Microbio review (Kinder) Flashcards
Bordetella pertussis
Whooping cough Highly contagious Spread by large droplets Gram negative aerobic coccobacillus capsulate Humans are only known reservoir
Clinical Manifestations
of whooping cough
Onset of symptoms 1-3 weeks after exposure
Catarrhal Phase
Rhinorrhea, lacrimation, conjunctival injection, low grade fever – lasts days to a week
Paroxysmal phase
Uncontrollable expirations, followed by gasping inhalation – whooping cough
Cough Associated with post cough cyanosis, gagging, and vomiting
Lasts up to 4 weeks
Convalescent Phase
Reduction in frequency and severity of cough can last from weeks to months
Bordetella pertussis complications, dx, tretment and prevention
Complications- pneumonia
Diagnosis
- Nasal swabs for culture or PCR
Treatment:
Supportive
Azithromycin
Chemoprophylaxis to control outbreaks
Prevention – accellular pertussis vaccine
Klebsiella pneumonia
Gram negative, non-motile, capsulate rods
Facultative anaerobes
UTI, soft tissue infections, endocarditis, central nervous system infections, and severe bronchopneumonia.
Community and hospital acquired pneumonias
Cavitary lung lesions
Currant Jelly sputum
Moraxella catarrhalis
Gram negative bacteria that grows well on blood or chocolate agar diplococci Catalase positive Oxidase positive Pneumonia, especially in the elderly Otitis media in young children
Neisseria meningitidis
Aerobic gram negative kidney shaped diplococci, capsule
Oxidase positive, ferments maltose and glucose Grows on Thayer-Martin media, chocolate agar
Commensal of the human upper respiratory tract
Transmitted through close contact via larger respiratory droplets.
Clinical manifestation
- Meningitis
- Septicemia
- Pneumonia
- Septic arthritis, pericarditis, chronic bactermia, or conjunctivitis
Neisseria meningitidis, dx, treatment and prevention
Diagnosis
Gram stain from CSF
CSF PCR
CSF culture, blood culture, or skin culture
Treatment
Penicillin
3rd generation cephalosporin
Prevention
Chemoprophylaxis with rifampin in close contacts
Meningococcal polysaccharide-protein conjugate vaccines
Neisseria meningitidis prognosis
Untreated systemic disease with 70-90% mortality
10% mortality with treatment
Morbidity
Limb loss, hearing loss, long-term neurologic disability
Pseudomonas aeruginosa
Aerobic gram-negative rod
Produces pyocyanin on laboratory medium – blue/green pigment
Primarily nosocomial pathogen
In hospital can colonize moist surfaces of the axilla, ear, and perineum
Isolated from water in sinks, drains, toilets, and showers
Even isolated from flowers in patients rooms
Pseudomonas aeruginosa infections
Hospital acquired pneumonia, Ventilator Associated Pneumonia
Community acquired infections related to hot tubs, whirlpools, swimming pools, and extended contact lenses
Otitis externa
Puncture wounds through tennis shoes
Endopthalmitis – complication of eye surgery
Endocarditis, from sharing contaminated needles
UTI
Skin Infections, burns, ecthyma gangrenosum
Pseudomonas aeruginosa host factors, bacterial factors, treatment
Host Factors – Neutropenia increases risk
Bacterial Factors
exotoxins, endotoxins, type III secreted toxins, pili, flagella, proteases, phospholipases, iron-binding proteins, exopolysaccharides, the ability to form biofilms, and elaboration of toxic small molecules such as pyocyanin
Treatment
Extended spectrum penicillin and aminoglycoside combination
Always treat with 2 antibiotics: Pseudo? Duo!
Chlamydophila psittaci
Gram negative obligate intracellular bacteria
Macrophages are the principal host cell
Diseases - Psittacosis (birds) - Atypical pneumonia - Febrile illness Transmission Aerosolized bird secretions, dust Diagnosis - Serology
Chlamydophila psitacci treatment, prevention
Treatment : tetracyclines, macrolides, fluoroquinolones
Prevention
30 day quarantine for all imported psittacine birds and their treatment with feed containing chlortetracycline
Chlamydophila pneumoniae
80% of adults are seropositive
Common infection in children under 5 years old
Atypical pneumonia
- Incubation several weeks
- Non productive cough
- Preceded by nasal congestion, sore throat, and hoarseness
- Headaches in ½ of patients
Examination Crackles, rhonchi Chest x-ray Pneumonitis Labs Normal white count Prolonged course over several weeks
Diagnosis
- Serology
- Direct detection of organism in respiratory specimens
Treatment:
Tetracyclines
Macrolides
Fluoroquinolones
Coxiella burnetii
Gram negative that infects hosts monocytes
Incompletely eliminated after acute infection
Will continue to multiply in immunocompromised patients and endocarditis patients despite high antibody levels
Infects mammals, birds, and ticks
Mammals infected by aerosols and may shed Coxiella in feces, urine, milk, and birth products
Survives in environment and can be spread by the wind
Major outbreaks have been related to sheep and goats and associated during lambing season
Clinical Manifestations of Q-fever: Prolonged fever Pneumonia Hepatitis Rash Meningitis, encephalitis, meningoencephalitis, peripheral neuropathy Pericarditis, myocarditis
Chronic uterine infection may develop in half of patients infected during pregnancy, and may later experience multiple spontaneous abortions
Q-fever endocarditis
- Intermittent fever
- Vegetations frequently absent
- Cerebral emboli, renal insufficiency, splenomegaly, hepatomegaly
Diagnosis
Based on serology
Treatment
Doxycycline x 2 weeks in acute cases
Doxycycline + hydroxychloroquine(increases phagosomal pH) for 18-36 months for endocarditis
Francisella tularensis
Tularemia is an infectious zoonosis
Small aerobic pleomorphic gram-negative bacillus
Many animals harbor infection including rabbits, squirrels, and muskrats
Humans acquire the infection through direct contact with infected animal tissues, ingestion of contaminated water or meat, the bite of an infected tick or deer fly, or breathing an aerosol of bacteria – not communicated person to person
Extreme risk to lab personnel
Clinical Manifestations: Ulceroglandular Glandular Oculoglandular Typhoidal Oropharyngeal Pneumonic
Ulceroglandular Francisella tularensis
Fever and constitutional symptoms Swollen lymph nodes that drain an inoculation site Ulcer formation Sore throat Patchy infiltrates on chest x-ray
Glandular Francisella tularensis
Fever
Constitutional symptoms
Lymphadenopathy
Typhoidal Francisella tularensis
Fever of unknown cause
Oropharyngeal Disease Francisella tularensis
Uncommon in the United States
Mucous membranes of the mouth and pharynx are the portal of entry
Contaminated water or food such as inadequately cooked game meat is the source
Painful exudative pharyngitis and tonsillitis
Pharyngeal ulcers
Swollen retropharyngeal and cervical lymph nodes
Pneumonic disease Francisella tularensis
Inhalation exposure
Fever, malaise, dry cough, substernal discomfort, pleural effusion, dyspnea, and sore throat
Chest x-ray with peribronchial infiltrates to bronchopneumonia with effusion
Hilar adenopathy
Diagnosis
Serologic testing
Francisella tularensis treatment and prognosis
Treatment
Gentamcin or streptomycin
Doxycycline
Ciprofloxacin
Prognosis
When appropriately treated mortality is 1% or less
Bacillus anthracis
Spore forming gram-positive non motile rod that is aerobic or facultatively anaerobic, catalase positive, hemolysis negative
Grows on sheep agar
Zoonotic infection from goats, sheep, cattle, antelope, kudu, pigs, horses, zebu, and other animals.
Animal related products include meat, wool, hides, bones, and hair
Soil contaminated with spores
Clinical Manifestations Inhalation: Mediastinal adenopathy Mediastinal widening Pleural effusion Rapidly fatal if not treated with multiple antibiotics and pleural drainage
Cutaneous:
Most common
Gastrointestina:l
Oropharyngeal
Intestinal
Meningeal:
Nearly always fatal, can occur as complication of inhalation, cutaneous , or gastrointestinal disease
Diagnosis
Blood culture
Bacillus anthracis treatment, prevention, prognosis
Treatment
Multi-drug regimen
Pleural drainage
Prevention
Vaccination for possible exposure
Post-exposure antibiotics
Prognosis
45% mortality of inhalation in 2001 attacks
20% mortality in untreated cutaneous disease
Yersinia pestis
Gram negative coccobacillus, microaerophilic, nonmotile, and non spore forming
Transmission cycles involve rodents and fleas, which act as vectors.
Prairie dogs are a common host
Clinical Manifestations of Plague
- Bubonic
- Septicemic
- Pneumonic
Bubonic Plague
Yersinia pestis
Swollen, tender lymph nodes (buboes) closest to site of initial infection
Fevers, chills, myalgia, arthralgia, headache, malaise, and prostration
Untreated patients have continued fever, tachycardia, agitation, confusion, delirium, and convulsions
Septicemic plague (yersinia pestis)
Nausea, vomiting, diarrhea, and abdominal pain
Disseminated intravascular coagulation
Hypotension, renal failure, and obtundation
ARDS
Pneumonic Plague
Yersinia pestis
Fever, cough, chest discomfort, tachycardia, dyspnea, bacteria laden sputum, chills, headache, myalgias, weakness, and dizziness
Respiratory distress, hemoptysis, cardiopulmonary insufficiency, and circulatory collapse
Death within 24 hours of symptoms
yersinia pestis treatments
Streptomycin for pneumonic plague
Tetracyclines for bubonic plague
Chloramphenicol for meningitis
Leptospirosis
Spirochete with terminal hook
Identified on dark field microscopy or silver staining
Obligate aerobe
Clinical Manifestations
Weil’s Disease:
Pulmonary Hemorrhage Syndrome
Reservoir:
Persistent renal carriage from rodents, dogs, pigs, cattle, and sheep
Colonizes renal tubules, excreted in urine, and survives for weeks to months in the environment
Transmission:
Penetrates the skin or mucous membranes during contact with contaminated water, soil, or vegetation
Leptospirosis clinical manifestations
Early phase: First 3-7 days Fever, myalgia, and headache Nausea, vomiting, abdominal pain, diarrhea, cough, and photophobia Muscle tenderness Rash Conjunctival suffusion
Late Phase: Weil’s Disease Jaundice Acute hemorrhage Renal Failure Severe thrombocytopenia GI bleeding Pulmonary Hemorrhage Myocarditis Aseptic meningitis
Leptospirosis dx, treatment and prevention
Diagnosis
Agglutination test
Treatment
Doxycycline
Penicillin
Prevention
Doxycycline post-exposure
Haemophilus influenzae
Encapsulated gram negative coccobacilli Aerobic or facultative anaerobic Grows on chocolate agar X(hemin) Factor and V(NAD) Factor Nasopharynx of adults and children Transmission: respiratory droplets H influenza type b was most common cause of meningitis in young children prior to effective vaccines
Haemophilus influenzae clinical manifestations
Meningitis
Children under 5 years old and in adults with skull trauma or CSF leaks
Type B strains
Diagnosis made by detecting PRP capsular antigens in CSF
Epiglottitis
Life threatening infection in children that usually occurs in children younger than 5.
Symptoms include fever, drooling, dysphagia, and respiratory distress with stridor
Course is rapid over a couple of hours
Lateral neck film used for diagnosis
Pneumonia: Fever, cough, and lobar consolidation Parapneumonic effusion and empyema Diagnosed by blood culture or culture from pleural fluid Smoking – risk factor
Bronchitis
Risk factor is chronic lung disease ( COPD)
Acute Sinusitis
Otitis Media
H. influenzae treatment and prevention
Treatment:
3rd generation cephalosporin for meningitis
Prevention
Conjugate capsular polysaccharide-protein vaccine effective for type b disease
Antibiotic prophylaxis in nonimmunized household or daycare contacts of patients with H influenza type b
Rifampin
Corynebacterium diphtheriae
Gram-positive bacillus – club shaped Non-spore forming Aerobic Reservoir: Throat and pharynx Transmission: Bacterium or phage via respiratory droplets
Respiratory Diphtheria
Incubation of 1-7 days
Sore throat, malaise, and fever
Pharyngeal erythema followed by tonsillar exudate
Exudate changes into a grayish membrane that is tightly adherent and bleeds on attempted removal
Cervical adenopathy – Bull Neck
Stridor
Extension of membrane can lead to airway obstruction
Myocariditis, recurrent laryngeal nerve palsy, and peripheral neuritis
Treatment: Erythromycin Antitoxin Prevention: Vaccination with toxoid vaccine
Legionella pneumophila
Weakly gram-negative pleomorphic rod
Facultative intracellular
Requires cysteine and iron ( Charcoal yeast extract)
Water organism, amebae, air-conditioning water cooler tanks
Transmission: aerosols from contaminated air-conditioning, no human to human transfer
Risk Factors: smokers over age 55 with high alcohol intake and immunosuppression
Legionaire’s disease
Fevers, malaise, cough, chills , dyspnea, myalgias, * headache, chest pain, and diarrhea.**
Myalgias, severe headaches, and diarrhea distinguish it from other pneumonias
Mental Confusion
Pontiac Fever
Fever, sore throat myalgia, headache, and extreme fatigue
Short duration, lasting on average 3 days
Diagnosis
Antigen urine test
DFA ( direct fluorescent antibody)
Treatment
Fluoroquinolones, azithromycin, or erythromycin + rifampin for immunocompromised patients
Drug must penetrate human cells
Mycoplasma pneumonia
Smallest free-living bacteria
No cell wall – unaffected by cell-wall inhibiting antimicrobials such as B-lactams
Sterol containing membrane
Requires cholesterol for culture
Transmission: respiratory droplets, close contact, families, military recruits, dorms
Highest incidence age 5-20 years old
Respiratory Infection 2-3 weeks incubation Fevers, malaise, headache, and cough 5-10% progress to tracheobronchitis or pneumonia Cough usually non-productive Walking pneumonia
Diagnosis
Primarily clinical diagnosis
Positive cold agglutinins - positive in 65% of cases
Treatment
Macrolides: erythromycin, azithromycin, and clarithromycin
Tetracyclines
Streptococcus pneumonia
typical pneumonia
Gram positive diplococcus, lancet shaped Facultative anaerobe, grows on blood agar plates alpha hemolytic Optochin sensitive Lysed by bile
Reservoir – human upper respiratory tract
Transmission – respiratory droplets
Pathogenesis:
Polysaccharide capsule
Risk Factors
Influenza infection, COPD, CHF, Alcoholism, and asplenia
Pathobiology
Initially colonizes the nasopharynx then aspirated
Clinical manifestations: Typical Pneumonia Most common cause Shaking chills, high fever, chills, rigors, lobar consolidation, blood tinged (rusty) sputum Adult meningitis Most common cause in adults Otitis media and sinusitis Most common cause in children
Treatment of pneumonia
Beta lactams
Macrolides
Fluoroquinolones
Treatment of meningitis
3rd generation cephalosporins
Vancomycin added if penicillin resistant
Staphylococcus aureus
Gram positive cocci in clusters Catalase positive Coagulase positive Beta hemolytic Small yellow colonies on blood agar Ferments mannitol
Reservoir – nasal flora in 25% of population
Transmission Hands Sneezing Surgical wounds Contaminated food = Custards = Potato salad = Canned meats
Over 50 virulence factors including adhesins, toxins, enzymes, surface-binding proteins, and capsule polysaccharides
Pathogenesis from tissue invasion and toxin mediated
3 toxin mediated diseases
- Staphylococcal food poisoning
- Staphylococcal toxic shock syndrome
- Staphylococcal scalded skin syndrome
Clinical manifestations
Skin manifestations include impetigo, folliculitis, furuncle, abscess, erysipelas, cellulitis, mastitis, necrotizing fasciitis, and wound infections
Bacteremia
Endocarditis
- Roth’s spots, Osler’s nodes, Janeway lesions, and petichiae
Pericarditis
Osteomyelitis – hematogenous seeding
Septic Arthritis, Infected prosthetic joints
Pneumonia – nosocomial pneumonia, **salmon colored sputum
Toxin Mediated Diseases
Staphylococcal food poisoning – Enterotoxins A-E
- 2-6 hours after eating nausea, vomiting, diarrhea, and abdominal pain
- Self limited
Toxic Shock Syndrome TSST-1 a super antigen
- Fever, erythroderma, hypotension, involvement of 3 or more organ systems, and desquamation of the palms and soles
Scalded Skin Syndrome – exfoliative toxin A or B
Treatment
Gastroenteritis is self limiting
Nafcillin/Oxacillin
MRSA – Vancomycin
Pnemocystis jiroveci
Fungus
Obligate extracellular parasite
Silver stain
Opportunistic infection in HIV patients with CD4 count less than 200
Pneumonia:
Fever, nonproductive cough, and shortness of breath
X-ray with patchy infiltrate, ground glass appearance, lower lobe and periphery may be spared
Diagnosis : silver staining cysts in bronchial alveolar lavage fluids or biopsy
Treatment sulfamethoxazole/trimethoprim or dapsone
Prevention SMX/TMP prophylaxis for CD4 counts less than 200 in HIV patients
Histoplasma capsulatum
Dimorphic fungus
Facultative intracellular parasite – found in RES cells
Found in soil, caves, and abandoned buildings with bird and bat guano
Transmission
- Disruption of soil; cleaning attics, bridges, and barns; tearing down old structures, and spelunking
Endemic to Mississippi and Ohio River Valleys
Clinical Manifestations:
Acute pulmonary
- Most asymptomatic
- Several weeks after exposure fevers, chills, fatigue, non-productive cough, anterior chest discomfort, and myalgias
Chronic pulmonary
- Progressive, often fatal
- Elderly, immunocompromised, and COPD patients at risk
X-ray
- Acute Pneumonia with patchy lobar or multilobar infiltrate
- Chronic Pneumonia with upper lobe infiltrates, multiple cavities, fibrosis of lower lobes – mimics TB
Treatment
- Itraconazole
- Amphotericin B
Blastomyces dermatitidis
Thermally dimorphic fungus
Broad based budding yeast
Appears to be associated with soil and decaying vegetation, especially in areas associated with rivers and lakes.
Endemic in north central, south central, great lakes, and southeastern seaboard
Transmission – inhaled conidia
Clinical Manifestations:
- Acute Pulmonary
Most asymptomatic or thought to have community acquired pneumonia
Fever, malaise, nonproductive cough
Chest x-ray with lobar, multilobar, or nodular infiltrates
Skin lesions - Chronic Pulmonary
Fever, night sweats, fatigue, weight loss, cough, hemoptysis, and dyspnea
Chest x-ray with cavitary, nodular, fibrosis, mass like
Treatment
All patients should be treated
Itraconazole in mild disease
Amphotericin B in severe disease
Coccidioides immitis
Dimorphic fungi
Inhaled arthroconidia enlarge and form spherules
Spherules undergo internal septation producing endospores
Endemic in southwest deserts
Clinical Manifestations
- Most asymptomatic
- Pulmonary Infection:
Symptoms develop 5-21 days after exposure
Fever, weight loss, fatigue, dry cough, and pleuritic chest pain
Arthralgias
Erythema nodosum
Chest x-ray with pulmonary infiltrates, hilar adenopathy, and peripneumonic effusion
Pulmonary Nodule, cavitary
Disseminated infection
Immunocompromised , e.g. AIDS
3rd trimester pregnancy
Skin, joints, and bones
Treatment
Itraconazole
Amphotericin B
Paracoccidioidomycosis brasiliensis
Thermally dimorphic fungus
Endemic to humid areas of Central and South America
Lives in soil
Most prevalent in middle-aged to elderly men
Paracoccidioidomycosis develops after inhalation of aerosolized conidia encountered in the environment
- Acute-Subacute Paracoccidioidomycosis – less than 10%
—-RES (reticulo-endothelial system) with dissemination to the liver, spleen, lymph nodes, and bone marrow
Chronic Paracoccidioidomycosis
Progressive over many years
Most patients older men
Pulmonary involvement mimics tuberculosis
Chest x-ray with nodular, interstitial, and cavitary lesions in the middle or lower lung fields
Ulcerative lesions in the anterior nares, oral cavity, and larynx that are slowly destructive
Chronic Paracoccidioidomycosis
Diagnosis
Growth in culture
Morphology
Thick-walled yeast cells that have multiple small circumferentially attached, narrow-based budding daughter yeast cells
Ship’s steering wheel
Strongyloides stercoralis
Endemic in warm climates worldwide
Transmission
Exposed skin comes in contact with free-living filiariform larvae living in contaminated soil. After skin penetration, larvae enter the afferent circulation and travel to the pulmonary vasculature, where they rupture into the alveolar spaces, ascend the respiratory tree, and are swallowed into the GI tract. Development into adult worms occurs in the upper part of the small intestine. Female worms begin laying eggs. Eggs hatch in the lumen of the small intestine. Rhabditiform larvae migrate to the colon and are passed in the feces.
Pulmonary Manifestations
Can be severe in immunocompromised
Resembles ARDS with acute onset of dyspnea, productive cough, and hemoptysis accompanied by fever, tachypnea, and hypoxemia
Treatment
ivermectin
Aspergillosis
Aspergillus are ubiquitous organisms found in soil, decaying matter, and air.
Spore like conidia are aerosolized from the mold form of the organism. They reach tissue and form invasive hyphae.
Can be isolated from basements, crawl spaces, bedding, humidifiers, ventilation ducts, potted plants, dust, condiments, and marijuana
Invasive Aspergillosis
Immunocompromised host Fever Pulmonary infiltrates Nodules Wedge-shaped densities resembling infarcts Sinusitis Extrapulmonary sites CNS abscesses, endophthalmitis, MI, GI, renal, osteomyelitis, endocarditis
Diagnosis
Diagnosis: BAL, needle aspiration, thoracoscopic biopsy, or open lung biopsy
Treatment
Antifungal- Voriconazole or liposomal amphotericin B
Reversal of immunosuppression
Surgical resection of infected lesions
Chronic Pulmonary Aspergillosis
Aspergilloma
Ball in cavity
Debris in preformed cavity from TB, Histoplamosis, or fibrocystic sarcoidosis
Treatment
Limited benefit with aspergilloma
Antifungal – itraconazole or voriconazole in chronic cavitary pulmonary aspergillosis
Allergic Bronchopulmonary Aspergillosis (ABPA)
History of chronic asthma or cystic fibrosis
Airway obstruction, fever, eosinophilia, positive sputum cultures, mucous plugs containing hyphae, brown flecks in sputum, transient infiltrates, proximal bronchiectasis, upper lobe contraction, elevated IgE.
Eosinophilia in blood, sputum, and lung tissue
Allergic Pulmonary Aspergillosis Diagnosis
Asthma Immediate cutaneous reaction to A. fumigatus antigen Serum IgE greater than 1000 ng/ml A. fumigatus specific serum IgE levels Precipitating serum antibodies to A. fumigatus Central bronchiectasis Peripheral eosinophilia Pulmonary infiltrates
Treatment
Corticosteroids and itraconazole
Cryptococcosis
Occurs most often in the immunosuppressed – HIV
Meningitis is most common clinical manifestation
Pulmonary and other organ involvement can occur
Cryptococcus neoformans
Yeast
Environment and tissues
Polysaccharide capsule is the major virulence factor
Patients at highest risk are those with AIDS and CD4 counts less than 50.
Inhaled from the environment and causes pulmonary infection initially. Most patient asymptomatic.
If the host becomes immunosuppressed the organism can reactivate and disseminate to other sites.
C. neoformans is neurotropic
Central Nervous System Infection: Meningoencephalitis Headaches over several weeks Nuchal rigidity Lethargy Personality changes Confusion Visual abnormalities Nausea and vomiting
Pulmonary Infection
Risk factors include COPD, Corticosteroid use, and solid organ transplant
Fever, cough, and dyspnea
Treated with antifungals
Other organs affected
Skin, prostate, osteoarticular surfaces, breast, eye, and larynx.
Diagnosis
Yeast is grown in culture from CSF, Blood, sputum, skin lesions, or other body fluids
India Ink stain – visualization of budding yeast with large capsule
Latex agglutination for Cryptococcal polysaccharide antigen
Treatment of CNS infection
Non-AIDS Patients
Amphotericin B and flucytosine for 6 weeks
AIDS Patients
Amphotericin B and flucytosine for 2 weeks, followed by fluconazole 400 mg daily for 8 weeks, then suppressive therapy with fluconazole 200 mg daily
HACEK Organisms
Haemophilus spp Actinobacillus actinomycetemcomitans Cardiobacterium hominis Eikenella corrodens Kingella spp 5% of endocarditis cases Normal flora Common Cause of endocarditis in non-IV drug users Difficult to diagnose- often takes 3 months
Culture Requirements
H. influenzae Chocolate Agar with Factors V(NAD+) and X(Hematin)
N. meningitidis Thayer-Martin
B. pertussis Bordet-Gengou
C. diphtheriae Loffler medium
M. pneumoniae Eaton Agar – requires cholesterol
Legionella Charcoal Yeast Extract cysteine and iron
Special Stain Requirements
Chlamydia Giemsa
Cryptococcus India Ink
Pneumocystis Silver Stain
Mycobacteria Ziehl-Neelsen
