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General Pathology Theory > Infectious disease > Flashcards

Infectious disease Flashcards

1
Q

What are the classes of human pathogens? Give an example of each and a disease it causes

A

Prions: prion protein, Creutzfeld-Jacob
Virus: poliovirus, poliomyelitis
bacteria: Streptococcus pneumoniae, pneumonia
fungi: Candida, thrush
protozoa: Trypanosoma cruzi, Chagas disease
helminths: trichinella spiralis, trichinosis

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2
Q

What histochemical stain highlights Histoplasma capsulatum?

A

Romanowsky/Giemsa

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3
Q

Which coccobacillus is negative for Gram staining but stains with silver (causes necrotizing bronchopneumonia)

A

Legionella pneumophila serogroup 1

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4
Q

What is the typical pattern of injury in a kidney bx from post-streptococcal kidney failure?

A

Diffuse proliferative glomerulonephritis

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5
Q

Name 4 viruses that can cause interstitial nephritis

A

CMV, EBV, BK, Hantavirus

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6
Q

Name 4 organisms other than TB that stain with acid fast stain

A

Nocardia sp.
Mycobacterium marinum
Legionella micdadei
Rhodococcus equi

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7
Q

What is the causative organism in cat scratch associated lymphadenitis?

A

Bartonella henselae

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8
Q

What intracerebral infection (ring enhancing lesion) in an HIV patient with a CD4 count of 50?

A

Toxoplasma gondii

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9
Q

What morphology do dimorphic fungi show in histology samples?

A

yeast structures

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10
Q

Negri bodies are seen in which condition?

A

Rabies encephalitis

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11
Q

What are 3 conditions associated with HHV8?

A

Kaposi sarcoma
Multicentric Castleman disease
Primary effusion lymphoma

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12
Q

Name 4 viruses causing hemorrhagic fevers

A

Lassa virus
Ebola virus
Marburg virus
Machupo virus

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13
Q

What are the histologic findings in a colon bx from a patient infected with Shigella?

A

Cryptitis, crypt abcess, pseudomembranes

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14
Q

Name 4 category A disease/bioterrorism agent as classified by the CDC?

A

Bacillus anthracis
Yersinia pestis
Clostridium botulinum toxin
Variola major virus (smallpox)

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15
Q

What is a finding in pseudomonas infections?

A

Necrotizing pneumonia

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16
Q

Name features of primary, secondary, tertiary syphilis

A

1: chancre on the penis/scrotum/vulva/cervix
2: diffuse rash (palmar)
3: endarteritis of proximal aorta, gummas of skin, bone, liver
Argyll0Robertson pupils

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17
Q

What is a cause of elephantitis?

A

Worms in the lymphatic system causing damage to lymphatics; aka filariasis. Includes Wuchereria bancrofti and Brugia sp.

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18
Q

What species of fungi are the most frequent cause of human infections?

A

Candida species

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19
Q

What does symbiosis imply?

A

Organisms that live on or in other organisms (hosts), with a mutually advantageous arrangement

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20
Q

Give 4 features of Whipple disease

A
  • caused by gram-positive actinomycete Tropheryma whippelii
  • histology shows dense accumulation of distended, foamy macrophages in the small intestinal lamina propria
  • Ddx includles intestinal tuberculosis
  • foamy macrophages are positive for PASD, but do not stain with acid fast stain
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21
Q

Name at least 4 human prion diseases

A 
Creutzfeld-Jacob 
Variant Creutzfeld-Jacob
Kuru
Fatal familial insomnia
Gerstmann-Straussler-Scheinker syndrome
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22
Q

What is the condition caused by prions?

A

Transmissible spongiform encephalopathies

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23
Q

What are prions, and how do they differ from other infectious organisms?

A

Infectious agents composed of misfolded proteins, that cause transmissible neurodegenerative disorders
They differ from others in that they do not contain nucleic acids

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24
Q

Describe the pathogenesis of prion disease

A

Normal prion protein (PrP), normally present in neurons undergoes a conformational change to abnormal form making it indigestible to proteases
Infectious (PrPsc) binds to normal (PrP) protein, catalyzing it into the abnormal form
- The new PrPsc continues to catalyze the transformation of more prion protein
- Abnormal prion protein accumulates in neural tissues, causing pathology

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25
Q

What are the 3 methods by which prion disease arises in humans?

A
  • Acquired
  • Familial
  • Sporadic
26
Q

What are the clinical presentations of prion diseases?

A
  • Personality changes
  • Psychiatric disorders (depression)
  • Lack of coordination
  • Ataxia
  • Myoclonus
  • Sensory changes
  • Insomnia
  • Confusion
  • Memory deficits
  • Dementia
  • Paralysis
27
Q

List 5 types of CJD

A
  • Classic CJD
  • Iatrogenic CJD
  • Variant CJD
  • Familial CJD
  • Sporadic CJD
28
Q

Compare and contrast classical and variant CJD

A

Classic:
age at death: 68
duration of illness: 4 months
s/s: dementia, neurologic
EEG with periodic short waves: present in 75%
florid plaques on histology: absent
IHC: variable accumulation
immunoblot for protease-resistant protein: not reported
detection of infective prion in lymphoid tissue: not detected

Variant: 
age at death: 28 yrs
duration of illness: 13 months
s/s: psychiatric, behavioural, sensory symptoms
EEG periodic short waves: absent
pulvinar sign on MRI: present
florid plaques on histology
PrP accumulation significant on IHC
Significant PrP accumulation on immunoblot
prion detected in lymphoid tissue
29
Q

What are the microscopic features of CJD?

A
  • Spongiform transformation of cerebral cortex, caudate, putamen
  • Uneven distribution of variably sized small microscopic vacuoles within neuropil and perikaryon of neurons, expanding into cyst-like spaces
  • Severe neuronal loss and reactive gliosis in advanced cases
  • Kuru plaques (aggregates of PrPsc) frequently in cerebellum
  • Kuru plaques also found in cerebral cortex in variant CJD
  • Plaques are Congo red and PAS positive
30
Q

Which prion disease does not show spongiform change? What are the characteristic histologic findings?

A
  • Fatal familial insomnia
  • Shows neuronal loss in anterior ventral and dorsomedial nuclei of thalamus, inferior olivary nuclei
  • Reactive gliosis in anterior ventral and dorsomedial nuclei of thalamus
31
Q

What four factors affect viral tropism?

A
  • Host cell receptors
  • Cellular transcription factors that respond to viral enhancers and promoter sequences
  • Anatomic barriers
  • Local environment including temperature, pH, host defenses
32
Q

Through what 3 mechanisms do viruses cause damage to human hosts?

A
  • Direct cytopathic effects
  • Eliciting immune response that damages tissues
  • Transforming infected cells into neoplastic cells
33
Q

What are the three components of the viral particle?

A
  • Envelope
  • Capsid
  • Core
34
Q

List the Baltimore classification of viruses and give an example of each.

A
  • dsDNA: herpesvirus
  • ssDNA: parvovirus
  • dsRNA: reovirus
  • +ssRNA: West Nile virus
  • -ssRNA: rabies virus
  • ssRNA-RT: HIV
  • dsDNA-RT: hepatitis B
35
Q

What is the classification of viral hepatitis?

A
  • can be classified by virus or by clinical syndrome
  • clinical: acute symptomatic infection with recovery, acute symptomatic hepatitis with recovery, chronic hepatitis (+/- progression), fulminant hepatitis (massive/submassive hepatic necrosis)
  • by virus type:
    hepatotrophic: hepatitis A,B,C,D, E
    non-hepatotrophic: CMV, EBV, herpes, adenovirus, HIV
36
Q

What is the definition of chronic hepatitis?

A

Symptomatic, biochemical or serologic evidence of continuing/relapsing hepatic disease for greater than 6 months

37
Q

What is the frequency of chronic liver disease for each hepatotrophic virus?

A
  • Hep A: 0%
  • Hep B: 10%
  • Hep C: 80%
  • Hep D (coinfection): 80% with HepB
  • Hep E: 0%
38
Q

What genotypes of HCV have the best response to treatment

A
  • Genotypes 2 and 3
39
Q

What defines the carrier state of HBV?

A
  • Infected individual who can transmit the virus, but is asymptomatic (no liver disease or non-progressive damage)
  • serologically have anti-HBe, normal AST/ALT, low serum HBV DNA
  • do not have HBe-Ag
40
Q

What are the laboratory and histologic findings in a healthy carrier of HBV?

A
  • HBsAG+, HBeAG-
  • AntiHBe+
  • HBV-DNA low or negative
  • ALT/AST normal
  • bx: lack of inflammation or necrosis
41
Q

What are the histologic findings in acute hepatitis

A

Hepatocyte ballooning degeneration
Cholestasis
Lymphocytic infiltrate, zone 3
Apoptotic hepatocytes with fragmented nuclei and eosinophilic cytoplasm
focal hepatocyte dropout w/ macrophages
Kupffer cell hypertrophy and hyperplasia with lipofuscin pigment
portal tract infiltrate with mixed inflammatory cells

42
Q

What are some specific histologic features of acute HAV and HBV?

A

HAV: plasma-cell predominant inflammatory infiltrate of portal, periportal, lobular areas with perivenular cholestasis, extensive microvesicular steatosis
HBV: ground glass hepatocytes caused by cytoplasm packed with spheres of HBsAg

43
Q

What are the histologic findings of chronic hepatitis?

A
  • Lymphocytic portal infiltrate, +/- interface hepatitis
  • varying degrees of necrosis/bridging necrosis
  • varying degrees of fibrosis periportal–bridging
44
Q

What are some specific histologic features of chronic HBV and HCV?

A

HBV: ground glass hepatocytes
HCV: lymphoid aggregates +/- germinal centres and reactive bile duct changes, focal macrovesicular steatosis esp. with genotype 3

45
Q

What are the histologic findings in cirrhosis?

A

Hepatocytes divided into irregularly sized nodules separated by thick bands of fibrosis

46
Q

What are several common grading/staging systems for viral hepatitis?

A 
Hepatic activity index
Ishak modification
Scheuer classification
Metavir classification
Batts-Ludwig
47
Q

What is reported in a grading/staging system for viral hepatitis

A
  • Grade: degree of inflammation/necrosis

- Stage: degree of fibrosis

48
Q

What is fulminant hepatic failure

A

Hepatic insufficiency that progresses from the onset of symptoms to hepatic encephalopathy in 2-3 weeks in an individual who does not have chronic liver disease

49
Q

What are the morphologic features of fulminant hepatitis?

A
  • Loss of liver mass
  • Limp, red tissue
  • Wrinkled capsule
  • Necrotic red interior with hemorrhage
  • Complete destruction of hepatocytes, with collapsed reticulin and preserved portal tracts
50
Q

Describe transmission incubation period diagnostic investigations for the hepatotrophic viruses

A

A: F/O, 2-6 weeks anti-HAV (IgM)
B: parenteral, vertical, 6wks-6mo, HbSAg, HBVAg antibody
C: parenteral, 5-10wks, HCV RNA or anti-HCV (IgG/IgM)
D: parenteral, close contact; 6wks-6mo, Anti-HDV (IgG/IgM), HDV RNA, HDVAg in liver
E: F/O, 2-6wks, Anti HEV (IgG/IGM) or HEV RNA

51
Q

What IHC stains are useful in HBV, and how are they used?

A
  • HBV core antigen and HBV surface antigen
  • can be negative in acute HBV
  • positive in chronic, with decreased staining when +++Inflammation
  • HBsAg stains cytoplasm
  • HBcAg stains nucleus, represents active viral replication
  • if HBsAG is membranous and HBcAg cytoplasmic=unopposed replication
52
Q

Describe the serological/PCR findings of HBV in the following:

  • Acute
  • Chronic (high-infectivity)
  • Chronic (low-infectivity)
  • Recovered
  • Immunized
A

Acute: HBsAG+, HBeAg+, Anti-HBC IgM, HBV DNA+
Chronic/infective: HBsAG+, HBeAg+, Anti-HBc IgG, HBV DNA+
Chronic/non-inf.: HBsAg+, HBeAg-, Anti-HBe+, Anti-HBC IgG, HBV DNA-
recovered: HBsAg-, AntiHBs+, HBeAg-, AntiHBe+, AntiHBc-IgG, HBV DNA-
immunized: Anti-HBs + (all the rest negative)

53
Q

What are risk factors for HCV?

A
  • IV drug use
  • multiple sex partners
  • recent surgery (6 mo)
  • Needle stick injury
  • Multiple contacts with HCV infected popuation
  • employment in medical/dental fields
54
Q

What is the natural history of HCV infection?

A
  • Persistent infection/chronic hepatitis in 80%

- cirrhosis in 5-20 yrs in 1/3 of pts with persistent infection

55
Q

Describe the morphology and IHC of HDV

A
  • Same features as HBV

- HDAg

56
Q

Describe HDV co-infection, superinfection and helper independant latent infection

A
  • Acute co-infection: occurs on exposure to both HBV/HDV; HBV establised first, providing HBSAg necessary for HDV virions; hepatitis ranges from mild to fulminant (rarely chronic)
  • Superinfection; occurs when chronic HBV exposed to new HDV; acute hepatitis 30-50d later, fequently develops into chronic disease/cirrhosis
  • Helper independant: in liver transplants, HDV detected in nuclei of liver w/o HBV (prevented with HBV immunoglobulins)
57
Q

What is hepatitis F

A

Various undesignated viruses causing hepatitis

some cause hemorrhagic hepatitis with toga-virus like particle on EM

58
Q

Define Hepatitis G

A

Flavavirus related to HCV, transmitted by blood/sexual contact
- no known human disease, not hepatotrophic and no elevations in ALT/AST

59
Q

What is relationship between HGV/HIV

A
  • commonly co-infect

- dual infection protective against HIV

60
Q

What should you do if you cut your finger during an autopsy?

A
  • Follow facility’s procedures
  • Wash wound with warm water/soap
  • Hold affected limb down to get it to bleed
  • Do not squeeze wound or soak in bleach
  • apply antiseptic if necessary (poviodine-iodine 10%)
  • contact occ heath or ED ASAP
61
Q

What is the usual clinical presentation of infectious mononucleosis?

A
  • Fever, generalized lymphadenopathy, splenomegally, sore throat, fatigue, atypical activated T lymphocytes (mononucleosis cells) in the blood
62
Q

What are the uncommon complications of acute EBV infection?

A

splenic rupture, upper airway obstruction, hepatitis, encephalitis, pneumonitis, hemophagocytic lymphohistiocytosis

General Pathology Theory (6 decks)

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