or by direct contact of lesions
Primary infx with VZV causes:
chicken pox
reactivation causes:
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
erythromatous rash in thoracic region, severe pain
predispostion to zoster if:
-increasing age
-leukemia, lymphoma, AIDS, renal transplant (ImunoComp)
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
intimate contact-airborne droplets, salivary secretions and possibly urine
-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
painful tender and swollen parotid gland: classic 30-40% of cases
1 week, life long resistance
none, live attenuated vaccine
how many serotypes of rubella?
droplet infx
more or less contagious than measles
-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
after 14-21 days, milde disease, fever, malaise, and maculopapular rash lasting 3 days
live attenuated vaccine
what is the lgst human herpes virus
how many serotypes
saliva "salivary gland virus", urine, semen, cervical secretions, blood transfusions, organ transplant
-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
assymptomatic; mabye fever in young adults
may lead to:
1. fetal malformations
2. interstitial pneumonia
ganciclovir; no vaccine
EBV transmission
saliva, kissing
-replicates in B lymphocytes binding to Cd3 receptors
-T lymphos respond to infected B's
-remains latent in some B's
what are sn/sx attributed to?
immunologic response--cytokines released
-infants/children: none or weak
- mono, fever, sore throat, petechiae on hard palate, lymphadenopathy, splenomegaly, anorexia, lethargia
Immunodeficiency can lead to:
reactivation with no symptoms
no antivirals; acyclovir useful; no vaccine
EBV is closely related to
Burkitts lymphoma; co-carcinogen is marlaria (weakens t cells)
where is it restricted to
Africa and papua new guinea
Smallpox (variola) caused by:
person to person via contact with skin lesions and via respiratory tract
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)
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
Africa, central/south america, and caribean
-virus enters blood vessel
-spreads to vascular epithelium and liver
-2-6 days incubation
fever, headache, muscle ache; severe- shock, severe liver damage
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
-virus replicates in monocytes and in vascular epithelium
-incubation 4-8 days
-increased cytokine release into circulation
malaise, fever, nausea, vomiting, maculopapular rash
dengue hemorrhagic fever syndrome- children endemic 10% mortality
what does incre'd cytokine release cause
vascular damage, shock, hemorhging into GI tract and skin