Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
256 Cards in this Set
- Front
- Back
|
Gram, catalase, hemolysis, and coagulase for Staph aureus?
|
Gram positive
Catalase + beta-hemolytic coagulase + |
|
|
What two possible organisms for:
gram+, catalase+, beta-hemolytic, coagulase- |
Staph epidermidis, or Staph saprophyticus
|
|
|
3 Toxins of Staph aureus
|
Exfoliatin, enterotoxin (food poisoning), and toxic shock syndrome toxin (TSST-1).
|
|
|
Tissue-destroying proteins of Staph aureus?
|
Hyaluronidase, staphlyokinase (lyses clots), and lipase.
|
|
|
What is the 2nd most common cause of UTI in young, sexually active women?
|
Staphylococcus saprophyticus.
|
|
|
What type of metabolism is the Staphylococci species?
|
Facultative anaerobe
|
|
|
First three lines of drugs for non-MR Staph aureus?
|
1. nafcillin
2. 1st gen cephalosporin 3. Clindamycin |
|
|
First 5 lines of treatments for MRSA?
|
1. Vancomycin IV
2. Daptomycin IV 3. Clindamycin IV and oral 4. Trimethaprim-Sulfamethoxazole (Bactrim) 5. Linezolid IV and oral |
|
|
Treatment for Staph saprophyticus?
|
Penicillin
|
|
|
What are the two important gram-positive spore-forming rods?
|
Bacillus and Clostridium
|
|
|
What is the main illness that Bacillus cereus causes? What virulence factors are responsible for that?
|
Food poisoning. 2 enterotoxins: heat-labile toxin (diarrhea+), and heat-stable toxin (diarrhea-)
|
|
|
How does Bacillus cause food poisoning?
|
B. cerus deposits spores in food, which then survive the cooking process. They germinate in the food and begin releasing enterotoxin.
|
|
|
What metabolism are the Bacillus species?
|
Aerobic
|
|
|
What 2 types of food are associated with botulism?
|
Smoked fish and home-canned vegetables.
|
|
|
How is Clostridium similar and different from Bacillus?
|
Similar because they are both gram-positive, spore-forming rods. Different because Clostridium is anaerobic.
|
|
|
How does botulinum toxin work? What does it cause?
|
Blocks the release of ACh at presynaptic terminals in ANS and motor endplates. Causes flaccid paralysis.
|
|
|
Describe how food gets contaminated with Botulinum toxin?
|
Clostridium botulinum spores float through the air and land on food. If food is undercooked and placed into an anaerobic environment (canned goods, ziplock bags), the spores mature and bacteria release their toxin. Eating the contents weeks later results in botulism.
|
|
|
How does infant botulism occur?
|
When infants ingest food contaminated with C. botulinum spores.
|
|
|
What is the toxin released by Clostridium tetani?
|
Tetanospasmin
|
|
|
How does tetanus toxin act?
|
Taken up at the NMJ, and transported to the CNS. There is acts on inhibitory interneurons to prevent the release of GABA. This allows motor neurons to send many impulses to muscle cells, which results in sustained tetanic contraction
|
|
|
What causes gas gangrene?
|
Clostridium perfringens
|
|
|
What environment is favorable for C. perfringens?
|
Deep wounds with lots of dead tissue creates an anaerobic environment.
|
|
|
What is a classic sign of cellulitis caused by C. perfringens?
|
Crepitus: crackling upon wound palpation due to pockets of gas.
|
|
|
What is the most dangerous condition caused by Clostridium perfringens?
|
Clostridial myonecrosis.
|
|
|
How are Clostridium and Bacillus species transmitted?
|
endospores
|
|
|
What is the heat-labile entertoxin of B. cereus similar to?
|
The cholera enterotoxin.
|
|
|
What exotoxins does Clostridium difficile produce?
|
Toxin A: diarrhea
Toxin B: Cytotoxic to colonic epithelial cells. |
|
|
what is the metabolism of Listeria monocytogenes?
|
facultative anaerobe
|
|
|
describe listeria in terms of spores, morphology, and gram stain
|
Non-spore forming and gram-positive rod.
|
|
|
describe the motility of listeria
|
Flagellar motility outside host. Non-motile at 37degrees (inside host)
|
|
|
Is listeria intra- or extracellular?
|
Facultative intracellular
|
|
|
What food source(s) is Listeria most commonly contracted from?
|
Contaminated raw milk or cheese from infected cows.
|
|
|
What toxins do Listeria produce, and what do they do?
|
Listeriolysin O and phospholipases. They allow escape from the phagolysosomes of macrophages.
|
|
|
What metabolism is Neisseria gonorrhoeae?
|
Facultative anaerobe
|
|
|
What is the name of the syndrome if N. gonorrhoeae enters the bloodstream?
|
bacteremia-arthritis syndrome
|
|
|
What endo- and exotoxins does gonococcus have?
|
Only endotoxin: LPS.
|
|
|
What are the virulence factors of N. gonnorrhoeae?
|
Pili, IgA protease, porins, opacity proteins.
|
|
|
What does Neisseria gonorrhoeae cause?
|
Urethritis in men, and cervicitis in women. Cervicitis can progress to PID.
|
|
|
Treatment for N. gonorrhoeae?
|
Third-generation cephalosporin, plus a macrolide or tetracycline to cover Chlamydia.
|
|
|
Does infection with gonococcus induce future immunity?
|
NO. A person can be reinfected multiple times.
|
|
|
What is the main reason that N. gonorrhoeae does not disseminate like N. meningititis?
|
Gonococcus does not have a polysaccharide capsule
|
|
|
What are the virulence factors of pathogenic E. coli?
|
Fimbriae: colonization factor.
Siderophores Adhesins Capsule (K-antigen) Flagella (H-antigen) |
|
|
What toxins does E. coli produce?
|
LT (heat labile): increases cAMP like cholera toxin.
ST (heat stable): increase cGMP. Shiga-like toxin: Inhibits protein synthesis by inactivating 60S subunit. |
|
|
Enterotoxigenic E coli (ETEC)
|
Infection similar to cholera due to ST and LT toxins. Traveler's diarrhea.
|
|
|
What is EIEC similar to?
|
shigellosis
|
|
|
Symptoms of shigellosis (or EIEC)?
|
abdominal cramps with pus and blood in stools.
|
|
|
What is enteropathogenic E coli (EPEC) associated with?
|
Outbreaks of infant's diarrhea.
|
|
|
What strain is EHEC?
|
O157:H7
|
|
|
How does EHEC exert its ill effects?
|
A shiga-like toxin that is responsible for damage to colonic epithelium and mesenteric blood vessels.
|
|
|
What serious complication is there for EHEC?
|
Hemolytic uremic syndrome (HUS)
|
|
|
What two symptoms differentiate EIEC from EHEC?
|
EIEC has fever and pus in the stool while EHEC has neither of those symptoms.
|
|
|
What is the first-line treatment of E. coli?
|
cephalosporins
|
|
|
What are four major diseases caused by E. coli?
|
Newborn meningitis, UTI, sepsis, diarrhea.
|
|
|
What is the causative agent of bacillary dysentery?
|
Shigella dysenteriae
|
|
|
What are the symptoms of dysentery?
|
painful cramping; bloody, mucous-tinged stools of small volume; prostration; fever.
|
|
|
What is blood and mucous in stool indicative of?
|
An invasive organism.
|
|
|
How is Shigella transmitted?
|
fecal-oral route
|
|
|
What does Shigella invade?
|
submucosa of intestinal tract, but not the lamina propria
|
|
|
How does Shiga toxin work?
|
Inactivates the 60S ribosome
|
|
|
What type of E. coli are Shigellosis symptoms similar to?
|
EIEC
|
|
|
Treatment for Shigella?
|
Fluoroquinolones only for severe cases. It could cause HUS.
|
|
|
What type of antibody is best for immunity to Shigella?
|
IgA
|
|
|
Are Shigella species motile?
|
NO
|
|
|
Who are the two typical populations infected by Shigella?
|
Pre-school age children, and people in nursing homes
|
|
|
Is Shigella ever a part of the normal flora?
|
NO!
|
|
|
Do ETEC and cholera elicit fever? Why?
|
They do NOT elicit fever because they don't invade the mucosa.
|
|
|
Describe the structure of Shiga toxin
|
A-B toxin. One A unit bound to 5 B units. B binds to the microvillus membrane in the colon, allowing entry of the deadly A subunit.
|
|
|
What serious sequela is possible after Shigellosis?
|
HUS
|
|
|
What is the single most important factor affecting virulence of Shigella?
|
The ability to invade M cells.
|
|
|
What are the 6 enteroinvasive pathogens?
|
Salmonella, Shigella, Yersinia, Campylobacter, Listeria, and EIEC
|
|
|
What characterizes enteropathogenic infection?
|
Destruction of epithelial cells without invasion.
|
|
|
Describe Salmonella in terms of shape and gram stain
|
Gram-negative rod
|
|
|
What causes Typhoid Fever?
|
Salmonella typhi
|
|
|
How is Typhoid Fever transmitted?
|
Person to person by contaminated food.
|
|
|
What is the other name of Typhoid fever?
|
Enteric Fever
|
|
|
In what way does Salmonella typhi go beyond Shigella and EIEC?
|
After invading the epithelium, it invades the regional lymph nodes to seed multiple organ systems. They are phagocytosed and survive intracellularly
|
|
|
What is the most common kind of Salmonella infection?
|
Salmonella enterica causing gastroenteritis
|
|
|
What is the reservoir of Salmonella enterica? How is it transmitted?
|
Animals. Animal feces contaminating human food
|
|
|
Where is the Salmonella typhi located in chronic carriers?
|
In their gallbladder.
|
|
|
What helps Salmonella typhi evade phagocytosis? How is that different from non-typhoid Salmonella?
|
Encapsulation. Non-typhoid species are NOT encapsulated.
|
|
|
Is Yersinia motile?
|
yes
|
|
|
In what symptom is Yersinia infection different than other invasive bacteria?
|
Diarrhea is watery
|
|
|
What condition does infection by Yersinia mimic?
|
Appendicitis
|
|
|
What does Campylobacter jejuni look like?
|
Vibrio cholerae
|
|
|
What are the 3 most common causes of diarrhea in the world?
|
Campylobacter, ETEC, and rotavirus
|
|
|
What is the metabolism of Campylobacter?
|
Microaerophilic
|
|
|
What can 50% of Campylobacter infections be traced back to?
|
Contaminated chickens
|
|
|
How does cholera toxin work?
|
It is an A+B toxin. The A1 subunit ADP-ribosylates the Gs subunit and thus stabilizies adenylate cyclase in its active conformation. This results in rise in cAMP levels.
|
|
|
Describe the shape and gram stain of Helicobacter pylori
|
Spiral-shaped gram negative
|
|
|
What allows H. pylori to survive in the stomach?
|
Urease breaks down urea into CO2 and ammonia, which reduces the acidity around it.
|
|
|
What toxin does H. pylori release?
|
vacA, which causes vacuolation of cells and leads to apoptosis.
|
|
|
What is the treatment for H. pylori infection?
|
Antibiotics+Pepto-bismal
|
|
|
Why is antibiotic use for EHEC risky?
|
HUS
|
|
|
What are the two mechanisms of entry for invasive bacteria into non-phagocytic cells?
|
Zipper and trigger (endocytosis).
|
|
|
What is the difference in carriers between S. typhi and non-typhoid Salmonella species?
|
S. typhi is only humans. Non-typhoid species are zoonotic.
|
|
|
What is the genome of rotavirus?
|
Segmented dsRNA
|
|
|
What is the major viral attachment protein of rotavirus?
|
VP4
|
|
|
What must happen to VP4 for rotavirus to become infectious?
|
Must be cleaved by intestinal trypsin
|
|
|
What type of diarrhea does rotavirus cause?
|
watery
|
|
|
genome of norovirus
|
+sense ssRNA
|
|
|
Does rotavirus produce an enterotoxin?
|
yes
|
|
|
Does norovirus produce an enterotoxin?
|
no
|
|
|
What is the antibody response to norovirus?
|
IgG but not much IgA
|
|
|
Genome of astrovirus?
|
+sense ssRNA
|
|
|
What 3 viruses are classified as enteroviruses?
|
Poliovirus, Coxsackievirus, and echovirus.
|
|
|
What is abortive poliomyelitis?
|
When the symptoms of malaise, headache, fever, and nausea resolve in a few days.
|
|
|
What do ribosomes load on to for enterovirus genomes?
|
IRES sequences
|
|
|
How are enteroviral proteins produced?
|
Ribosomes load on to IRES, translate entire genome to one peptide. VIRAL proteases then cleave the single peptide into the many proteins of the virus.
|
|
|
How does poliovirus shut down host cell translation?
|
Its protease degrades host cell cap-binding complex (CBC)
|
|
|
Describe the antibody response to the inactivate poliovirus vaccine. What is the implication of that?
|
Good IgG response, but NO IgA response in the gut or nose. The vaccine protects against paralytic polio, but not gut infection. Therefore the vaccinee still sheds virus in their feces.
|
|
|
Describe the oral polio vaccine
|
Attenuated virus replicates in the oropharynx to stimulate nasal IgA and duodenal IgA. The viruses disseminate into the blood to induce IgG response. The vaccinees shed live attenuated virus in their feces.
|
|
|
What are the two differences between the live attenuated and killed virus vaccines in terms of their antibody response?
|
Live attenuated virus vaccine induces duodenal IgA and Nasal IgA, while the killed virus does not. All the other antibody responses (e.g. serum IgG) are the same.
|
|
|
What is the genome of Hepatitis A virus?
|
+sense RNA
|
|
|
How many ORFs for HAV?
|
One ORF
|
|
|
Describe the HAV effect on host cell
|
Host cell can still translate its own proteins CAP-dependently while virus has its RNA translated via IRES. The virus does not directly kill the cell per se.
|
|
|
How is HAV acquired?
|
Orally
|
|
|
What causes the damage to the liver in Hepatitis A?
|
The immune system.
|
|
|
Is Hepatitis A ever chronic?
|
NO. The cell-mediated immunity clears the virus.
|
|
|
What two hepatitis viruses cause only transient infection?
|
A and E
|
|
|
What is it that only HAV and HEV are transmissible through the feces?
|
They are naked while the other hepatitis viruses are enveloped. The others' envelopes get digested by the bile.
|
|
|
By how many days does virus shedding precede HAV symptoms?
|
10-14 days
|
|
|
Is there progression to hepatocellular carcinoma for HAV infection?
|
NO. Also there is no chronic carrier state.
|
|
|
How many ORFs for HEV?
|
3
|
|
|
Is HEV infection ever chronic?
|
NO
|
|
|
Define definitive host.
|
The host in which a parasite completes the sexual phase of its life cycle.
|
|
|
What is a trophozoite?
|
The motile lifecycle phase of a protozoan parasite.
|
|
|
Do trophozoites usually live outside in the environment?
|
no. The parasite is spread through cysts.
|
|
|
How is giardia spread?
|
Contaminated water or person-to-person (especially daycares)
|
|
|
What type of diarrhea does giardia cause?
|
Steatorrhea and flatulence.
|
|
|
What is the most important pathogenic amoeba?
|
Entamoeba histolytica
|
|
|
How is E. histlytica transmitted?
|
Cysts in feces contaminate food or water, and cysts mature in human intestinal tract.
|
|
|
What is a severe amoebic infection called?
|
Amoebic dysentery.
|
|
|
Where do amoeba frequently form abscesses?
|
liver
|
|
|
Why is it difficult to diagnose E. histolytica from feces? 2 reasons
|
1. Cyst excretion during chronic infection is very low.
2. During acute infection, E. histolytica cysts are indistinguishable from the non-pathogenic E. dispar cysts. |
|
|
What animal is a host for Cryptosporidium parvum?
|
Cows
|
|
|
For which Cryptosporidium species are humans the only host for?
|
C. hominis
|
|
|
What pathogen is associated with public swimming pools?
|
Cryptosporidium
|
|
|
What is the infective stage of Cryptosporidium?
|
Oocysts
|
|
|
What type of diarrhea does Cryptosporidium cause? For how long after resolution do patients still shed oocysts?
|
Watery. Weeks after resolution of symptoms.
|
|
|
Is Cryptosporidium intra- or extracellular in the GI tract?
|
Intracellular
|
|
|
What are the 3 ways amoeba damage host cells?
|
Direct cell-cell contact via lectins; contact-dependent killing via insertion of amebapores into host membrane; Ingestion of killed host cell (like RBCs)
|
|
|
For what types of nutrients does Giardiasis cause malabsorption?
|
Fat-soluble vitamins.
|
|
|
Common name of Enterobius vermicularis? What type of helminth is it?
|
Pinworm. It is a nematode
|
|
|
Describe how pinworm gets spread
|
Female at night crawls to the perianal area and lays eggs. Eggs get spread by hand to clothes, furniture, and food. The larvae hatch in the intestine and establish in the colon.
|
|
|
What are nematodes also known as?
|
roundworms
|
|
|
What is the largest human intestinal roundworm?
|
Ascaris lumbricoides
|
|
|
Describe the life cycle of Ascaris lumbicoides
|
Female lays eggs in intestine, which are passed in feces. Eggs take 18 days in the environment to become infective (ingested unfertilized eggs are not infectious). Larvae hatch in intestinal mucosa, and are carried via portal system to the lungs. They mature there and ascend the bronchial tree to the throat and are swallowed. Once they reach the small intestine again, they mature into adults.
|
|
|
what is the common name of Necator americanus?
|
hookworm
|
|
|
Describe the life cycle of hookworm
|
Eggs shed in feces. Larvae hatch in feces/soil and after 3 days become filariform larvae, which are infective. When they come in contact with human skin, they burrow in to the vessels, travel to the heart then lungs, ascend the bronchial tree, and are swallowed to reach the intestine.
|
|
|
What other nematode besides Hookworm burrows into human skin?
|
Strongyloides stercoralis
|
|
|
Where do Strongyloides eggs hatch?
|
In the human intestine
|
|
|
What is unique about Strongyloides stercoralis life cycle?
|
It has two of them: free-living and parasitic.
|
|
|
For which nematode is reinfection and auto-reinfection a common occurrence?
|
Strongyloides stercoralis
|
|
|
What is the common name for cestodes?
|
tapeworm
|
|
|
Common names of Taenia saginata and Taenia solium?
|
Beef tapeworm and pork tapeworm.
|
|
|
What is the attachment head of the tapeworm called?
|
Scolex
|
|
|
What is the definitive host for T. saginata and T. solium?
|
humans. beef and pigs are intermediate hosts.
|
|
|
What is a cysticercus?
|
A larval tapeworm in a fluid-filled sac.
|
|
|
what happens when a cow or pig ingests tapeworm eggs?
|
They hatch in the intestine, invade the blood stream, and establish themselves in the muscle, brain, etc.
|
|
|
What is cysticercosis?
|
When a human ingests the EGGS of the pork tapeworm. The eggs hatch in intestine and travel to the muscle and brain where they form cysticerci.
|
|
|
What is neurocysticercosis?
|
When a human ingests pork tapeworm eggs, which hatch into larvae that travel to the brain and form cysticerci.
|
|
|
What is neurocysticercosis a major cause of in Africa?
|
epilepsy
|
|
|
What is the small tapeworm that has a dog-sheep lifecycle?
|
Echinococcus granulosus
|
|
|
What is the definitive host of E. granulosus?
|
dog
|
|
|
What helminth forms hydatid cysts in humans?
|
Echinococcus granulosus
|
|
|
What is a serum marker of active (acute or chronic) and highly infectious HBV infection?
|
HBeAg: a cleavage product of the viral core structural polypeptide.
|
|
|
Antibodies against which HBV antigen provide immunity against HBV infection?
|
HBsAg: surface antigen.
|
|
|
What is the shorthand for the HBV core?
|
HBcAg
|
|
|
How is HBV transmitted?
|
via any body fluids
|
|
|
Can HBV cause chronic hepatitis?
|
YES
|
|
|
What causes the actualy hepatitis during HBV infection?
|
Cell-mediated immune system injury to the liver
|
|
|
What group of people are more likely to be asymptomatic carriers of HBV?
|
immunosuppressed people
|
|
|
What is cirrhosis?
|
Scarring of the liver and loss of hepatocytes
|
|
|
What does the HBV vaccine consist of?
|
Recombinant HBsAg
|
|
|
What does HDV require to replicate? Why?
|
coinfection with HBV. It does not have its own envelope or replication genes.
|
|
|
Specifically what antigen from HBV does HDV use?
|
HBsAg for its coat
|
|
|
How is hepatitis C virus transmitted?
|
Parenterally (body fluids), most often via IV drug use
|
|
|
What percentage of HCV infected patients go on to develop chronic hepatitis? What is the percentage for HBV infected patients?
|
85% for HCV. 10% for HBV
|
|
|
What is the treatment for HCV?
|
Combo treatment of interferon and ribavirin
|
|
|
What 5 things do all retroviruses contain in their RNA?
|
Two long terminal repeats (LTR), as well as the gag gene, pol gene, and env gene.
|
|
|
What are the 2 important functions of LTRs?
|
1. They are sticky ends recognized by integrase, and are involved in insertion in the host DNA.
2. Promotor/enhancer function. Once the LTRs are incorporated into the host DNA, proteins bind to them that can modify viral DNA transcription. |
|
|
what does the "gag" gene stand for? What does it encode?
|
Group antigen. It encodes sequences for proteins INSIDE the envelope: Nucleocapsid, capsid (p24), and matrix proteins. Thus, gag codes for the virion's major structural proteins that are antigenic.
|
|
|
What does the pol gene of HIV encode?
|
It encodes the viral protease, integrase, and reverse transcriptase enzymes.
|
|
|
What does the env gene of HIV code for?
|
Codes for the ENVelope proteins that, once glycosylated, form the glycoprotein spikes gp120 and gp41.
|
|
|
What two herpes species are part of the alphaherpes subfamily?
|
Herpes simplex and varicella-zoster
|
|
|
What two herpes species are part of the betaherpes subfamily?
|
CMV and HHV-6 and 7
|
|
|
What three viruses are part of the gammaherpes subfamily?
|
HHV8, Kaposi's Sarcoma-associated Herpesvirus, and Epstein-Barr virus
|
|
|
Where are alphaherpes viruses latent?
|
neurons
|
|
|
Where are betaherpes viruses latent?
|
macrophages and T cells
|
|
|
Where are gammaherpes viruses latent?
|
B cells
|
|
|
What disease can all 3 virus subfamilies cause?
|
Mononucleosis
|
|
|
What is the pathogenesis of HSV?
|
Extreme cytolytic replication
|
|
|
In what form is HSV DNA latent in DRG neurons?
|
A separate circular viral genome without gene expression.
|
|
|
what are the two most common presentations of HSV-1 infection?
|
Gingivostomatitis: sores on lips, tongue, buccal mucosa.
Pharyngitis with flu-like symptoms. |
|
|
Where is latent infection of HSV-2?
|
Sacral ganglia
|
|
|
What is a serious complicated of primary or reactivated HSV infection?
|
Encephalitis
|
|
|
How can HSV cause keratitis?
|
HSV reaches the cornea via the ophthalmic branch of CN V. Immune system attacks and causes scarring and eventual blindness.
|
|
|
Why is serology not useful for diagnosis of HSV?
|
High prevalence of IgG in the normal population.
|
|
|
What converts acyclovir to its active form?
|
Viral thymidine kinase
|
|
|
How can EBV promote tumorigenesis?
|
Its DNA genome does not integrate into the host cell's DNA. It exists as a separate episome, and during latent infection certain proteins are continually expressed. These proteins are growth-promoters.
|
|
|
What are two types of cancers that EBV can cause?
|
Burkitt's lymphoma, Hodgkin's Disease.
|
|
|
How does HPV cause tumorigenesis?
|
Accidental integration into host DNA can silence the E2 regulatory gene, which allows uncontrolled expression of E6 and E7. They block the Rb and p53 pathways, respectively. This causes genome instability.
|
|
|
What two pathways are mutated in almost all cancers? What are the consequences of each mutation?
|
p53 and Rb tumor suppressors. p53 pathway is a checkpoint, so inactivating it allows unregulated progression into S phase. Rb regulates G1 progression, and inactivation leads to uncontrolled progression through G1.
|
|
|
What protein class primarily determines progression through the phases of the cell cycle?
|
Cyclin-dependent kinases (Cdks).
|
|
|
What are the 3 factors that determine the rate of movement of an STI through a population?
|
1. Transmissibility
2. Rate of new partner acquisition and partners' sexual history. 3. Duration of infectiousness. |
|
|
What segment of the population is primarily responsible for sustained STI prevalence?
|
A small number of individuals with large amounts of sexual partners.
|
|
|
What 3 STI pathogens cause genital ulcers?
|
HSV-2, Treponema pallidum, and Haemophilus ducreyi
|
|
|
What three STI pathogens cause mucosal inflammation?
|
Chlamydia trachomatis, Neisseria gonorrhoeae, Trichomonas vaginalis
|
|
|
What STI pathogen causes epithelial cell changes?
|
HPV
|
|
|
What 4 STIs are reportable in all states?
|
HIV, Chlamydia trachomatis, Treponema pallidum, and Neisseria gonorrhoeae.
|
|
|
What cures Treponemas infection?
|
Penicillin
|
|
|
What forms at the site of innoculation during primary infection with Treponemas (Syphilis)
|
A painless ulcer called a chancre
|
|
|
What are 3 classic signs of the secondary stage of syphilis?
|
Rash on palms and soles, low-grade fever, and generalized enlargement of lymph nodes.
|
|
|
What is a classic sign of tertiary syphilis?
|
Nodular, ulcerative lesions called gummas.
|
|
|
Describe the cell covering of Treponemas
|
Double membrane of cell envelope like in typical gram-negative bacteria, however there is NO LPS and few proteins.
|
|
|
What is the most common non-viral STI worldwide?
|
Trichomonas vaginalis
|
|
|
What are 3 presenting symptoms of female T. vaginalis infection? How often is infection asymptomatic in both sexes? What is the classic physical finding on infected women?
|
Vaginal discharge, itching, and/or dysuria, but asymptomatic infection is common. Asymptomatic infection is even more common in men. "Strawberry cervix" is the classic physical finding.
|
|
|
What is the gold standard for Trich diagnosis?
|
Culture
|
|
|
Is N. gonorrhoeae intra- or extracellular?
|
Intracellular. It invades epithelial cells in the genital mucosa.
|
|
|
How frequent is asymptomatic infection with Gonorrhea?
|
Most women are asymptomatic and many men are, too.
|
|
|
What are the 3 virulence factors of N. gonorrhoeae?
|
1. Pili that are hypervariable
2. Outer membrane porins 3. Opa proteins for adherence and invasion. |
|
|
What happens if N. gonnorrhoeae reaches the blood?
|
It localizes to joints, but causes other systemic symptoms as well.
|
|
|
Does gonnococcus have a polysaccharide capsule?
|
No
|
|
|
Treatment of choice for gonorrhea?
|
3rd-gen cephalisporin.
|
|
|
Why is gonococcus entry to male urethral cells more likely to be symptomatic than entry into female genital cells?
|
They enter male epithelial cells via endocytosis, which elicits a large inflammatory response. They enter female epithelial cells via macropinocytic entry, which is more likely to be asymptomatic.
|
|
|
How is gonorrhea diagnosed in men? Women?
|
Men: Gram stain of urethral discharge.
Women: Culture |
|
|
Which STI bacterial pathogen is an obligate intracellular bacteria?
|
Chlamydia
|
|
|
What is trachoma?
|
Ocular strains of Chlamydia trachomatis can cause trachomas, which lead to blindness.
|
|
|
Is chlamydia genital infection most often asymptomatic?
|
yes
|
|
|
What causes Lymphogranuloma venereum?
|
LGV strain of Chlamydia trachomatis
|
|
|
What is Lymphogranuloma venerum (LGV)?
|
Chlamydia trachomatis penetrates genital mucosa and causes systemic infection.
|
|
|
What does Chlamydia psittacosis cause?
|
a flu-like respiratory infection.
|
|
|
Describe elementary bodies
|
Infectious but non-growing particles of Chlamydiae
|
|
|
Describe reticular bodies
|
Non-infectious but actively growing particles of Chlamydiae
|
|
|
What largely causes fallopian tube scarring in Chlamydia infection?
|
Cell-mediated immunity
|
|
|
What must an antibiotic be able to do to clear a Chlamydia infection? What are the 2 most common antibiotics?
|
They must be able to penetrate the epithelial cell and reach high intracellular concentrations. Doxycycline and Azithromycin.
|
|
|
Describe Neisseria by gram stain, oxidase, and shape.
|
Gram-negative diplococci and oxidase positive.
|
|
|
What is the main reason that disseminated N. gonorrhoeae is not life-threatening but N. meningitidis is?
|
Unlike N. meningitidis, N. gonorrhoeae lacks a polysaccharide capsule. therefore it does not evade phagocytosis well.
|
|
|
Does gonococcus have LPS?
|
yes. This is different from a polysaccharide CAPSULE
|
|
|
What is the discharge like with a patient presenting with bacterial vaginosis?
|
Fishy-smelling discharge.
|
|
|
Diagnosis of bacterial vaginosis requires evidence of 3 of the following symptoms:
|
1. Presence of "clue cells": exfoliated cells with large numbers of Gardnerella vaginalis.
2. Vaginal pH>4.5 3. Homogenous adherent discharge. 4. Fishy odor after adding KOH to discharge |
|
|
What is the first-line treatment of bacterial vaginosis? What is a problem with it?
|
Metronidazole. Recurrence is common.
|
|
|
What fungi causes most vulvovaginal yeast infection?
|
Candida albicans
|
|
|
Is discharge commonly present with vulvovaginal candidiasis?
|
no
|
|
|
What is cystitis?
|
Infection of lower urinary tract (urethra and bladder).
|
|
|
What is pyelonephritis?
|
Infection of the kidney
|
|
|
What is the most common nosocomial infection?
|
Catheter-associated UTI
|
|
|
What is Tamm-Horsfall protein?
|
Glycoprotein produced by some renal cells that binds to UPEC strains. This prevents them from binding to uroepithelial cells.
|
|
|
What is a major factor determining recurrence of UTIs?
|
Density of adherence receptors.
|
|
|
What is a bladder infection usually indicative of in men?
|
an underlying disorder like a tumor or obstruction of the urinary tract.
|
|
|
Where do most uropathogens originate from?
|
The intestine
|
|
|
What is the pathogenesis of UTI bacteria?
|
Adherence to uroepithelium and invasion of cells.
|
|
|
What is the most common cause of UTI?
|
Uropathogenic E. coli (UPEC). 80% of cases.
|
|
|
What is the most important virulence factor for UPEC?
|
Ability to adhere to epithelial cells by expression of fimbrial adhesins.
|
|
|
What is the 2nd most common cause of UTI?
|
Staphylococcus saprophyticus
|
|
|
What is an essential virulence factor for Staph saprophyticus?
|
Urease
|
