Bacteria V

Question 1

Anthrax: bacillus anthracis

Answer 1

encapsulated
G+
large, spore producing rod

Question 2

method of transmission with antrax

Answer 2

contact with animals, animal hides, animal products

• sheep and goats
• inhaled as a powder

Question 3

what kind of diseases does anthrax cause?

Answer 3

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

Question 4

pathological mechanism of anthrax

Answer 4

antiphagocytic activity

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

Question 5

mycobacterium tuberculosis

Answer 5

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

Question 6

virulence factors of TB

Answer 6

glycolipids promote resistance to intracellular killing

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

Question 7

histological hallmarks of mycobacterium TB

Answer 7

caseating granulomas

-associated with elderly, AIDS and alcoholism

Question 8

TB pathogenesis

Answer 8

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

Question 9

how does granuloma formation occur in TB?

Answer 9

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

Question 10

what is the gold stand of diagnosing TB

Answer 10

seeing bacteria on stain

-takes 30 days though

Question 11

Key features of granuloma formation

Answer 11

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

Question 12

what causes the epithelioid changes for granuloma formation?

Answer 12

interferon-gamma

Question 13

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

Answer 13

PPD test

Question 14

primary (or latent) TB

Answer 14

-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

Question 15

what are Ghon complexes?

Answer 15

primary lung lesion with caseating granulomas in draining lymph nodes

Question 16

secondary TB

Answer 16

• 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

Question 17

what are the characteristics symptoms with secondary infection

Answer 17

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

Question 18

tertiary TB

Answer 18

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)

Question 19

how does TB get into the blood?

Answer 19

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

Question 20

gold standard of diagnosis for TB

Answer 20

positive culture of organism

Question 21

diagnosis of TB

Answer 21

AFB in sputum

Question 22

what are characteristics of X-ray with someone with TB

Answer 22

cavitary lesions

-calcifications of lymph nodes

Question 23

what is the Quanti-feron test

Answer 23

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

Question 24

clinical progression of TB

Answer 24

• 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

Question 25

Leprosy (mycobacterium leprae) pathogenesis

Answer 25

infection affecting skin and nerves - coolest parts of body - skin: macular, papular, or nodular lesions - nerves: ulnar, peroneal

Question 26

leprosy forms of diseases

Answer 26

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

Question 27

T. pallidum: Syphilis

Answer 27

microaerophilic spirochete - covered in outer sheath that masks bacterial antigens - sexual/transplacental transmission

Question 28

diagnosis of syphilis

Answer 28

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)

Question 29

In primary stage, what would the serology show?

Answer 29

no antibodies, organism present

Question 30

In secondary stage, what would the serology show?

Answer 30

antibodies and organism present

Question 31

In tertiary stage, what would the serology show?

Answer 31

antibodies, NO organism

Question 32

pathogenesis of syphilis

Answer 32

- 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

Question 33

primary syphilis

Answer 33

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

Question 34

secondary syphilis

Answer 34

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

Question 35

tertiary syphilis

Answer 35

-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

Question 36

neurosyphilis

Answer 36

chronic meningoecephalitis | -tabes dorsalis-> charcot joints (sensory)

Question 37

CSF findings for neurosyphilis

Answer 37

pleiocytosis, increased protein and decreased glucose

Question 38

benign tertiary syphilis

Answer 38

formation of gummas | -skin, subcut. tissue, bone, joints

Question 39

pathology of tertiary syphilis

Answer 39

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

Question 40

congenital syphilis

Answer 40

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