Bacteria V Flashcards
Anthrax: bacillus anthracis
encapsulated
G+
large, spore producing rod
method of transmission with antrax
contact with animals, animal hides, animal products
- sheep and goats
- inhaled as a powder
what kind of diseases does anthrax cause?
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
pathological mechanism of anthrax
antiphagocytic activity
- edema factor
- cytotoxic factor
- leukopenia (kills neutrophils)
- bacteremia-> meningitis
- electrolyte imbalance, hemoconcentration, DIC-> leads to death
mycobacterium tuberculosis
acid fast-> waxes in their cell wall
-slow growing
facultative intracellular invaders
virulence factors of TB
glycolipids promote resistance to intracellular killing
- inhibit interferon activation of macrophages, prevent phago-lysosome membrane fusion
- stimulate destructive cell-mediated inflammatory injury
histological hallmarks of mycobacterium TB
caseating granulomas
-associated with elderly, AIDS and alcoholism
TB pathogenesis
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
how does granuloma formation occur in TB?
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
what is the gold stand of diagnosing TB
seeing bacteria on stain
-takes 30 days though
Key features of granuloma formation
- persistent infection by mycobacterium
- type IV hypersensitivity reaction
- synthesis of interferon gamma as a result of a specific T cell mediated response
- formation of granuloma-> chronic immune mediated reaction, chronic inflammation, fibrosis, and caseous necrosis
what causes the epithelioid changes for granuloma formation?
interferon-gamma
what must you give someone before you give an anti-interferon drug?
PPD test
primary (or latent) TB
-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
what are Ghon complexes?
primary lung lesion with caseating granulomas in draining lymph nodes
secondary TB
- 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
what are the characteristics symptoms with secondary infection
fever, night sweats, weakness, loss of appetite, weight loss, productive cough, blood-streaked sputum
tertiary TB
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)
how does TB get into the blood?
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
gold standard of diagnosis for TB
positive culture of organism
diagnosis of TB
AFB in sputum
what are characteristics of X-ray with someone with TB
cavitary lesions
-calcifications of lymph nodes
what is the Quanti-feron test
in vitro measure of interferon production in response to exposure to M.TB
clinical progression of TB
- 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
Leprosy (mycobacterium leprae) pathogenesis
infection affecting skin and nerves
- coolest parts of body
- skin: macular, papular, or nodular lesions
- nerves: ulnar, peroneal
leprosy forms of diseases
- Tuberculoid leprosy: granulomas
- lepromatous: associated with lack of Th1 mediated immunity and proliferation of organism in macrophages (foam cells), contagious form
T. pallidum: Syphilis
microaerophilic spirochete
- covered in outer sheath that masks bacterial antigens
- sexual/transplacental transmission
diagnosis of syphilis
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)
In primary stage, what would the serology show?
no antibodies, organism present
In secondary stage, what would the serology show?
antibodies and organism present
In tertiary stage, what would the serology show?
antibodies, NO organism
pathogenesis of syphilis
- 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
primary syphilis
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
secondary syphilis
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
tertiary syphilis
-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
neurosyphilis
chronic meningoecephalitis
-tabes dorsalis-> charcot joints (sensory)
CSF findings for neurosyphilis
pleiocytosis, increased protein and decreased glucose
benign tertiary syphilis
formation of gummas
-skin, subcut. tissue, bone, joints
pathology of tertiary syphilis
lymphoplasmacytic infiltrates
- obliterative endarteritis-> endothelial proliferation and intimal fibrosis
- focal epitheloid granulomas-> delayed-type hypersensitivity reaction: central necrosis surrounded by palisading macrophages and fibroblasts
congenital syphilis
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
