Week 6 Flashcards

1
Q

Name the 3 causes of genital ulcer disease.

A
  1. HSV 1/2
  2. Syphilis (T. pallidum)
  3. Chancroid
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2
Q

Name the causes of urethritis/cervicitis.

A
  1. Chlamydia

2. Gonorrhea

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3
Q

Name the causes of vaginitis.

A
  1. Candida (not a STI)
  2. Bacteria vaginosis (not a STI)
  3. Trichomonas
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4
Q

Genital lesions caused by HSV are _________, while chancres from T. pallidum are not.

A

painful

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5
Q

In which phase of the syphilis disease process does neurosyphilis occur?

A

Trick question!

It can occur in any phase of the disease

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6
Q

Anterior bowing of the tibia in a kid. What is high on your DDx?

A

congenital T. pallidum (syphilis)

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7
Q

Hutchinson’s incisors. What is high on your DDx?

A

T. pallidum (syphilis)

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8
Q

What bug causes chancroid?

A

Haemophilus ducreyi

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9
Q

What are the clinical manifestations of chancroid?

A

Painful genital ulcers and regional lymphadenopathy

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10
Q

What is lymphogranuloma venerum and what causes it (including serovars)?

A

Clinical manifestations are fluctuant buboes, markedly swollen inguinal nodes w/ groove sign, proctitis, ulcers.

Caused by Chlamydia trachomatis L1-L3

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11
Q

Which one is true?

  1. You should treat for gonorrhea every time you Dx chlamydia.
  2. You should treat for chlamydia every time you Dx gonococcus.
A

2 - assume that someone with gonorrhea also has chlamydia

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12
Q

Describe the life cycle of Chlamydia species.

A

Infection w/ elementary bodies –> reticular bodies inside cells w/ replication –> release from host cells as elementary bodies

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13
Q

What bacterial species is the predominant one found in the vagina?

A

Lactobacillus

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14
Q

What bug causes bacterial vaginosis? Is this an STI?

A

Gardnerella vaginalis. Not an STI

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15
Q

What is a clue cell and what bug does it clue you in on?

A

Epithelial cell w/ borders that are obscured by bacteria - seen in Gardnerella vaginosis infection

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16
Q

Compare condyloma acuminata with condyloma lata in terms of appearance and the bugs that cause each.

A

Acuminata looks like a cauliflower - caused by genital HPV

Lata lesions are flatter, broader, and usually more moist - caused by T. pallidum

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17
Q

Name four high-risk HPV types.

A

16, 18, 31, 33

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18
Q

Describe the life cycle of plasmodium.

A

Anopholes mosquito injects sporozoites during a bite –> sporozoites go to liver.

Liver phase: sporozoites –> schizonts –> shizonts rupture hepatocytes and release merozoites –> merozoites exit liver into blood

RBC phase: merozoites infect RBCs –> merozoites turn into trophozoites in RBCs –> trophozoites lyse RBCs and are released as schizonts –> schizonts infect more RBCs

Note that gametocytes can form from merozoites during the RBC phase; these are what are take up by mosquitos when they bite an infected person

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19
Q

What treatments work for malaria in the blood phase?

What treatment is used for the latent liver phase? What is one important thing to remember about this?

A

Blood phase: atovaquone + proguanil

For liver phase: primaquine - but test for G6PDH deficiency first or else anemia

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20
Q

Maltese cross

A

Babesia

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21
Q

Which tick transmits Babesia? What parts of the US are endemic?

A

Ixodes tick (deer tick) found in the NE and Midwest

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22
Q

Flask-shaped lesions in the colon.

A

Entamoeba histolytica

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23
Q

Steatorrhea and abdominal bloating and cramps after traveling to developing country to do some backpacking. What is high on your DDx? How do you treat it?

A

Giardia lamblia. Tx is metronidazole

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24
Q

Severe watery diarrhea in an AIDS patient. You see acid-fast cysts on O&P. What is your Dx?

A

Cryptosporidium

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25
Q

Crazy cat lady with HIV and ring-enhancing brain lesions on MRI. What is your Dx?

A

Toxo gondii

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26
Q

What is Winterbottom’s sign?

A

Posterior cervical lymphadenopathy associated with Trypanosoma brucei infection (African sleeping sickness)

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27
Q

Where is rocky mountain spotted fever endemic in the US?

A

Throughout US but most commonly seen in SE US.

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28
Q

What is ehrlichiosis?

A

Transmitted by lone star tick (Amblyomma americanum), E. chafeensis/ewingii are intracellular bacteria that live inside leukocytes and cause fever, headache, myalgias/arthralgias, and a maculopapular/petechial rash in 30% of adult patients. Fever can last for months if untreated.

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29
Q

What parts of the US are endemic for ehrlichiosis? What time of year is it seen?

A

Mostly central and SE US

E. ewingii is seen in California.

Seen mostly April-September

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30
Q

How is ehrlichiosis diagnosed? What is the treatment?

A

Clinical Dx but there is also leukopenia, thrombocytopenia, and elevated LFTs

Tx is doxycycline for kids and adults and chloramphenicol or rifampin for pregnant women

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31
Q

What is Anaplasmosis?

A

Anaplasma phagocytophilia is an intracellular bacteria that infects leukocytes and is transmitted by the Ixodes tick.

It causes fever that can last for months, myalgias/arthralgias, headache.

Rash is rare!

32
Q

What is the treatment for anaplasmosis?

A

Same as ehrlichiosis.

Doxycycline for kids and adults and chrloramphenicol or rifampin for pregnant women

33
Q

What areas of the US are endemic for Lyme disease?

A

Midwest and NE US

34
Q

Your patient presents with recurrent episodes of fever and myalgias and tells you they just did a long backpacking trip in the Sierra Nevadas but did frequent tick checks and noted no bites. What test do you order to confirm your Dx? Explain why.

A

Peripheral blood smear looking for spirochetes.

Top of DDx is Tick-borne relapsing fever caused by Borrelia hermsii. Seen in the western US. Transmitted by Ornithodoros soft ticks that feed in 1 hr and drop off so are usually unnoticed.

Associated w/ mountain cabins and rodents.

35
Q

What is tularemia?

A

Caused by gram-neg coccobacillus that infects macrophages.

Associated with contact with dead animals like rabbits and rodents.

Many types of clinical presentations; includes skin ulcers, lymphadenopathy, may cause fever, pneumonia. Can be life-threatening.

36
Q

Your patient presents with erythema migrans after having a known tick bite, but you’re in the SE US where Lyme disease is not endemic. What is at the top of your DDx?

A

STARI (Southern Tick Associated Rash Illness) - unknown microbial etiology; Tx is same as for Lyme

37
Q

Name a sequelae of chronic Q fever.

A

Endocarditis

38
Q

Patient presents with fever, headache, muscle aches, lymphadenopathy, and history of recent travel to the Phillipines. You note a bug bite with a black center surrounded by a rim of erythema. What is at the top of your DDx?

A

Scrub typhus - caused by Orientia tsutsugamuchi (Rickettsial bacteria)

Note that 50% of patients present with a pale macular rash.

Constitutional symptoms + Western Pacific/East Asia + eschar = scrub typhus

39
Q

What is trench fever? Describe the bacterial etiology, transmission, clinical manifestations, and at-risk populations, and how to diagnose.

A

Bartonella quintana - intracellular bacteria that infects epithelial cells and RBCs. Transmitted by body louse.

Clinical findings: constitutional symptoms and leg pain, endocarditis.

Homelessness and alcholism are risk-factors.

Dx w/ PCR or histology.

40
Q

Name two drug regimens for malaria prophylaxis.

A
  1. Mefloquine

2. Atovaquone/proguanil

41
Q

Immune reconstitution inflammatory syndrome is a risk for AIDS patients with what fungal infection?

A

Cryptococcus neoformans

42
Q

Is candida found on IV catheters?

A

Yeah!

43
Q

Describe the life cycle of Enterobius vermicularis.

A

Pinworm!

Starts when a person eats food contaminated with eggs —> stomach —> hatch, releasing a worm —> cecum —> sexual reproduction in the cecum —> female crawls out of the anus and lays eggs in the perianal area along with a sticky goo (itchy)

44
Q

How would you diagnose pinworms?

A

Scotch tape –> microscope to look for eggs

45
Q

Describe the life cycle of Ascaris lumbricoides.

A

Giant roundworm!

  • Begins in soil, where eggs mature (put there by peeps that shit on the ground) - takes 1-2 weeks for maturation
  • Eggs get on hands and are ingested —> larval worm (microscopic) emerges from eggs —> worms burrow out of the GI lumen into venous circulation —> right heart —> lungs —> coughed up —> swallowed back into GI tract –> grow into huge worms
46
Q

Name some major complications of Ascaris lumbricoides infection.

A
  1. Bowel blockage
  2. Migration up biliary tree –> pancreatitis and biliary sepsis
  3. Migration into the peritoneum –> peritonitis
47
Q

How do you diagnose Ascaris lumbricoides?

A
  1. Ask patient to bring in pooped-out worm.
  2. O&P, look for eggs
  3. ID during colonoscopy or contrast GI XR
48
Q

Name the three hookworms we are supposed to know.

A
  1. Ancylostoma duodenale
  2. Ancylostoma brazilense
  3. Necator americanus
49
Q

Describe the life cycle of the hookworms.

A

Starts by walking barefoot through contaminated soil —> microscopic worms burrow through intact skin —> into vasculature —> right side of heart —> lungs where they mature —> coughed up, swallowed —> maturation in intestines and sexual reproduction and egg production —> eggs into feces —> hatching and maturation so they can penetrate skin of someone else

50
Q

What early clinical finding is associated with the hookworms?

A

Cutaneous larva migrans

51
Q

What type of parasite is Strongyloides stercoralis?

A

GI roundworm (nematode)

52
Q

Describe the life cycle of Strongyloides stercoralis.

A

Barefoot in contaminated soil —> microscopic worms burrow through skin —> vasculature —> right side of heart —> lungs, maturation —> coughed up and swallowed —> into GI, maturation in the small intestine —> burrow into wall of small intestine to lay eggs —> eggs hatch inside bowel —> pooped out as infectious larvae or autoinfection in the perirectal area or through rectal mucosa (does not need to exit body to complete life cycle)

53
Q

What type of skin rash does Strongyloides cause?

A

Larva currens - shorter-lived than larva migrans, also itchy (IgE-mediated)

54
Q

What can people with T cell lymphocytopenia from illness/chemo/steroids develop if they also have Strongyloides infection? Explain how this works.

A

Hyper-infection: the worms burrow their way all over the body, carrying fecal bacteria along the way –> sepsis and death

55
Q

Describe the life cycle of Toxocara canis/cati.

A

Puppies or cats w/ worms poop out eggs that mature in the soil —> another dog or cat eats the eggs off the soil —> intestine to blood to heart to lungs to GI —> reproduction —> start over…

Unless a human eats an egg from the soil —> worm hatches out —> worm invades organs in the human like the gut (visceral larva migrans) or eyes (ocular larva migrans)

56
Q

Describe the life cycle of Trichinella spiralis.

A

Ingestion of undercooked meat w/ cysts —> larval worms come out in GI tract —> sex in the duodenum —> females stick tail into duodenal wall —> give birth to live worms straight into the wall of the duodenum –> swept into bloodstream (dissemination to everywhere!) so they can become dormant as cysts in tissues —> eventual death and calcification of cysts

57
Q

Name the three trematodes/flukes/flatworms we are supposed to know.

A

Schistosoma mansoni, japonicum, haematobium

58
Q

Describe the life cycle of Schistosoma.

A

Starts when infected human urinates or defecates eggs into body of water —> eggs hatch —> infects a snail (intermediate host) —> schistosome develops into a cercaria (motile animal) —> cercaria burrows into intact human skin —> loses its tail like a salamander and head goes into circulation —> head develops into mature worm and they like to do this in the portal blood because of nutrients —> crawl against venous blood to the mesenteric plexus or the veins that drain the bladder and seminal vesicles —> lay eggs —> sometimes the eggs don’t get into the GI lumen or into the bladder and get trapped in the walls of these organs —> eosinophilic reaction, hematuria, bladder cancer

59
Q

What bug causes cercarial dermatitis?

A

This is aka “swimmer’s itch” caused by Schistosoma that normally infect birds or other animals burrow into a human’s skin, causing a IgE reaction that is itchy. Self-limiting - worms do not get very far.

60
Q

What is Katayama syndrome?

A

When there is a systemic allergic reaction to egg antigens of Schistosoma flatworms.

Characterized by fever, chills, rigors, joint and muscle pain, lymphadenopathy and hepatomegaly. Lasts days to weeks, then resolves.

61
Q

Name the three tapeworms we are supposed to know.

A
  1. Diphylloborthrium latum
  2. Taenia soleum
  3. Taenia saginata
62
Q

Describe the life cycle of Diphyllobotrhium latum.

A

Person ingests uncooked freshwater fish that contains a plerocercoid (tiny worm with just a few segments in a cyst) —> small intestine —> hatches —> grows —> person poops into water —> water flea takes it up —> fish eat the flea —> people eat fish

63
Q

What is the difference between taeniasis and cysticercosis?

A

We are talkin’ bout tapeworms!

Taeniasis is when a person eats undercooked meat that contains a cyst. Cyst grows into a tapeworm in the GI.

Cysticercosis is when a person eats feces containing an egg. Egg –> larvae that borrows through GI mucosa and travels to visceral organs & muscles to create a cyst (cuz it wants someone to come along and eat the meat). When the larvae goes to the brain it is neurocysticercosis.

64
Q

True or false:

Neurological damage and seizures from neurocysticercosis are due to mechanical damage caused by larval migration.

A

False. It is from cysts dying –> immune response and inflammation in the brain (so treat w/ steroids!)

65
Q

Name two ways fungi evade the immune system.

A
  1. Make molecules that inhibit the production of TNF and IL-12 and that stimulate production of IL-10.
  2. Inhibition of phagolysosome formation –> granulomas
66
Q

Name three ways that parasites evade the immune system.

A
  1. Antigenic variation
  2. Concealment via intracellular infection
  3. Production of molecules that turn down the immune response
67
Q

Name four things that immune cells make to fight parasites and what each does.

A
  1. Histamine - toxic to parasites, vasodilation and increased permeability, smooth m. contraction.
  2. Proteases
  3. Leukotrienes - increased vascular permeability, smooth m. contraction, mucus production
  4. Prostaglandins - vasodilation
68
Q

What disease does one have if they have no FOXP3?

A

X-linked polyendocrinopathy and enteropathy syndrome (IPEX) - no Tregs –> overwhelming autoimmune disease

69
Q

What are the clinical manifestations of IL-10 receptor deficiency? What is the treatment?

A
  1. Infant-onset severe fistulating colitis
  2. Rash

Bone marrow transplant

70
Q

Describe the two mechanisms by which an infectious agent can cause autoimmune disease.

A
  1. Molecular mimicry - when the infectious antigen looks a lot like a self-peptide.
  2. Bystander activation - when there is inadvertent activation of a self-reactive T cell that made it out to the periphery.
71
Q

What makes C. galbrata unique from C. albicans?

A

C. galbrata is smaller, no hyphae, more resistant to fluconazole, and is more common in line infections

72
Q

What is the most common cause of chronic meningitis in AIDS patients?

A

Cryptococcus

73
Q

What are the three classic presentations of Aspergillus infection?

A
  1. Allergic brohcnopulmonary aspergillosis (ABPA)
  2. Fungus ball
  3. Invasive aspergillosis
74
Q

What are the key features of invasive aspergillosis?

A
  • It loves to get into blood vessels
  • Resistant to fluconazole
  • High mortality rate
75
Q

What is unique about Cryptococcus in form, histology, pathophys, and diagnosis?

A

Only has a yeast form, large polysaccharide capsule, high tropism for CNS, minimal white cells in CSF, high opening pressure, cryptococcal antigen (GXM) is helpful for Dx

76
Q

How do parasites evade the immune system?

A
  1. Stage-specific antigenic variation
  2. Continuous variation
  3. Hide inside cells or in cysts
  4. Production of molecules that inhibit immune response
77
Q

Your patient is a 9 year old with new onset of leukocoria (no red reflex). What is at the top of your DDx?

A

Ocular larva migrans from Toxocara canis/cati