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Pathobiology > Pathology of Infectious Diseases > Flashcards

Pathology of Infectious Diseases Flashcards

1
Q

In Creutzfeldt-Jakob Disease, what mediates the change from PrPc to PrPsc?

A

Change in conformation from normal alpha-helix structure to abnormal, beta-pleated sheet structure

PrPsc = scrapie, the abnormal protein resistant to proteolysis

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2
Q

What gives rise to the majority of Creutzfelt-Jakob disease cases? Minority?

A

Majority - sporadic cases

Minority - Familial mutations in PRNP gene or direct, infectious transmission of prion protein (especially iatrogenic)

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3
Q

What are the macroscopic and microscopic findings of CJD?

A

Macroscopic - appears grossly normal

Microscopic - formation of intracytoplasmic, clear vacuoles within neuropia of cerebral cortex and basal ganglia
-> eventual neuronal loss and secondary reactive gliosis

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4
Q

What will secondary reactive gliosis show?

A

The presence of cytoplasm of glial cells like astrocytes, which should basically never be seen..

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5
Q

What are the clinical manifestations of CJD?

A

Rapidly progressive dementia and prominent startle myoclonus (clapping will make the patient shake)

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6
Q

What will commonly be seen in the parotid gland with mumps virus infection? What lab marker will be elevated?

A

Lymphocytic infiltration (Acute viral infection appears as chronic inflammation due to cell-mediated response)

  • > causes unilateral or bilateral parotid gland swelling which is painful
  • > elevated serum amylase (due to salivary amylase)
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7
Q

What pathology occurs in the testes in mumps infection and does it lead to infertility? Also, give one other organ which is infected other than brain / parotid gland.

A

Causes orchitis in postpubertal males, only causes testicular atrophy but rarely sterility (large reserve of seminiferous tubules).

Pancreas is uncommonly involved since it is glandular tissue -> can produce a transient hyperglycemia due to loss of insulin

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8
Q

What are the microscopic features of active VZV infection, and how does it differ from HSV?

A

Intraepithelial vesicles (blisters) with multinucleated epithelial (keratinocytes) cells with ground-glass chromatin around the periphery. Intranuclear inclusions are eosinophilic, with no cytoplasmic inclusions.

These look exactly the same as HSV under the microscope because VZV is a herpesvirus.

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9
Q

What are some complications of herpes zoster?

A

Herpes zoster ophthalmicus -> possible blindness if virus reactivates from V1

Postherpetic neuralgia

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10
Q

Is CMV a latent infection? And how do you normally get it?

A

Yes - it is a herpesvirus, actually thought to stay latent in the hematopoieitic myeloid cell line.

Because CMV tends to infect glandular epithelium rather than squamous, it is spread via contact with body fluids (saliva, breast milk, etc, which is why it’s called mono)

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11
Q

What does CMV look like pathologically? Make sure to contrast this with VZV.

A

“Owl’s eye” - according to sketchy

Enlarged, basophilic intranuclear inclusion sourrounded by a halo and (unlike VZV) multiple, smaller, basophilic intraCYTOPLASMIC inclusions.

-> nuclei do not tend to aggregate together like VZV

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12
Q

What are the common characteristics of the CMV TORCH infection which are unique?

A

Periventricular calcifications (only present in Toxoplasmosis otherwise), sensorineural hearing loss, microcephaly, chorioretinitis, blueberry muffin rash

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13
Q

What causes the blueberry muffin rash in CMV?

A

Thought to be due to extramedullary hematopoiesis

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14
Q

What are the shared features of ALL torch infections?

A

Hepatosplenomegaly, thrombocytopenia, intrauterine growth retardation

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15
Q

What are common sites of involvement for CMV in immuncompromised patients? (i.e. AIDS or organ transplant)

A

Organ transplant - lungs, especially CMV pneumonia

AIDS - GI tract, retina

  • > ulcers in the colon
  • > Chorioretinitis (pizza pie retinopathy)
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16
Q

How do hepatocytes appear with active HBV infection? Why?

A

Ground-glass appearance, almost like hydropic change

-> due to buildup of spherule and filamentous particles which are not infective

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17
Q

How does the liver appear generally with active HBV infection? What labs will be elevated?

A

Random hepatocyte injury and regeneration, with lymphocyte infiltration to fight the viral infection

ALT/AST will be elevated

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18
Q

Who is the hepatitis B carrier state more common in and why?

A

Infants / very young people -> immune system cannot fight off the infection and grows accustomed to it

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19
Q

What is the definition of the carrier state and what are the range of symptoms?

A

Evidence of HBsAg for greater than 6 months
Ranges from no symptoms (carrier state) to severe, progressive disease with cirrhosis (diffuse hepatic fibrosis with regenerative nodules).

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20
Q

Does cirrhosis need to precede hepatocellular carcinoma?

A

Not in the case of hepatitis B infection -> cancer can develop as a result of the virus.

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21
Q

What is the structure of HPV?

A

NON-ENVELOPED (statue of david)

Double-stranded, circular (remember the table is circular in sketchy) DNA virus

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22
Q

What differentiates the high risk vs low risk strains of HPV mechanistically in terms of ability to cause cancer?

A

Low risk: i.e. 1-4, 6, 11 = HPV replicates as an extrachromosomal episome

High risk: HPV is integrated into host cell DNA

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23
Q

How can HPV be recognized microscopically during active infection? Provide the name of the abnormal cell type.

A

It replicates in cutaneous epithelial cells (especially squamous), replicating in basal layers and actually producing viral particles in the top layer.

Top layer will still have a nucleus -> KOILOCYTES = squamous epithelial cells containing hyperchromatic, wrinkled nuclei with perinuclear clearing.

-> there will often be abnormal keratinization nearby

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24
Q

What is the most common manifestation of HPV called and where does it appear? Microscopically?

A

Verruca vulgaris - common wart

Appears as small, pale papules with a roughened surface, often on dorsum of hands or soles of feet.

  • > major thickening of squamous epithelium (mitosis is induced by virus)
  • > thick keratin makes the warts appear white
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25
Q

How does the field affect apply to HPV? What is being detected in a PAP smear?

A

The anogenital lesions will affect a wide variety of sites, including vulva, vagina, cervix, and anus

-> we are detecting koilocytes on PAP smear (the most superficial layer of squamous epithelium should never contain large, defined nuclei)

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26
Q

What viruses normally cause the venereal wart (spread by sexual contact) of HPV and what is it called? What does it look like grossly?

A

HPV types 6 and 11

Called condyloma acuminatum

Looks like a fleshy, exophytic (outward-growing), cauliflower-like perineal mass, in which multiple lesions can become confluent

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27
Q

What three things from the virus cause increased risk of dysplasia -> invasive carcinoma?

A
  1. E6 - degradation of p53
  2. E7 - inhibition of Rb / E2F interaction
  3. Upregulation of telomerase
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28
Q

What are the major virulence factors of S. pneumoniae?

A
  1. Polysaccharide capsule

2. Pneumolysin - membrane-damaging cytolysin, response for alpha-hemolytic properties

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29
Q

Who is especially at risk for pneumococcus infection?

A

Young children, older adults, and immundeficient individuals (functional asplenia or defective pulmonary clearance)

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30
Q

What type of pneumonia does pneumococcus cause, and what will be found microscopically?

A

Lobar pneumonia -> acute bacterial pneumonia associated with PMNs, hyperemia, and exudative edema

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31
Q

What are two major virulence factors of Clostridium perfringens? How does this relate to its plating appearance?

A
  1. Alpha toxin - a lecithinase / phospholipase
  2. Hemolysins - beta-hemolytic on blood agar

These two toxins together are responsible for the double-zone of hemolysis on blood agar.

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32
Q

What are the two diseases caused by clostridium perfringens? Describe the pathogenesis of both.

A
  1. Food poisoning - slow onset, due to ingestion of spoors -> associated with abdominal cramps and diarrhea from bacterial enterotoxin
  2. Gas gangrene - myonecrosis. Following wound infection, anaerobic growth of spores in poorly oxygenated tissue allows use of exotoxins to kill immune cells and soft tissue / skeletal muscle around -> dissemination and sepsis, as well as formation of gas bubbles from fermentation of sugars in wound
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33
Q

How does gas gangrene look under the microscope?

A

Like coagulative necrosis with large vacuoles -> gas bubbles, death of immune cells which try to save the muscle tissue from necrosis

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34
Q

How does syphilis infection look pathologically? What feature of tertiary syphilis does this explain?

A
  1. Many plasma cells nearby trying to clear the infection (nonspecific antibodies generated which are picked up by VDRL test, reacting with beef cardiolipin)
  2. Obliterative endarteritis -
    vascular pathology causes compression of blood vessels
    -> explains death of vasa vasorum leading to thoracic aortic aneurysm in tertiary syphilis
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35
Q

What are the smooth, wart-like lesion appearing on the anogenital region in secondary syphilis called?

A

Condylomata lata

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36
Q

What is the generalized finding in secondary syphilis?

A

Full body rash, even including palms and soles (very rare), 4-8 weeks after primary infection

  • > resolves spontaneously
  • > lesions are highly infectious
  • > lymphadenopathy and patchy hair loss
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37
Q

What are the three primary findings of tertiary syphilis? Are these lesions infectious?

A
  1. Aortitis with aneurysm (vasa vasorum degeneration)
  2. Neurosyphilis -> tabes dorsalis (Demyelination of dorsal column), Argyll-Robertson pupils (miosis on accommodation, but does not react to light)
  3. Gummas - lesions of skin, liver, and bone -> NOT INFECTIOUS. Perhaps due to immune response
38
Q

What is the micropathology of gummas?

A

Granulomatous inflammation surrounding the treponema

39
Q

What are the features of congenital syphilis?

A
  1. Snuffles - rhinitis
  2. Saber shins - periostitis leading to bowing of tibia
  3. Hutchinson teeth - notched front teeth
  4. Saddle nose - Destruction of nasal bridge
  5. Common findings of all TORCH infections, including neurologic / ocular abnormalities
  6. Deafness - kids with earmuffs in sketchy
40
Q

What is the life cycle of Chlamydia trachomatis / what type of cells does it like to infect?

A
  1. Elementary body - enfectious former when enters columnar epithelial cells / mucosal membranes (does not prefer squamous, thus, will prefer glandular / secretory epithelium. This includes transitional epithelium of the urethra, conjunctiva, pharynx (PSCC), uterine endocervix, and rectum).
  2. Elementary body inhibits phagolysosome fusion, replicates in phagosome as reticulate body.
  3. Reticulate body will replicate, then swap back to elementary body for release
41
Q

Who is Chlamydia often asymptomatic in? How is diagnosis made? What is the primary risk of this group?

A

Asymptomatic in women, diagnosis made by nucleic acid amplification test

-> chlamydia will cause cervicitis. If it ascends to the fallopian tubes / ovaries, this is also secretory epithelium and can cause pelvic inflammatory disease -> ectopic pregnancies, infertility, pelvic pain, bleeding, and vertical transmission

42
Q

What do men typically develop in chlamydia infection? Complications?

A

Urethritis -> irritation and watery discharge

-> can cause epididymitis and infertility

43
Q

What is lymphogranuloma venereum? What will it cause?

A

Small, painless ulcers or vesicles on penis (similar to syphillis), followed by major lymphadenopathy / constitutional symptoms.
->suppurative inflammation blocks the lymph nodes and can cause strictures / lymphatic obstruction due to fibrosis

-> strains typically seen in Africa / Asia (L1-L3)

44
Q

What is trachoma? How can it cause its worse manifestation?

A

Ocular infection caused by Chlamydia trachomatis

  • > Conjunctiva becomes inflamed
  • > eyelid becomes scarred, which turns the eyelid inward
  • > eyelashes scratch the cornea, causing blindness
  • > seen in areas of poor hygiene. leading cause of blindness
45
Q

What is inclusion body conjunctivitis vs ophthalmia neonatorum?

A

Inclusion body conjunctivitis - conjunctivitis caused by C. trachomatis, usually due to perinatal transmission, but may occur in adults due to touching genitals then face

Ophthalmia neonatorum - conjunctivitis of newborn / infants, can be caused by gonorrhea or chlamydia, or even chemical irritants

46
Q

What one feature would make you suspect ophthalmia neonatorum is due to Chlamydia and not gonorrhea (other than time of onset)?

A

Often associated with infant pneumonia (staccato cough)

47
Q

What is Reiter syndrome and who is this more common in? Clinical triad?

A

Reactive arthritis -
Autoimmune response to chlamydial infection, more common in men

Clinical triad includes: Polyarthritis (especially sacroiliac joint / knees), urethritis, and conjunctivitis (uveitis)
-> think of the three monkeys in the sketchy video

48
Q

What is the morphology of Rickettsia rickettsii and how is it spread?

A

Gram-negative, poorly-staining, obligate intracellular coccobacillus
-> spread by saliva of the Dermacentor American dog tick (it’s Chagas disease which is spread by poop of tic, NOT this one)

49
Q

What cell type does Rickettsia rickettsii have tropism towards? When should its primary infection be treated?

A

Tropism towards vascular endothelial cells -> causes vasculitis
-> Rocky Mountain Spotted Fever is potentially life threatening, treatment with doxycycline should not be delayed if you think it is possible

50
Q

What are the clinical features of RMSF? What type of rash is it?

A

Fever and headache early on, followed by a rash with centripetal spread (spread from extremities towards the trunk

  • > will include palms and soles
  • > Rash is a petechial rash which is nonblanching due to bleeding into the dermis
  • > thrombocytopenia is caused by clotting forming around vasculitis areas
51
Q

What are the late stage findings of RMSF?

A

Systemic organ involvement -> including GI tract, CNS, heart, etc.

52
Q

What three diseases are associated with a rash on the palms and soles?

A
  1. Secondary syphilis
  2. Rocky Mountain Spotted Fever
  3. Coxsackievirus A - hand, foot, and mouth disease
53
Q

What is the structure, reservoir, and transmission pattern of mycobacterium leprae? Is it highly contagious?

A

Structure - acid-fast bacillus,

Reservoir - armadillos

Transmission - respiratory in the lepromatous form only

Not highly contagious -> only genetically susceptible patients can be infected

54
Q

What areas of the body are particularly susceptible to leprosy and why?

A

Skin and peripheral nerves -> likes to travel to cooler spots on the body, especially extensor surfaces turned away from the body and distal extremities

55
Q

How is Leprosy treated? Specify by the two subtypes.

A

Tuberculoid subtype - dapsone and rifampicin (think of dapsone deputy and his rifampin rifle)

Lepromatous subtype - dapsone, rifampicin, and clofazimine (think of the extra cloth rope hanging next to the deputy)

56
Q

What type of skin lesions exist in the paucibacillary form of leprosy, and what will be seen pathologically? What is the other name for this form?

A

Tuberculoid - paucibacillary just means few bacilli since the infection is well-controlled by Th1 immune response

Pathology - many well-formed granulomas

Skin - hypopigmented, hypoesthetic

57
Q

What type of skin lesions exist in the multibacillary form of leprosy, and what will be seen pathologically? What is the other name for this form?

A

Lepromatous- there will be many bacilli in the skin lesions since the infection is poorly-controlled by a Th2 immune response

Pathology - Sheets of foamy macrophages containing bacilli, which will also be present in endothelial and Schwann cells

Skin - larger, deep, more destructive skin lesions, with saddle-nose and lion-like faces

58
Q

What causes the majority of disfigurement in lepromatous leprosy?

A

Peripheral neuropathy leads to trauma and secondary infections which cannot be felt -> limbs often need to be amputated.

59
Q

What are the pseudohyphae of yeast and how do you tell this from actual hyphae?

A

They are elongated germ tubes of the dividing yeast form of Candida species

-> told from actual hyphae because these will taper before the “pseudoseptae”, indicating elongated budding. Regularly hyphae will not taper between septae.

60
Q

Which form of the dimorphic endemic fungi are infectious?

A 
The mycelial (environmental form, with spores) form
-> note that the yeast form it is not transmissible, as would be present in a patient with a respiratory infection with one of these
61
Q

How is Blastomyces infection diagnosed histologically? Describe the inflammation stages.

A

Presence of broad-based budding yeasts

Initial neutrophilic invasion into the lung, followed by chronic granulomatous inflammation / being walled off by macrophages

62
Q

What are the early findings of blastomycosis? What are the skin findings of blastomycosis? Who tends to get this?

A

Following an acute or chronic pneumonia with systemic symptoms (due to granuloma cytokines)

Small papules and pustules which can enlarge to ulcerated plaques with scarring

  • > can later spread to bones
  • > generally immunocompromised
63
Q

How does coccidioides differ from blastomycosis histologically and pathogenically?

A

Histologically - will appear much larger, with big balls of endospores reproducing by endosporulation

  • > initial acute inflammation followed by granulomatous inflammation, like blasto
  • > will appear similar to TB, and can disseminate to skin, basically the same as blasto.
64
Q

What does a coin lesion on X-ray mean and what pathogen is responsible?

A

Small lesion on X-ray or CT of the lung which corresponds to histoplasmosis which has been walled off in granulomas and calcified.

65
Q

How does Histoplasma capsulatum appear in histology? How can disseminated disease happen?

A

Very small little spores (much smaller than coccidoides spherules which are each are the size of lymphocytes) which are smaller than lymphocytes arranged in macrophages (appear like clusters)

-Disseminated disease happens with reactivation following immunosuppression (loss of TNF / IL12)

66
Q

What is the defining feature of Cryptococcus as a fungal infection? What defines whether or not it can spread in the body?

A

It has a heavy polysaccharide capsule -> the only fungus with a polysaccharide capsule

-> Spreading determined by presence of intact cell-mediated immunity

67
Q

What form of Cryptococcus is transmissible, and what is the normal vector which spreads it?

A

Spread most often by pigeon droppings and bat guano

Cryptococcus is NOT dimorphic -> only has an encapsulated yeast form, which is transmissible

68
Q

What are the two forms of aspergillosis which are NOT associated with being immuncompromised?

A
  1. Allergic bronchopulmonary aspergillosis (ABPA) -
    Type 1 hypersensitivity to aspergillus colonizing the airway, especially in asthma and CF patients
  2. Aspergilloma - collection of Aspergillus growing in a pre-exisiting pulmonary cavity (especially past TB infection), hemoptysis will be common
69
Q

What are the two forms of aspergillosis which ARE associated with being immunocompromised? What defect makes you susceptible?

A

Especially neutropenia

  1. Chronic necrotizing Aspergillus pneumonia - chronic lung disease
  2. Angioinvasive aspergillosis - causes thrombotic / hemorrhagic complications by invading vessels with acute angle hyphae, with dissemination to extrapulmonary organs and ring-enhancing lesions on CT.
70
Q

How are zygomycetes (Mucor / Rhizopus) identified under the microscope?

A

Wide-angle branching (i.e. 90 degrees) as well as nonseptate hyphae

71
Q

What patients are most susceptible to zygomycetes infection and how does the pathogen like to invade?

A

Neutropenic patients (i.e. leukemia) and uncontrolled diabetic ketoacidosis (high glucose environment which allowed molds to survive)

Pathogen invades vascular tissue first, causing hemorrhage, thrombosis, and infarction

72
Q

Where do zygomycetes invade and what is the treatment?

A
  1. Rhinocerebral disease -> infection of sinuses with orbital involvement, tissue necrosis, facial paralysis, and frontal lobe abscess due to CNS penetration thru cribriform plate
  2. Can have pulmonary / GI / disseminated involvement

Treatment: Surgical debridement and amphotericin B

73
Q

What is the major descriptive symptom of Giardiasis and how is it typically diagnosed?

A

Steatorrhea - fat-rich Ghirardelli Giardia fatty stools

Diagnosed via cysts / trophozoites in stool. In the past, diagnosed with the string test or duodeonal aspirate / biopsy.

74
Q

What is the life cycle of Trypanosoma cruzi / how is it spread to humans? What cells do they replicate in?

A

Epimastigotes in insets replicate, before becoming trypomastigote which is infectious.

Triatomine / kissing bug will bite around the human’s face and night then poop in the trypomastigotes into the wound. These can circulate in the bloodstream and replicate intracellularly as the amastigote form (within CARDIAC and SMOOTH muscle cells)

75
Q

What is American trypanosomiasis also called and how is it diagnosed?

A

Chagas disease, diagnosed via blood smear containing trypomastigote, serological testing, or PCR

76
Q

What sign is associated with acute infection with Trypanosoma cruzi?

A
  1. Chagoma - inflammation of bug bite

2. Romana’s sign - edema of eyelids / conjunctiva if trypanosome enters through conjunctiva

77
Q

What heart problems characterize Chaga’s disease

A

Myocarditis -> tryptomastigote burrows through endocardium and replicates in cardiomyocytes, leading to dilated cardiomyopathy, congestive heart failure, and conduction abnormalities

-> can be visualized on biopsy

78
Q

Other than heart problems, what characterizes the chronic phase of Chaga’s disease?

A
  1. Megaesophagus - difficulty swallowing, from smooth muscle involvement
  2. Megacolon - severe constipation, from smooth muscle involvement
79
Q

How do you get elephantiasis?

A

Years of repeated exposure to mosquito vector infected with the nematode (roundworm) Wuchereria bancrofti.

80
Q

What is the life cycle of Wuchereria bancrofti?

A

Adult female worms in human host produces thousands of microfilariae -> ingested by feeding mosquito -> two larval changes in mosquito -> inoculated back into human host to complete life cycle as adult worms which live in lungs by day and peripheral blood by night when the mosquitos feed

81
Q

What are the signs / symptoms of filariasis? Can it be treated?

A

Fever, lymphadenopathy, chronic limb and genital swelling because of adult worms blocking lymph nodes and vessels producing inflammation and lymphatic damage (lymph backs up)

Only the microfilariae can be treated -> with diethylcarbamazine

82
Q

Which species cause hepatic / intestinal schistosomiasis vs urinary schitosomiasis?

A

Hepatic / intestinal - S. mansoni and S. japonicum

Urinary - S. haematobium

83
Q

What is the life cycle of Schistosoma, including where they diverge between the two subtypes? What is their intermediate host

A

Snails are intermediate host, release cercariae into water which penetrate human skin, then disseminate to portal circulation hematogenously.

  • > Hepatic / intestinal will migrate as a pair to mesenteric veins
  • > Urinary will migrate to vesicular veins
  • > eggs are released in stool or urine respectively, which are taken up by snails after hatching
84
Q

What does early infection with Schistosoma cause?

A

Swimmer’s itch -> pruritic or papular rash where cercariae penetrated

Still in early stage: lymphadenopathy, hepatosplenomegaly, and reactive eosinophilia
-> may be subclinical

85
Q

What will be the late complications of the hepatic / intestinal forms of schistosomiasis (months to yeras later)?

A

Abdominal pain / bloody diarrhea, with development of intestinal obstruction / hepatic periportal “pipestem” fibrosis due to granulomatous inflammation

-> portal hypertension and associated symptoms are likely

86
Q

What are the symptoms of portal hypertension?

A

Ascites, hematemesis (esophageal varices), splenomegaly (splenic vein can’t drain)

87
Q

What will urinary schistosomiasis cause long-term? Most important association?

A

Dysuria, hematuria, urinary tract obstruction secondary to granuloma formation.

Can lead to chronic UTIs, chronic kidney disease

All this inflammation leads to squamous metaplasia
-> can cause SQUAMOUS CELL carcinoma of the BLADDER

88
Q

What type of worm is Trichinella spiralis and how is it transmitted?

A

It is an intestinal nematode

-> all stages of development occur in a single host who eats meat of another host with cysts in their muscle tissue

89
Q

What is the life cycle of Trichinella spiralis?

A

Ingestion of undercooked infected meat (usually pork) with encysted larvae -> cysts penetrate villi of small intestine after ingestion and develop into adult worms

  • > gravid female produces new larvae deep in the mucosa which disseminated via lymphatics / bloodstream
  • > larvae remain viable as cysts in skeletal muscle for months to ears
90
Q

What are the usual symptoms of Trichinella infection?

A

Usually asymptomatic or undiagnosed if a small number of larvae

91
Q

What are the symptoms of the three phases of Trichinella infection if the inoculum is heavy?

A
  1. Enteral phase (week one) -> vomiting, diarrhea, nausea, hemorrhage, ulceration
  2. Parental / migratory phase (past 1 week) -> eosinophilia, periorbital edema, systemic symptoms. Muscle swelling / pain as they encyst, can even cause elevated muscle enzymes
  3. Encystation phase with tissue repair -> larvae become surrounded by fibrosis and skeletal muscle as cyst wall calcifies, with resolution of clinical symptoms.
92
Q

What is a nurse cell?

A

Multinucleated skeletal muscle cells which surround the encysted Trichinella spiralis larvae

Pathobiology (20 decks)

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