Microbiology lecture note terminology



Drug of first choice

S. pneumoniae


H. influenzae


M. pneumoniae

Erythromycin or tetracycline

C. pneumoniae


L. pneumophila

Macrolide or fluoroquine

K. pneumoniae


P. aeruginosa

Aminoglycoside + antipseudomonal penicillin. Resistant to many antibiotics.

Typical v. atypical pneumonias






General appearance


Malaise, fatigue


Yes, > 39 degrees

Low < 39 degrees










Gram stain

Bactera + WBC

Mixed oral flora


Elevated, left shift

Normal +/- lymphocytes


Lobar consolidation

Brochiopneumonia (patchy)

Organism invovled

S. peumoniae, H. influenzae, S. aureus

M. pneumoniae, C. pneumoniae, L. pneumoniae

Respiratory Fungal infections

Ajellomycces dermatidis

Formerly Blastomyces dermatidis. North american blastomycosis. True dimorphic fungi. Largely sourtheastern United States. Spread by droplets. Usually comes from breathing spores from ground living animals. Primary walking pneumonia (infectious). Secondary: Cutaneous granulomatous lesions (often on the face and extremities). Slow growing, lesions take years to get as bad as the pictures. Cross reactivity w/ histoplasmosis. Delayed hypersensitivity skin test. Immunodiffusion test. Identify organism in tissue. Treatment: systemic (topical is useless); use amphotericin B for pulmonary diseases or immunosuppressed patients. Normally FLUCANOZOLE

Paracoccidioides dermatidis

Formerly Blastomyces brasilensis. South american blastomycosis. Loosely located in central and South America. Rare. Primary walking pneumonia. Secondary: disfiguring granulomatous lesions in oral cavity. Often discovered by dentists and oral surgeons.

Ajellomyces capsulatum

Formerly Histoplasma capsulatum. Histoplasmosis. Common. Found in the missouri and mississippi valleys. Occasional cases found in Greater Antilles (Cuba, peurto rico, Hispaniola). Walking pneumonia. Usually disappears in 3-6 weeks. Occasionally develop mediastinal fibrosis as a result of over-active immune response. In immunosuppressed, disease may metstasize to anywhere. Caseated lung nodule. Similar to tuberculosis, often indistinguishable. Yeasts observed in WBC. Tuberculate macroconidia grow in Sabouraud's . amphitericin B for severe cases. Life-long suppressive therapy.


Coccidiodes immitis. Desert fever. Found in high desert dust. Walking pneumonia. 1-2 week course. If it gets to secondary state usually goes to meningitis. See spherules on slide. Serodiagnosis: delayed hypersensitive skin test. Laboratory acquired infections. Specific exoantigen test.


Cryptococcus neoformans. Birds are not vectors, but there droppings make fertile growth areas. Walking pneumonia. Secondary usually meningitis. Most common fungal infection of AIDS patients. Backwards serodiagnosis. India ink negative stain (stains everything but the yeast). Culture is definitive diagnosis. Treatment: Combination of amphotericin B and 5-flurocytosine. Urease positive, encapsulated and inhibited by cycloheximide


Formally Pneumocystis carnii. Reproduces like a sporozoan parasite. New name is Pneumocystis jiroveci. PCP: pneumocystis pneumonia. No ergosterol in cell wall. Difficult to grow in culture.

Aspergillus sp.

Aspergillus fumigatus. Opportunistic infection. Different organ systems may be infected. Usually immunocompromised URT and LRT infections, sometimes brain or eye. Fungus balls. Gummatus lesion.

Mucor sp.

Rhizopus sp.

Pneumonic aspergillosis

Requires predisposing factors: neutropenia. Large amounts of amphotericin B. Usually lethal (immunocompromised patients). Worldwide distribution. Progressive diffuse pneumonitis. Direct FA stain of organism in sputum for diagnosis. Treat w/ trimethoprim-sulfamethoxazole. Prognosis is poor.

Myobacterium sp


Fungus-like bacteria. Aerobic, gram+ (if stained), large rods. No true branching. Strongly acid fast. Not penicllin usceptible. Resists drying but sensitive to heat. Do not form spores. Grow slowly (12-24 hour generation time) (6 weeks to culture and claim negative). Like egg media (Lowenstein-Jensen agar) (oleic acid -albumin broth).

M. smegmatis

Will grow anywhere (faucets, walls....)

M. leprae

Will not grow in artificial culture or tissue culture at all

Muramic acid

Component of mycobacterium cell wall. Polymer consists of N-glycolylmuramic acid (instead of N-acetylmuramic acid) alternating w/ N-acetylglucosamine.

Mycolic acid

Component of cell wall. Lipid. ~84 carbons

Wax D

15-20 molecules of mycolic acid esterified to a large polysaccharide. Allows resistance to drying. Heat is not impeded. Slow growth because nutrients are impeded as well. Allows for acid fast properties. Wax holds acid dye in place.


In a thin layer to outer surface of the muramimc acid layer

Trehalose dimicolate

Complex lipid on outer surface. Responsible for the aggregation of cells in parallel bundles or “Cords”

Cord factor

Trehalose dimicolate. Only found in virulent strains. Inhibits migration of neutrophils. Binds to mitochondrial membrane, damages respiration and oxidative phosphorylation, induces synthesis of cachectin --> cachexia


Tumor necrosis factor


Wait loss resulting from the presence of cachectin

M. tuberculosis

Causes TB.

M. bovis

Causes TB in cattle and humans

A. avium

TB in birds and humans (more highly drug resistant)

M. marinum

TB in fish. Leads to cutaneous lesions in humans

M. ulcerans

Leads to skin ulcers in humans

M. kansasii

TB-like disease in humans. Same pathologenesis and symptoms

M. inracellulare

TB-like disease in humans. Same pathologenesis and symptoms

M. scrofulaceum

Lymph node infection in humans

M. fortuitum

Various human diseases

M. leprae



Runyan group II. Scrofulaceum, szulgai


Need light. Runyan group I. Kansani, marinum, simii


Don't need light. Runyan group III. Avium, intracellulare, ulcerans


Rapid growers. Runyan group IV. Fortuitum


Men (and women). M. bovix and M. avium have animal reservoirs


Density dependent. 1/3 to ¼ of world population carries the latent type of infection. Minimum infectious dose is relatively small. High level of immunity. People w/o long exposure to TB have higher incidence and death rates


Coughed TB --> inhaled by close contacts (usually aborted but if not)--> bacilli are ingested by macrophages(usually killed, but if not) --> latent infection (bacteria lives in granuloma --> 10% active disease (weight loss, fever, coughing) infective

Primary tuberculosis

Inhaled bacilli reach the bronchi. Bacilli outlive macrophage and are released unharmed. Granuloma forms eventually becoming caseated. Self limiting

Reactivation tuberculosis

The most active clinical disease. Areas of high oxygen tension and low drainage (apex of lungs). Spreads w/ frequent coalescing. Bronchules and small blood vessels are frequently eroded. Can occur in other organs: brain, kidney, bone marrow, meninges. Major symptoms don't occur until disease is fairly well progressed: coughing up blood (haemoptysis), cachexia (wasting away), loss of vitality, death to wasting, respiratory insufficiency


Cells w/ no seperating membranes (giant cells)

Ghon complex

Granuloma (multinucleated giant cells w/ caseating necrosis)+ enlarged regional lymph nodes

Tuberculosis in AIDS

~10% of HIV pop has TB. CNS invasion in up to 10%. CD4 cells important in immune response

Coin lesion

Presumptive diagnosis


Ziehl Neelsen staining. Culture from sputum sample

Antimicrobial resistance testing

Must be done on culture since resistance to vairous antibiotics is wide spread


Cell-free culture. Used in PPD test. Originally developed to develop immunity







Vaccine. Live attenuated strain derived from M. bovis. Varying reports of effectiveness, ranging from useless to 80%

Bronx box

Determines antibiotic resistance in TB.