Micro final 24,25,26

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croth247  on December 8, 2010

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microbiology

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Micro final 24,25,26

S. pyogenes (GAS) Group A Strep
Streptococcal pharyngitis (Strep Throat)
-local inflammation and fever
complications may include tonsillitis and otitis media
Diagnosis- agglutionation test
**penicillin is drug of choice
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S. pyogenes (GAS) Group A Strep Streptococcal pharyngitis (Strep Throat)
-local inflammation and fever
complications may include tonsillitis and otitis media
Diagnosis- agglutionation test
**penicillin is drug of choice
S. pyogenes - lysogenized produces erythrogenic toxin (red producing, strawberry) and sandpaper rash
-Scarlet fever,
Corynebacterium diphtheriae begins with sore throat and fever, followed by malaise and swelling of the neck and pseudomembrane formation which blocks airflow.
Lysogenized C. diphtheriae produces diptheria toxin, and ***exotoxin--very potent
*Treatment- Antitoxin therapy, DTaP
-clubbed cells
Otitis media middle ear infection -> earache ( pressure on eardrum)
-caused by many different bacteria/viruses
-Upper respiratory infection.
- characterized by the production of pus which created pressure on the eardrum.
Amoxicillin??
Rhinoviruses, coronaviruses (families) Common cold, S/S include sinus infection, laryngitis, otitis media, --transmission may be airborne
prevent/treat= ICAM decoy
Bordetella pertussis Whooping cough (aka Pertussis)
-aerobic, gram negative, coccobacillus, virulent strains produce a capsule. has a Tracheal cytotoxin, and pertussis toxin
Tracheal cytotoxin kills ciliated cells
pertussis toxin systemic effects of the disease
-M/O may attach to trachea and block ciliary escalator.
Stage of whooping cough - cararrhal similar to common cold
Stage of whooping cough - Paroxysmal typically lasts 1-6 weeks
-characterized by sieges of coughing (clear mucus) and gasping inbetween breaths=whooping sound
Mycobacterium tuberculosis "consumption" airbone transmission only in active cases
**BCG vaccine (Bacillus of Calmette and Guerin)
--live, but avirulent, culture of M. bovis
-cells contain mycolic acid> acid-fast
TB pathogenesism/o enter lungs=phagocytosed by macrophages
- enzymes/cytokines cause tissue inflam, if disease arrested, tubericales become calcified, **visiable as ghon complexes
- if defenses fail--> **military TB- turbicles burst releasing the pathogen into the airway. (active)
----S/s include - weight loss, coughting (w/blood) malaise
Tb treatment isonizid, rifampin, pyrazinamide, ethambutol,
-WHO recommends 6mo minimus of antimicrobial therapy with 2 first line and 1or2 second line drugs
= lack of patient treatment compliance->drug Resistance
MDR Mixed drug resistant
XDR Extensively drug resistant
TB diagnosis skin test (mantoux) look for "wheal"
sputum smears, chest X-Ray, PCR
S. Pneumoniae generally, lower lobe infections
S/S - rapid onset, fever, breathing difficulty, chest pain, ***rust-colored sputum.
"atypical" pheumonia may be caused by other m/o such as fungi, viruses and other bacteria
-----slower onset and less chest pain than typical
Heamophilis influenzae "atypical" pheumonia - affects those with *pre-disposing conditions such as poor nutrition, cancer, diabetes, alcoholism
Mycoplasma pheumoniae "atypical" pheumonia - "walking pneumonia" - pretty mild, m/o doesnt have a cell wall
Legionella pneumophilia Gram-neg rod characterized by high fever (105F) cough
-droplett transmission
- found in a/c tower
Burkholderia pseudomallei Meliodosis (Lower resp)
S/S include bone/joint infections, liver/speen abcesses, Genito-urinary infection
other- pneumonia, abscesses, encaphalitis, sepsis, fever, night sweats, myalgia, headache
***Transmission is primarlily inhalatior, Zoonotic(transfer to human)
Viral pneumonia -seldom confirmed by culture
-somst common RSV - respiratory syncytical virus
Influenza (virus) S/S- chills, fever, headache, muscle aches
--virus has 2 types of envelope "spikes"
Variations in the H and N proteins(antigens) account for the "types of the flu"
- segmented genome for easy exchange with other viruses
antigenic shift (responsible for major outbreaks) major change due to recombination of the viral genome
-"mixing vessels"
Histoplasma capsulatum dimorphic fungi>disease resembles TB-pathogens spread from lungs to blood to lymph
Blastomyces dermatitidis S/s cutaneous ulcers, abscesses, lungs
-affects hunting dogs
Streptococcus mutans gram positive coccus,Cariogenic-caries or tooth decay causing
M/O+biofilms accumulate> dental plaque
Tartar "old Plaque"
S. mutans must attach via a pellicle (proteins that allow attachent to teeth) and avoid "defense mechanisms" - salvia/ lysozome
Hydrolyze sucrose -> glucose and frutose
glucose is assembled into dextran (Hold MO on teeth)
bacteria + dextran = plaque
Frutoseis fermented to.. lactic acid which breaks down tooth enamel
-enamel low in fluoride is expecially susceptable
Preventing tooth decay minimal ingestion of sucrose - sugar alcohols are good though
-brushing, flossing, professional cleaning, fluoride treatment, mouthwash
** the invading population of bacteria is not the same as the colonizing population.
Periodontal disease inflamm and degen of structures that support the teeth
Gingivitis streptococcim actinomycetes, anaerobes, gram-neg
***-characterized by bleeding while brushing
Porphyromonas gingivalis Periodontitis, progressive gingivitis- gums are inflamed and bleed easily, - supportive tissue and bone are destroyed= bone loss
Staph food poisoning an intoxication: injestion of a pre-formed toxin(like botulism)
heat-stable enterotoxin produced by * S. aureus
S/S -NVD, 1-6 hours after ingestion
--Superantigen-intense non-specific immune response.
Staph food poisoning cause suspect foods are contaminated on fingers or in skin lesions and "outcompete" other bacteria - other bacteria killed
**all other bacteria killed in cooking but somebody touched the food
-- Food prepared in advance and not properly chilled allows proliferation of the organism/ toxin production
salmonella spp. gram neg, facultative rod, over 2400 serovars (types)
-m/o are ingested/multiply in the lower GI tract - infection
**can invade intestional mucose and may enter CLS
*** M/O can replicate in macrophages
- meat/poulty/egg products are most common source of contamination
Salmonellosis incubation time typically 12-36 hours
S/S - moderate fever, nausea, diarrhea abdominal cramps
Salmonella typhi Typhoid Fever, highly virulent, Fecal-oral contamination
Humans are only reservoir,
typical incubation period is 2-3 wk
M/O multiply in phagocytic cells > disseminated thoughout the body
Salmonella typhi symptoms fever (104F), headache, diarrhea (possibly bloody)
---treated with antibiotics, longer if carrier
-Some indiviiduals may be "carriers"
shigellosis etiologic agent members of the Shigella genus
-S. sonnei, S. dysenteriae, S. flexneri, S. boydii
-small infective dose--produces *shiga toxin
shiga toxin inhibits protein synthesis and kills cells (exp macrophages) destroyes the intestinal mucosa
shigellosis symp and treat s/s ***Severe dysentery- 20 bm/day (possibly bloody), cramps, fever
treat- antibiotics (fluocoquinolones)+ oral hydration
anytime there is an invasion of tissue there is a fever
Virbrio cholera MO enter the GI tract and proliferate in the **Small intestine (olny one to be in the small intestine)
- produces an **enterotoxin that results in rapid loss of body fluids and electrolytes
-pathogen is associated with brackish water and is endemic in US coastal waters
Cholera S/S "rice water stools" and vomiting, generally no fever (no invasion) Blood becomes viscous-- organ shutdown, shock, death
Cholera Treatment fluid and electrolyte replacement
--- 0:1 and 0:139 are primary epidemic strains
Vibro parahaemolyticus common in salt water
- assoc with raw oysters, shrimp, and crabs
Yersinia enterocolitica and Y.pseudotuberculosis transmitted in meat and milk
S/S include diarrhea, fever, headache and abdominal pain
Clostridium perfringens (gangrene) Produce Exotoxin-> abdominal pain/ diarrhea
S/S appear 8-12 hr after injestion
Escherichia coli pathogenic strains produce toxins and have specialized fimbriae to attach to cells - 3 types
Escherichia coli - Entertoxigenic (ETEC) "travelers diarrhea" watery, copious
"boil it, peel it, or don't eat it"
Escherichia coli - Enteroinvasive (EIEC) Invade epthelial cells causing inflammation, fever, and dysentery
Escherichia coli - Enterohemorrhagic (EHEC) 0157:H7, produce shiga toxins, associated with hemolytic uremic syndrome and hemorrhagic colitis.
--low infective dose
Campylobacter jejuni Gram-negative, **spiral-shaped bacteria
Nearly all poultry is comtaminated
S/S fever, cramping, ab pain, diarrhea that may progess to dysentery
Campylobacter jejuni complication Guillain-barre syndrome (1:1000)
-body attacks our nerves because it thinks that its the MO
Helicobacter pylori Infection in stomach= enxyme to combat stomach acid
-_- MO eats away at stomach mucosa
Paramyxovirus Mumps - *parotid glands, fever, and pain.
Transmitted via saliva and respiratory secretions
Incubation - 16days post exposure
*** MMR vaccine
Mumps complications Orchitis (swelling of the testes), meningitis, inflam of the ovaries and pancreatitis
Hepatitis inflam of the liver
Hepatitis A infectious - Fecal-oral transmission (shed in feces
incubation 2-6 wk
S/S - subclinical - fecer, headache, malaise, diarrhea, jaundice
Inactivated Vaccine
Hepatitis B Serum - parenteral transmisson, gen more severe hep A
Vaccine available
liver cancer is subsequent complication
Hepatitis C paternal transmission
-no vaccine
S/S like that of HBV
Hepatitis D Host must be coinfected with *HBV
Paternal transmission, associated with severe liver damage and high mortality rate, vaccine for HBV
Hepatitis E Fecal-oral transmission
symptoms similar to HAV (same transmissson)
high mortality rate for preg women, vaccine developing
Rotavirus most common cause of viral gastroenteritis
Self limiting ~7 days
Low grade fever, diarrhea, vomiting
Nortoviruses (norwalk agent) Fecal-oral and aerosol transmission
20 million (lots) of cases in US
S/S - NVD, cramps
Self limiting ~ 3 days
Urine should be sterile may become contaminated near the end of the urethra
E. Coli is the usual case for UTI's may be dangerous as "ascending" infections --> pyelonephritis
urethritis--> Cystitis usual suspects are E. Coli and S. saprophyticus
Neisseria gonorrhoeae attaches to oral or urogenitial mucosa by fimbriae, invades columnar epithelial cells. aquired at any point of contact. Invasion leads to an inflammatory response and PUS formation.
Neisseria gonorrhoeae symptoms females asymptomatic -->sterility, complication PID
Males --> painful urination, PUS discharge, sterility
Untreated can become systemic-----> Endocarditis, meningitis, arthritis, opthalmia neoatorum
Neisseria gonorrhoeae treatment/ diagnosis detecting pus or cervical swab, M/o can be found in phagocytic leukocytes.
----treated with antibiotics (cipro)
********** recovery does not lead to immunity
Nongonococcal urethritis any inflamm of the urethra not caused by N. gonorrhoeae.
5x more in females than males.
infects same cells as gonnorhea -- columnar epithelium
Chlamydia trachomatis more common cause of Nongonococcal urethritis
-Treatment inlcueds tetracyclines--gets into the infected cells
Pelvic inflammatory disease any bacterial infection of the FEMALE pelvic organs
--characterized by abdominal pain, blocked uterine tubes may lead to Ectopic pregnancy/ salpingitis
--M/o hitch ride on sperm cells and be transported to uterine tubes --- treatment doxycyline/ cefoxitin
Pelvic inflammatory disease caused by N. gonorrhoeae
C. trachomatis is common co-infection
Salpingitis results from scarring that blocks passage of the egg to the uterus. Diagnosis inflives laparoscopy
Treponema pallidum syphalis, transmitted via ANY sexual contact, typical incubation period is 3 weeks. disease has 4 stages
syphalis Primary stage painless CHANCRE AT SITE OF INFECTION, exudate is highly infectious
-treated with penicillin
syphalis secondary stage Several weeks after frimary state, skin and mucosal rashes, HAIR LOSS, malaise, fever
-treated with penicillin
syphalis latent period no symptoms, not normally infectious
syphalis Tertiary Gumas on many organs (rubbery lesions) ---> CNS
Gardnerella vaginalis Bacterial vaginosis---> infection of the vagina (NO SIGN OF inflammation) vaginal PH aboce 4.5, odor, frothy discharge
diagnosis based on smell and "clue cells"
Treatment-- metronidazole- allows normal flora to grow
"clue cells" sloughed off vaginal cells covered with G. vaginalis
candidiasis odor-- yeasty/ none
color of discharge--- white
apprearance of vaginal mucosa--- dry, red
ph---below 4
Bacterial VaginOsis odor-- fishy*
color of discharge--- grey/white
apprearance of vaginal mucosa--- pink
ph--- above 4.5
Trichomoniasis odor-- Foul
color of discharge--- Greenish-yellow*
apprearance of vaginal mucosa--- Tender, red
ph--- 5-6
Human papillomaviruses Genital warts/ Genital herpes/ condyloma acuminata
Treatment- patient applied gels0 Imiquidmod (aldara) to stimulate inferferon production
Ceravix and gardasil --- vaccine
condyloma acuminata Genital warts, HPV16 associated with cancer
women: cervix Men:penis
if have visual on genital warts, you are not infected with strains that lead to cancer

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