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Pathology: Infectious disease section > Bacteria V > Flashcards

Bacteria V Flashcards

1
Q

Anthrax: bacillus anthracis

A

encapsulated
G+
large, spore producing rod

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2
Q

method of transmission with antrax

A

contact with animals, animal hides, animal products

  • sheep and goats
  • inhaled as a powder
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3
Q

what kind of diseases does anthrax cause?

A

cutaneous disease
-small hemorrhagic pustule develops into black eschar with very painful lymphadenitis

pulmonary disease

  • woolsorter’s disease, extensive pneumonia with serofibrinous (mixture of edema and fibrin) exudation
  • sepitemia
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4
Q

pathological mechanism of anthrax

A

antiphagocytic activity

  • edema factor
  • cytotoxic factor
  • leukopenia (kills neutrophils)
  • bacteremia-> meningitis
  • electrolyte imbalance, hemoconcentration, DIC-> leads to death
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5
Q

mycobacterium tuberculosis

A

acid fast-> waxes in their cell wall
-slow growing
facultative intracellular invaders

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6
Q

virulence factors of TB

A

glycolipids promote resistance to intracellular killing

  • inhibit interferon activation of macrophages, prevent phago-lysosome membrane fusion
  • stimulate destructive cell-mediated inflammatory injury
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7
Q

histological hallmarks of mycobacterium TB

A

caseating granulomas

-associated with elderly, AIDS and alcoholism

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8
Q

TB pathogenesis

A

no know endotoxins, exotoxins or hystiolytic enzymes

  • hypersensitivity reactions (delayed, type IV) plays dominant role
  • tubercle (granuloma) consists of plump, round histiocytes (epithelial cells), langhans mutlinucleated giant cells, peripheral collar of fibroblasts, with lymphocytes
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9
Q

how does granuloma formation occur in TB?

A

inability of macrophages to kill bacteria results in persistent infection

  • presentation of TB antigen by infected macrophages to lymphocytes
  • Th1 cells-> secretion of interferon gamma
  • TNF induces chemotaxis and collection of more monocytes, interferon gamma results in aggregation of epithelioid macrophages
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10
Q

what is the gold stand of diagnosing TB

A

seeing bacteria on stain

-takes 30 days though

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11
Q

Key features of granuloma formation

A
  1. persistent infection by mycobacterium
  2. type IV hypersensitivity reaction
  3. synthesis of interferon gamma as a result of a specific T cell mediated response
  4. formation of granuloma-> chronic immune mediated reaction, chronic inflammation, fibrosis, and caseous necrosis
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12
Q

what causes the epithelioid changes for granuloma formation?

A

interferon-gamma

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13
Q

what must you give someone before you give an anti-interferon drug?

A

PPD test

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14
Q

primary (or latent) TB

A

-local infection
lack previous contact with TB
-most show no symptoms
-Ghonus focus in lower part of upper lobes or upper lobes or upper part of lower lobes (unilateral)
-most cases result in fibrosis, calcification, but rarely progressive disease
-direct progression more common in children and may lead to disseminated (miliary) lesions and meningitis

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15
Q

what are Ghon complexes?

A

primary lung lesion with caseating granulomas in draining lymph nodes

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16
Q

secondary TB

A
  • disease in PREVIOUSLY sensitized individual either by reactivation or reinfection
  • cavitary lesion in apical lobes-> high oxygen tension
  • satellite lesions in nodes are distinctly rare
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17
Q

what are the characteristics symptoms with secondary infection

A

fever, night sweats, weakness, loss of appetite, weight loss, productive cough, blood-streaked sputum

18
Q

tertiary TB

A

progressive secondary infection may lead to:

  • extension of other parts of lung, empyema
  • miliary TB in other organs (bacteremia)
  • isolated organ TB (cervical lymph nodes, meninges, kidney, adrena, bones)
19
Q

how does TB get into the blood?

A

drainage of organisms into lymphatics leads to dumping of organisms into the bloodstream via thoracic duct
-redistribution to other lung fields via pulmonary recirculation as miliary TB

20
Q

gold standard of diagnosis for TB

A

positive culture of organism

21
Q

diagnosis of TB

A

AFB in sputum

22
Q

what are characteristics of X-ray with someone with TB

A

cavitary lesions

-calcifications of lymph nodes

23
Q

what is the Quanti-feron test

A

in vitro measure of interferon production in response to exposure to M.TB

24
Q

clinical progression of TB

A
  • most exposed either develop no infection or latent infection
  • progression to secondary disease leads to pulmonary symptoms, AFB in sputum, and x-ray changes
  • tertiary disease is rare, miliary TB in lung is most common presentation
25
Q

Leprosy (mycobacterium leprae) pathogenesis

A

infection affecting skin and nerves

  • coolest parts of body
  • skin: macular, papular, or nodular lesions
  • nerves: ulnar, peroneal
26
Q

leprosy forms of diseases

A
  1. Tuberculoid leprosy: granulomas
  2. lepromatous: associated with lack of Th1 mediated immunity and proliferation of organism in macrophages (foam cells), contagious form
27
Q

T. pallidum: Syphilis

A

microaerophilic spirochete

  • covered in outer sheath that masks bacterial antigens
  • sexual/transplacental transmission
28
Q

diagnosis of syphilis

A

RPR, VDRL-> nonspecific tests for antibody to cardiolipin
-false positive with mono and lupus

dark field microscopy-> silver stain for organism

Specific fluorescent treponemal antibody absorption test (FTA-Abs)

29
Q

In primary stage, what would the serology show?

A

no antibodies, organism present

30
Q

In secondary stage, what would the serology show?

A

antibodies and organism present

31
Q

In tertiary stage, what would the serology show?

A

antibodies, NO organism

32
Q

pathogenesis of syphilis

A
  • scarcity of treponemes and intense inflammatory infiltrate suggest central role for immune response in lesions
  • chancres infiltrated with Th1 cells
  • antibody response does not eliminate the infection
  • endarteritis central to the pathology of all lesions
33
Q

primary syphilis

A

development of hard chancre at site of spirochete invasion

  • intense mononuclear infiltrate with plasma cells
  • obliterative endarteritis, vessel wall infiltrates
  • VDRL AND ANTI-TREPONEMAL antibodies are NEGATIVE
  • organism can be extracted from lesion
34
Q

secondary syphilis

A

2-10 weeks after primary chancre
painless macular plaques of skin and mucous membranes
-elevated broad plaques in the region of the penis or vulva-condylomata lata
-widespread mucocutaneous lesoins-> macular discrete red-brown lesions, especially soles and palms
-contain spirochetes and are infectious (histology similar to chancre)
-enter into latent disease after several weeks
-VDRL/ANTI-TREPONEMAL antibodies POSITIVE
–organism can be extracted from lesion

35
Q

tertiary syphilis

A

-latent period of 5 years or more
-cardiovascular system most commonly affected
damage to proximal aorta and aortic root
obliterated endarteritis-> tree barking
aneurysms and dissections/coronary insufficiency
-neurosyphyilis/tabes dorsalis/charcot’s joint
-syphilitic gumma
–VDRL/ANTI-TREPONEMAL antibodies POSITIVE
-organism CANNOT be extracted from lesion

36
Q

neurosyphilis

A

chronic meningoecephalitis

-tabes dorsalis-> charcot joints (sensory)

37
Q

CSF findings for neurosyphilis

A

pleiocytosis, increased protein and decreased glucose

38
Q

benign tertiary syphilis

A

formation of gummas

-skin, subcut. tissue, bone, joints

39
Q

pathology of tertiary syphilis

A

lymphoplasmacytic infiltrates

  • obliterative endarteritis-> endothelial proliferation and intimal fibrosis
  • focal epitheloid granulomas-> delayed-type hypersensitivity reaction: central necrosis surrounded by palisading macrophages and fibroblasts
40
Q

congenital syphilis

A

may be contracted by a fetus born up to five years after mother first become infected
-late abortion
-diffuse rash, disseminated lesions, including destruction of bridge of nose “saddle nose”
-Hutchinson teeth, saber chin: infection of bones and teeth
liver lung involvement
-late occurring form: interstitial keratitis and eighth nerve deafness

Pathology: Infectious disease section (11 decks)

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