Path 8 except for pp. 381-388
Infectious Diseases
Principles and Categorization
1. If a microbe is 1 μm in size, in what category could it be? What about nm scale?
a. Protozoa and bacteria can be 1 μm around the low end
b. Only viruses exist on the nanometer scale
2. What are CMV, herpesvirus, and rabies viruses are all known to form?
a. they all form inclusion bodies (CMV: eosinophillic nuclear inclusions & cytoplasmic
inclusions, herpes: nuclear inclusion with halo, rabies: negri bodies)
3. Who is usualy affected by the bacterium Pneumocystis jirovecii?
(~Jared has aides)
a. AIDS patients are affected by this opportunistic infection
(PJ has AIDs)
4. How would you detect an infection of herpes simplex virus encephalitis using CSF fluid?
a. HSV encephalitis is best detected with PCR of the cerebrospinal fluid
i. Viral culture of CSF has terrible sensitivity
b. The same is true for chlamydia, although of course not in the CSF
5. What is the most serious category of Bioterrorism agents?
a. Category A Diseases/Agents are the most severe, and include stuff like smallpox, plague,
anthrax, etc.
b. Category C doesn’t really include anything besides “emerging threats”
6. When will Ascaris lumbricoides start to cause disease? What about Hookworms?
a. Helminths like Ascaris lumbricoides usualy cause disease only when they are present in
large numbers because they obstruct the gut
b. Hookworms however will cause anemia by drinking blood and stealing vit. B12
7. Which virus mediates interactions with sialic acid through hemagglutinin and neuraminidase?
a. Influenza viruses use hemagglutinin to attach to sialic acid, and eventually use
neuraminidase to cleave the sialic acid and allow the virus to release from the host
8. When does the transmission of treponemes to fetuses occur:
a. Treponema pallidum causes congenital syphillis only when the mother is infected late in
the second trimester
b. It causes miscarraige or severe fetal oseochondritis and periostitis
9. How do HIV and EBV enter human cells?
a. These two viruses use normal cellular receptors (HIV binds to CD4 on T cells and EBV
to B cells) to gain access to human leukocytes
10. What is “quorum sensing?”
a. Bacteria coordinate in gene expression within a large population
b. Example: some S. aureus cells secrete autoinducers, the others respond by producing
toxin
11. What are two injurious effects of host immunity in response to infection with S. pyogenes?
a. Rheumatic heart disease and glomerulonephritis can occur after an S. pyogenes infection
12. List three effective means of evading the immunse system:
a. Modification of LPS to reduce Toll-Like Receptor activation (Salmonella)
b. Replicating within phagocytic cells (Mycobacteria, Listeria)
c. Altering MHC class I proteins (DNA viruses)
13. What is signified by chronic inflammation and “pipe-stem” fibrosis of the liver or bladder wall?
a. These are signs of inflammation in response to schistosomal eggs
14. How does a Klebsiella pneumoniae infection differ from a pneumoccoccus infection?
a. K. pneumoniae will not heal correctly, instead it causes abscess formation
15. 5 histologic types of inflammation:
a. Purulent, mononuclear/granulomatous, cytopathic-cytoproliferative reaction (viruses),
necrosis, chronic inflammation
Viral Infections (p. 348)
16. Which ssRNA virus has only one serotype? What viral protein is bound by the two cell-surface
receptors CD46 and SLAM?
a. Measles/rubeola
b. viral hemagglutinin protein is bound by CD46 and SLAM on host cells
17. What does a measles/rubeola infection look like?
a. Koplik spots are ulcerated mucosal lesions near the Stensen ducts
b. A blotchy, reddish brown rash forms on the face trunk and proximal extremities
c. Finkeldey cells, full of inclusion bodies, appear in lymphoid organs
18. What virus can cause orchitis, fat necrosis, and encephalitis (among other Sx)?
a. In addition to the much more common parotitis, mumps causes these symptoms
19. What receptor increases the risk of fatal West Nile virus, but protects against HIV?
a. A lack of CCR5 receptor is dangerous in regards to West Nile (fatal encephalitis), but
HIV uses the same receptor to enter cells
20. What kind of infection is caused by the arenaviruses, filoviruses, bunyaviruses, and flavaviruses?
What are the specific viruses?
a. viral hemorrhagic fevers,
b. Ebola, Marburg, and Lassa viruses
21. What group do the herpesviruses HSV-1, -2, and VZV belong to? CMV? EBV?
a. These are α group herpesviruses (alphaherpesviruses
b. β
c. γ
22. What lesions occur besides on the skin? What are the more rare symptoms of herpes?
a. HSV-1 is the major infectious cause of corneal blindness in the US
b. gingivostomatitis in kids, in the immunocompromised: Kaposi varicelliform eruption,
eczema herpeticum, herpes esophagitis, herpes bronchopneumonia, and herpes hepatitis
23. What do HSV-infected cells contain (2)?
a. Cowdry type A inclusions
b. multinucleated syncytia
24. What virus causes a skin lesion with a “dewdrop on a rosepetal” appearance?
a. VZV
25. What virus causes a characteristic “owl’s eye” intranuclear inclusion which is usually set off from
the nuclear membrane by a clear halo?
a. CMV
26. How is CMV transmitted (5)? Who needs to worry about infection? Symptoms in this group?
a. The routes are: Transplacental, neonatal, through saliva, veneral, and iatrogenic
(transplants/transfusions)
b. AIDS patients
i. pneumonitis and colitis
27. What are the latency-specific genes of EBV?
a. EBNA1, EBNA2, and LMP1 drive B cell activation and proliferation through the cell
cycle
b. A few infected B cells expressing only EBNA-1 and -2 genes allow some copies of the
virus to linger after recovery (see #28)
28. What lymphocytes transform into the characteristic “mononucleosis cells” (2)?
a. CD8+ cytotoxic T cells and some CD16+ NK cells
i. EBV invades B cells only
29. Latent Epstein-Barr Virus (EBV) can progress to which disease in the immunocompromised?
a. B-celllymphomas, particularly Burkitt lymphoma
Bacterial Infections (p. 357)
30. How does bordetella pertussis appear microscopically? [Test Q]
a. Gram-negative coccobacillus
31. Which Staphylococcus aureus hemolytic toxin lyses RBCs?
a. The gamma toxin targets erythrocytes and lyses them
32. What is hidradenitis (S. aureus)? How do you differentiate SSSS/Ritter from toxic epidermal
necrolysis/Lyell’s disease?
a. Chronic suppurative infection of apocrine glands, likely in the axilla
b. Desquamation of the epidermis in SSSS occurs at the level of the granulosa layer
c. Toxic epidermal necrolysis causes desquamation between epidermis and dermis
33. Which streptococcus species colonizes the female genital tract? What problems does it cause?
a. S. agalactiae (“group B streptococcus”) causes
i. sepsis and meningitis in neonates
ii. chorioamnionitis in pregnancy
34. Besides Vibrio vulnificus and Aeromonas hydrophila, which bacteria causes necrotizing fasciitis?
a. Streptococcus pyogenes also causes necrotizing fasciitis
35. A patient with sloughing respiratory epithelium also has phage-encoded A-B toxin in their blood.
What infection do they have, and how does it attack? How does it spread?
a. Cornyebacterium diptheriae’s A-B exotoxin prevents RNA translation
b. Spread by skin exudate and aerosols (affects the mouth and airways)
36. Which bacteria is often spread by raw chicken and is dangerous for pregnant women? [test Q]
What other problems can it cause? How is immune protection mediated? What other grampositive can cause meningitis?
a. Listeria monocytogenes—intracellular
i. Also spread by contaminated dairy products!
b. Also causes meningitis and focal abcesses in all organs
c. IFN-γ needs to be produced by NK cells and T cells in order to activate macrophages
d. Bacillus anthracis—boxcar shaped and extracellular
37. What are the two subunits of Bacillus anthracis toxin?
a. protective antigen (B) and alternately edema and lethal factors (A)
38. Which Nocardia bacteria tends to affect people with defects in T cell-mediated immunity or
prolonged steroid use, and can infect the CNS? Why is it hard to diagnose?
a. Nocardia asteroides tends to infect the immunocompromised (bad T cells)
b. can be tricky to diagnose because of its odd beaded appearance and nongranulomatous
but liquefactive infection pattern
i. Looks like TB
39. Can you describe N. meningitidis? How does N. meningitidis enter the blood? Which form of
immunity is most important to fight this form of meningitis? Which membrane protein helps all
Neiseriae to bind to host cells?
a. Gram-negative coccus, frequently causing meningitis
b. N. meningitidis enters the blood through the respiratory tract
c. complement attack is the first line defence (same is true for N. gonorrheae)
d. Pili; virulence factors undergo antigenic variation to escape the immune system
i. Proteins encoded by the OPA gene mediate entry to host cells
40. Is N. gonorrheae the most common STD? Who is more likely to have an asymptomatic infection?
a. Second most common STD
b. Women—diagnose with PCR/culture; possible in other sex but not nearly as likely
41. What is similar about whooping cough and cholera toxins? How about diptheria and
pseudomonas toxins?
a. Pertussis and cholera ADP-ribosylate G proteins to stop signal transduction
i. Bordetella pertussis paralyzes the cilia (“pertussis toxin”)
b. Diptheria (A-B toxin) and pseudomonas (exotoxin A) prevent protein production
i. ADP-ribosylate ribosomes
42. Which bacteria causes necrotizing pneumonia? What else?
a. Pseudomonas aeruginosa
i. Cystic fibrosis, neutropenia, nosocomial?
b. ecthyma gangrenosum in people with skin burns
43. What protein does Yersinia pestis express to prevent phagocytosis? How does it spread?
a. Plague uses Yops to wreck phagocytosis and cytokine production as it spreads through
the lymph nodes
b. Fleabites and aerosol
44. How does chancroid differ from syphilitic chancre? What is the causative microbe?
a. Chancroid is not indurated, and may be multiple
i. Also, covered by shaggy yellow-grey exudate
b. Hemophilus ducreyi
45. What you though was a carcinoma turns out to be granuloma inguinale. What bacteria is causing
it? How does granuloma inguinale appear microscopically?
a. Klebsiella granulomatis infections looks like cancer:
i. Pseudoepitheliomatous hyperplasia
ii. Surrounded by inflammatory cells, maybe indurated, moist, ulcerated, granulated
[GRANULOMAtis]
46. What disease states increase the risk of tuberculosis infection? What are some caveats to the
tuberculin (Mantoux) test?
a. Diabetes, Hodgkin lymphoma, silicosis, chornic renal failure, alcoholism, immune suppr.
b. Requires 2-4 weeks post infection for a positive result
c. Does not distinguish between disease and simple presence of antibodies (BCG vaccine)
d. False negatives can occur with severe disease or immunosuppression
47. What cells does TB infect? What part of the lung does primary tuberculosis affect? Secondary?
a. Primarily macrophages—certain NRAMP1 mutations cause susceptibility
b. primary tuberculosis attacks right between superior and inferior lobes, as well as in
lymph nodes; Ghon focus => Ranke complex (calcified)
i. affects those who have never been exposed before or those who have lost
immunity
c. secondary TB affects the apex of 1-2 lungs, and readily develops to cause cavitation
48. What is the critical mediator that allows macrophages to contain tuberculosis? What is the most
common presentation of extrapulmonary TB? Where does miliary spread occur?
a. IFN-γ is key, T cells need to release it to activate dem macrophages! [like Listeria]
49.
50.
51.
52.
53.
54.
55.
b. Lymphadenitis (“scrofula”) is the most common extrapulmonary symptom
c. miliary tuberculosis likes to extend to highly perfused tissues, including all over the lung
How can you determine that an HIV+ patient has M. avium-intracellulare complex?
a. People with MAC will have abundant acid-fast bacilli within their macrophages
b. Affects liver, spleen, lymph nodes, and only sometimes lungs
A person with a bacterial infection has dry, scaly lesions that lack sensation, and peripheral nerve
infl. What’s going on here? What might the other version of this disease look like?
a. leprosy! The patient has tuberculoid leprosy: dry scaly lesions which often have central
healing, peripheral nerve thickening/atrophy, intact T cell response
b. lepromatous (anergic/ multibacillary) leprosy: symmetric skin thickening, a weak T cell
response, and sterility because of massive invasion
What occurs in secondary syphilis? When does aortitis form? What are some tertiary signs?
Congenital? What are the two main tests?
a. Skin lesions on the palms or soles of the feet occur in secondary syphilis. It usually
occurs 2-10 weeks after the primary chancre, in 75% of those infected.
b. Aortitis occurs in cardiovascular [tertiary] syphilis, after a latent period of 5+ years
c. Besides aortitis, neurosyphillis, and gumma formation in bone, skin, and joints
d. Syphilitic osteochondritis and periostitis affect all bones, but especially nose (vomer
collapse) and tibias (saber shins)
i. Late triad is interstitial keratitis, Hutchinson teeth, CN VIII deafness
e. Use VDRL for screening, more expensive antibody test for added specificity
What causes epdiemic relapsing fever, and what is it? What disease causes erythema chronicum
migrans? [test Q]
a. Caused by the spirochete B. recurrentis, features multiorgan failure, fever, chills,
recurrs, with lesser severity each time or spontaneous cure
b. B. bugdorferi
What is the most important toxin of C. perfringens, and what does it do? How can you
differentiate it from an infection of pyogenic cocci?
a. α-toxin is the most important toxin of C. perfringens. It degrades lethicin
(indiscriminantly degrading cell membrane phosphatidylcholine) and sphingomyelin in
nerve sheaths
i. lecithinase causes myonecrosis=> classic gas gangrene
b. clostridial cellulitis originates in wounds, has a foul odor, thin discolored exudate, and
causes relatively quick and wide tissue destruction, disproportionate to # of bacteria
Which STD can be asymptomatic in men? Two presentations?
a. Chlamydia is the most common bacterial STD; it may be asymptomatic in men, and
women too!
i. In contrast, the second most common bacterial STD almost always causes
symptoms in men; HPV takes the crown for most common STD
b. Appears as either urethritis or lymphogranuloma venereum
What is the hallmark of Rocky Mountain Spotted Fever? What is common to Ricketsial
infections? What microbe causes typhus, and what are its symptoms? How about Erlichiosis?
a. A hemorrhagic rash that extends over the entire body, including palms and soles, is
characteristic of RMSF
b. Symptoms are caused by vascular leakage secondary to endothelial cell damage
c. Rickettsia prowazekii, causes thrombosis and gangrene of skin, nodules in the brain
d. Erlichia ewingii, Anaplamsa phagocytophilum, and Erlichia chaffeensis
i. Morulae cytoplasmic inclusions with abrupt fever=> respiratory insufficiency
Fungal Infections (p.382)
56. What are the different forms of Candida albicans during infection? What is the attack pattern of
invasive candidiasis? Where does it strike?
a. Yeast form: elicit protective antifungal TH1 response
b. Filamentous form: nonproductive TH2 response
c. Abcesses: kidney, heart, brain, liver, eye (endopthalmitis)
i. Most often in people immunosuppressed from leukemia treatment
57. What is the course of an infection of Cryptococcus neoformans? What is a classic lesion in the
immunosuppressed? What are its environmental resevoirs?
a. Primary infection in lung, mild, sometimes forming solitary pulmonary granuloma
b. Spreads to CNS, lesioning the meninges, cortices, and basal nuclei
c. Soap bubble lesions form in the Virchow-Robin spaces as gelatinous masses of fungi
grow unchecked
d. Pigeon droppings and soil
58. What fungus often causes allergies and produces aflatoxin when it grows on peanuts? What does
a simple infection look like? Invasive signs and lesion?
a. Aspergillus
b. Proliferating fungal balls lying free within lung cavities and invading blood vessels=>
hemoptysis
c. primary lesions are necrotizing pneumonia with sharply delineated hemorrhagic borders:
target lesions; spreads widely throughout the body
59. What common bread molds give rise to rhinocerebral mucormycosis in diabetics and others?
What are some risk factors?
a. Zygomycosis/mucormycosis: Mucor, Rhizopus, Absidia, Cunninghamella genuses
i. The infection tracks superiorly and is followed by meningoencephalitis
b. Iron overload, corticosteroid use, diabetes mellitus, and breakown of cutaneous barrier
Parasitic Infections
60. Name the stages of malria development in stages:
a. Sporozoite, trophozoite, schizont, merozoite/gametocyte
[ST. SMG (mosquito gun)]
61. Why are many Gambians immune to P. vivax infections?
a. Gambians tend to have no Duffy blood group antigens, which are the protein that P. vivax
binds to
62. How does P. falciparum cause erythrocytes to bind to endothelial cells? How do CNS problems
occur and what is this called? What histologic features are visible?
a. PfEMP1 (P. falciparum Erythrocyte Membran Protein 1)
b. malignant cerebral malaria: brain vessels are plugged by parasitized erythrocytes
c. malarial/Durck granulomas form
63. How can Babesia be distinguished from malarial microbes? In what circumstances is infection
serious?
a. Babesia forms Maltese crosses in erythrocytes, and symptoms tend to be milder
i. Is treated with an antimalarial drug, atavoquone
b. However if the patient has had a splenectomy, he will most likely die
64. What transmits Leishmania?
a. Sand flies
65. Which forms of Leishmania cause cutaneous, mucocutaneous, visceral, and diffuse cutaneous
disease?
a. Cutaneous: L. major, tropica, mexicana, and braziliensis
[hot places]
b. Mucocutaneous (espundia): L.brazilensis
c. Visceral (spleen, liver, bones): L. donovani, infantum, chagasi
d. Diffuse cutaneous: ?
66. What animal transmits African trypanosomiasis? What protein covers African trypanosomes?
How does it travel in the body? What are infected plasma cells called?
a. The tsetse fly
b. VSG (Variable Surface Glycoprotein)
c. bloodstream
d. Mott cells
67. What animal transmits Chagas disease? What often appears at the site of entry? Where does the
disease localize—give two examples?
a. Triatomids (parent family: reduviids; the “kissing bug”)
b. Chagoma: swelling and erythema, most often on the face or hand
i. Make sure that you realize other parasites cause similar signs (esp.
trypanosomiasis!)
c. The heart:
i. acute Chagas: acute mycoarditis from direct invasion
ii. chronic Chagas disease: dilated cardiomyopathy, frequent mural thrombi=>
emboli
[home is where the heart is]
68. Which metazoan infection can reinitiate infection, unlike other parasitic worms? What is their
lifecycle like?
a. Strongyloides stercoralis sticks around
b. Penetrate skin, travel to lungs in blood, travel up trachea, get swallowed, reproduce
69. What happens when Taenia solium (tapeworm) eggs are ingested? What other kinds of tapeworm
are there, and what to you have to eat to get worms?
a. Convulsions and increased intracranial pressure are caused by the cysts
b. (Taenia solium, pork)
c. Taenia saginata, beef
d. Diphyllobothrium latum, fish
70. How does hydatid disease occur?
a. Consumption of Echinococcus granulosus/multilocularis eggs
71. What other metazoan is transmitted by pork? How does it encyst? What chronic problem does it
cause?
a. T. spiralis
b. Become intracellular parasites in striated skeletal muscle, forming nurse cells
c. myositis
72. What animal carries schistosomiasis? How does schistosomiasis spread? Where do they cause
problems in humans (2)?
a. Freshwater snails
b. Penetrates the skin
c. Hepatic vessels! => hepatic “pipe stem” fibrosis
d. S. haematobium can also deposit tons of eggs in the bladder, causing a “sandy”
granulomatous appearance
73. Which parasites can penetrate the skin unaided?
a. Strongyloides stercoralis
b. Schistosoma species
i. Also the blood-sucking hookworms Necator duodenale and Ancylostoma
duodenale (chapter 17)
74. What species cause lymphatic filiariasis? How are they transmitted? What species is an
endosymbiote? What other species do they infect?
a. Wuchereria bancrofti and Brugia species (malayi or timori)
b. Mosquito vector
c. Wolbachia bacteria
d. Also infect O. volvulus
75. What causes river blindness? What does ivermectin treatment sometimes cause? What else can be
used to treat it?
a. Onchocerciasis, caused by O. volvulus
b. The Mazzotti reaction, which accentuates the punctate keratitis
c. You should also use doxycylcine, because it kills the endosymbiotic Wolbachia and
prevents the worms from reproducing
1.
2.
3.
4.
5.
6.
7.
Organism
o Exotoxin: Almost all Gram-positive
o Endotoxin: Almost all Gram-negative
Location
o Exotoxin: Extracellular, excreted by living organisms
o Endotoxin: Part of pathogen cell wall, released when cell dies
Chemistry
o Exotoxin: Polypeptide
o Endotoxin: Lipopolysaccharide complex
Stability
o Exotoxin: Unstable; denatured above 60 degrees C
o Endotoxin: Stable; can withstand 60 degrees C for hours
Toxicity
o Exotoxin: Among the most powerful toxins known (some 100 to 1 million times more lethal than
strychnine)
o Endotoxin: Weak, but fatal in high doses
Effects
o Exotoxin: Highly specific, several types
o Endotoxin: Nonspecific; local reactions, such as fever, aches, and possible shock
Fever production
o Exotoxin: No
o Endotoxin: Yes, rapid rise to very high fever
8.
Usefulness as antigen
o Exotoxin: Very good, long-lasting immunity confered
o Endotoxin: Weak, no immunity conferred
9. Conversion to toxoid form
o Exotoxin: Yes, by chemical treatment
o Endotoxin: No
10. Lethal dose
o Exotoxin: Small
o Endotoxin: Large
11. Typical Infections Caused
o Exotoxins: Botulism, gas gangrene, etanus, diptheria, cholera, plague, scarlet fever,
staphylococcal food poisening
o Endotoxins: Salmonellosis, typhoid fever, tularemia, meningococcal meningitis, endotoxic shock