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SPECIFIC INFLAMMATION
1. Immune granulomas=granulomatous patern
2. Specific immune response – T lymphocytes +
macrophages
3. Hypersensitivity – delayed type, cell-
mediated (IV)
4. Specific granulation tissue = 0 vessels
• TBC, atypical mycobacteria
• Leprosy (Hansen disease)
• Syphilis
• Rhinoscleroma
• Mesenterial lymphadenitis
• Lymhogranuloma venereum
• Fungi (histoplasmosis, blastomycosis, cryptococosis)
TUBERCULOSIS
• Mycobacterium tuberculosis complex (hominis, bovis, M. africanum
Koch´s bacillus (2-10mm) – Robert Koch, 1882
N O T other mycobacterial infections: m arinum, m. avium intracellulare, xenopi, kansasii, leprae
• Acid fast bacillus
• Intracellular replication
• Transmition - from person to person (aerosol, direct contact – skin forms – milker disease)
• Predisposing conditions – immunosupression (chronic alcoholism, diabetes, malnutrition, HIV)
EPIDEMIOLOGY
• US – annual incidence 12/100 000, mortality 2/100 000
• Developing countries - 450/100 000
• Racial and ethnic differences (Africans, Native Americans, Eskimos – more susceptible)
• Transmission – inhalation (aerosolized droplets – coughing, sneezing, talking)
- ingestion (non-pasteurized milk, infected sputum)
- direct inoculation (milkers´diseaes)
CLINICAL COURSE
balance between host resistence and organism virulence and antigenicity
1) Elimination
2) Persistence
3) Progression, reactivation
SYMPTOMS
• Asymptomatic
• Non specific - weigh loss, fatigue, night
sweats
• Abrupt- high fever, plural effusions,
lymphadenitis, hemoptysis
TUBERCULOSIS
Morhological features
Proliferative form (TBC granuloma,
Langhan´s cels, epitheloid histiocytes)
milliary granuloma x large granuloma
Exsudative form (serofibrinous exudate,
Orth´s cells) – caseous pneumonia,
basilary meningitis
TUBERCULOSIS
• Primary – unsensitized cells,
wall lipids block the fusion of phagosome and lysosomes – bacilli proliferate)
Ghon´s complex
90% self limited course x 10%progression
Lymphogenic, hematogenic propagation
• Secondary (high resistence, hypersensitivity
Porogenic propagation)
• Milliary
ATYPICAL MYCOBACTERIOSES
MYCOBACTERIUM AVIUM-
INTRACELLULARE COMPLEX (MAI)
• Soil, water, foodstuff worldwide
1)rare, slowly progressive (years, decades)
granulomatous pulmonary d. in immunocompetent patients (antedescent d.-COPD, TBC, pneumoconioses, bronchiectasias)
2) Progressive systemic d. –immunocompromized- AIDS (pulmonary and gut forms)
OTHER ATYPICAL MYCOBACTERIA
1. M. kansasii – soil, dust, water, chronic pulmonary d. similar to MAI, elderly
2. M. scrofulaceum – ingestion from soil, dust – cervical lymphadenitis, kids
3. M. Marrinum – direct inoculation from fish, swimming pools, all
4. M. ulcerans- Autralia, africa, youngs, large skin ulcers
5. M.fortiutum- inoculation due to trauma or iatrogenic injury, pyogenic infl., all,
SARCOIDOSIS – MORBUS BESNIER-BOECK-
SCHAUMANN •Sarcoidosis is a rare disease that
results from inflammation.
•90% of the cases of sarcoidosis are
found in the lungs, but it can occur in
almost any organ (multiorgan).
•Benign lymphogranulomatosis=it
causes small lumps, or granulomas,
which generally heal and disappear on
their own.
•Granulomas that do not heal, the
tissue can remain inflamed and
become scarred, or fibrotic.
•Pulmonary sarcoidosis can develop
into pulmonary fibrosis
•Myocarditis, meningitis rarely.
noncaseating granulomas
SYPHILIS – LUES
‘CUPID’S DISEASE’ OR THE ‘FRENCH
DISEASE.
PRIMARY S.
SECONDARY S.
TERTIARY S.
Tree -bark aorta
CONGENITAL SYPHILIS
1) Letal – fetus maceratus
2) Newborns – pneumonia
alba, hepatitis,
ostrochondritis syphilitica
(saber shins)
3) Syphilis congenita tarda –
Hutchinson trias –
keratitis, labyrintitis, peg
teeth
Saber shins
thin cortices;
generalized
osteopenia
» Hutchinson teeth – Peg shaped
LEPROSY
M. leprae grows best in the cooler areas of the body; skin,
peripheral nerves, anterior chamber of the eye, upper respiratory
tract, and testes. Its distribution is global and almost exclusively
affects individuals in the “developing world”.
L. Tuberculoid
Limited bacillus
proliferation and
Disease extend
(single lesion – face,
¨extremities, trunk)
Well demarcated,
Hypopigmented patches
Not infectious
L lepromatous
Tumor – like lesions, facies
leonine
Incubation – 3-20years
Direct contact
• Tuberculoid leprosy is characterized by
the presence of non-necrotizing
granulomas in the dermis and
peripheral nerves with acid fast bacilli
absent or few in number. The lepromin
skin test is positive and there is a
predominance of helper CD4+ over
CD8+ T lymphocytes at sites of
infection. Tuberculoid tissues are rich
in the TH1 family of cytokines.
• Lepromatous leprosy is characterized by the presence of sheets of foamy macrophages in the dermis (and other sites) containing numerous acid fast bacilli, and absence of granulomas. The lepromin skin test is negative and there is a predominance of suppressor CD8+ over CD4+ T lymphocytes. Lepromatous tissues are rich in the TH2 cytokines. The loss of ability to kill bacteria appears to be specific for M. leprae. Patients with lepromatous leprosy are not unusually susceptible to opportunistic infections, cancer, or AIDS and maintain delayed-type hypersensitivity to Candida, Trichophyton, mumps, tetanus toxoid, and tuberculin.
LEPRA – ANESTETIC MACULA
Rhinoscleroma
Klebsiella rhinoscleromatis
(G-rod)
Endemic disease–
Mediterranean c., Asia,
Africa, Latin America
Miculicz cells
Rhinoscleroma
LYMHOGRANULOMA VENEREUM
• LGV is primarily an infection of lymphatics and lymph nodes by Chlamydia trachomatis
• Primary stage: – LGV may begin as a self-limited painless genital ulcer
that occurs at the contact site 3–12 days after infection. Women rarely notice a primary infection because the initial ulceration where the organism penetrates the mucosal layer is often located out of sight, in the vaginal wall. In men fewer than 1/3 of those infected notice the first signs of LGV. This primary stage heals in a few days.
LYMHOGRANULOMA VENEREUM
• Secondary stage
– The secondary stage most often occurs 10–30 days later, but can present up to six
months later. The infection spreads to the lymph nodes through lymphatic drainage
pathways. The most frequent presenting clinical manifestation of LGV among males
whose primary exposure was genital is unilateral (in 2/3 of cases) lymphadenitis and
lymphangitis, often with tender inguinal and/or femoral lymphadenopathy because of
the drainage pathway for their likely infected areas.
– They may develop proctitis, inflammation limited to the rectum (the distal 10–12 cm)
that may be associated with anorectal pain, tenesmus, and rectal discharge, or
proctocolitis, inflammation of the colonic mucosa extending to 12 cm above the anus
and associated with symptoms of proctitis plus diarrhea or abdominal cramps. In
addition, symptoms may include inflammatory involvement of the perirectal or perianal
lymphatic tissues.
LYMPHADENITIS MESENTERIALIS
• Yersinia enterocolica
• May mimic acute appendicitis
• Often in kids
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