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