Microbiology Review Flashcards
Bordetella pertussis
Whooping cough
Gram negative aerobic coccobacillus capsulate
Humans are only known reservoir
Bordetella pertussis: clinical manifestations
Onset of symptoms 1-3 weeks after exposure
Catarrhal Phase
Paroxysmal phase - Uncontrollable expirations, followed by gasping inhalation – whooping cough, associated with post cough cyanosis, gagging, and vomiting
Convalescent Phase -Reduction in frequency and severity of cough can last from weeks to months
Bordetella pertussis: treatment
Supportive
Azithromycin
Chemoprophylaxis to control outbreaks
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
Neisseria meningitidis: clinical manifestations
Meningitis
Septicemia
Pneumonia
Septic arthritis, pericarditis, chronic bactermia, or conjunctivitis
Neisseria meningitidis: treatment & prevention
Penicillin
3rd generation cephalosporin
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
Pseudomonas aeruginosa: infections
HAP, VAP
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 & Bacterial Factors
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
Pseudomonas aeruginosa: treatment
Extended spectrum penicillin and aminoglycoside combination
Chlamydophila psittaci
Gram negative obligate intracellular bacteria Macrophages are the principal host cell Diseases Psittacosis 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
Chlamydophila pneumoniae: PE
Examination Crackles, rhonchi Chest x-ray Pneumonitis Labs Normal white count Prolonged course over several weeks
Chlamydophila pneumoniae: treatment
Tetracyclines
Macrolides
Fluoroquinolones
Coxiella burnetii
Gram negative that infects hosts monocytes
Will 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
Coxiella burnetii: Q fever
Prolonged fever, pneumonia, hepatitis, rash
Meningitis, encephalitis, meningoencephalitis, peripheral neuropathy
Pericarditis, myocarditis
Chronic uterine infection during pregnancy, may later experience multiple spontaneous abortions
Q-fever endocarditis
Intermittent fever
Vegetations frequently absent
Cerebral emboli, renal insufficiency, splenomegaly, hepatomegaly
Coxiella burnetii: treatment
Doxycycline x 2 weeks in acute cases
Doxycycline + hydroxychloroquine(increases phagosomal pH) for 18-36 months for endocarditis
Francisella tularensis
Small aerobic pleomorphic gram-negative bacillus
Not communicated person to person
Extreme risk to lab personnel
Francisella tularensis: Ulceroglandular
Fever and constitutional symptoms Swollen lymph nodes that drain an inoculation site Ulcer formation Sore throat Patchy infiltrates on chest x-ray
Francisella tularensis: Glandular & Typhoidal
Glandular
Fever
Constitutional symptoms
Lymphadenopathy
Typhoidal
Fever of unknown cause
Francisella tularensis: Oropharyngeal Disease
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
Francisella tularensis: Pneumonic disease
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
Fransicella tularensis: treatment
Gentamcin or streptomycin
Doxycycline
Ciprofloxacin
Bacillus anthracis
Spore forming gram-positive non motile rod, aerobic or facultatively anaerobic, catalase positive, hemolysis negative
Grows on sheep agar
Zoonotic infection
Animal related products include meat, wool, hides, bones, and hair
Soil contaminated with spores
Bacillus anthracis: clinical manifestations
Inhalation Mediastinal adenopathy Mediastinal widening Pleural effusion Rapidly fatal if not treated Meningeal Nearly always fatal, can occur as complication of inhalation, cutaneous , or gastrointestinal disease
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
Bubonic Plague
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
Nausea, vomiting, diarrhea, and abdominal pain
Disseminated intravascular coagulation
Hypotension, renal failure, and obtundation
ARDS
Pneumonic Plague
Fever, cough, chest discomfort, tachycardia, dyspnea, bacteria laden sputum, chills, headache, myalgias, weakness, and dizziness
Respiratory distress, hemoptysis, cardiopulmonary insufficiency, and circulatory collapse
Death within2 24 hours of symptoms
Yersinia pestis: treatment
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
Leptospirosis: early clinical manifestations
First 3-7 days Fever, myalgia, and headache Nausea, vomiting, abdominal pain, diarrhea, cough, and photophobia Muscle tenderness Rash Conjunctival suffusion
Leptospirosis: Late Phase-Weil’s Disease
Jaundice Acute hemorrhage Renal Failure Severe thrombocytopenia GI bleeding Pulmonary Hemorrhage Myocarditis Aseptic meningitis
Leptospirosis: diagnosis, treatment, prevention
Diagnosis Agglutination test Treatment Doxycycline Penicillin Prevention Doxycycline post-exposure
Haemophilus influenzae
Encapsulated gram negative pleomorphic rod
Aerobic or facultative anaerobic
Grows on chocolate agar
Factor X(hemin) and Factor V(NAD)
Nasopharynx of adults and children
H influenza type b was most common cause of meningitis in young children prior to effective vaccines
Haemophilus influenzae: 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
Haemophilus influezae: 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
Haemophilus influenzae: pneumonia & bronchitis
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
Haemophilus influenzae: treatment & 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 diptheriae
Gram-positive bacillus – club shaped Non-spore forming Aerobic Reservoir: Throat and pharynx Transmission: Bacterium or phage via respiratory droplets
Respiratory Diptheria
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
Corynebacterium diptheriae: clinical
Cervical adenopathy – Bull Neck
Stridor
Extension of membrane can lead to airway obstruction
Myocariditis, recurrent laryngeal nerve palsy, and peripheral neuritis
Corynebacterium diptheriae: treatment & prevention
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
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
Legionella pneumophila: diagnosis & treatment
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
Mycoplasma pneumonia: clinical manifestations
Respiratory Infection 2-3 weeks incubation Fevers, malaise, headache, and cough 5-10% progress to tracheobronchitis or pneumonia Cough usually non-productive Walking pneumonia Bullous myringitis
Mycoplasma pneumoniae: diagnosis & treatment
Diagnosis
Positive cold agglutinins - positive in 65% of cases
Treatment
Macrolides: erythromycin, azithromycin, and clarithromycin
Tetracyclines
Streptococcus 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
Streptococcus pneumonia: patho
Pathogenesis:
Polysaccharide capsule
Risk Factors
Influenzae infection, COPD, CHF, Alcoholism, and asplenia
Pathobiology
Initially colonizes the nasopharynx then aspirated
Streptococcus pneumonia: 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
Streptococcus pneumonia: treatment
Treatment of pneumonia
Beta lactams
Macrolides
Fluoroquinolones
Treatment of meningitis
3rd generation cephalosporins
Vancomicin added if penicillin resistant
Severe Acute Respiratory Syndrome (SARS)
Coronavirus – second most common cause of the common cold
Reservoir: birds and small mammals
Virus is also found in urine, sweat, and feces
Original case thought to be transmitted from animal to human
SARS: clinical manifestations
Fever greater than 100.4 F Flu-like illness Dry cough Dyspnea Progressive hypoxia
Diagnosis
Clinical history and history of travel to endemic area or association with a traveler
Travel to far east or Toronto.
SARS: treatment
Treatment is supportive
Mortality is 50% in the elderly
Varicella-Zoster Virus
Reservoir – human mucosa and nerves
Transmission – respiratory droplets
Virus infects epithelial cells and lymphocytes in the oropharynx and upper respiratory tract, then infected lymphocytes spread the virus throughout the body.
The virus enters the skin through endothelial cells in blood vessels and spreads to epithelial cells where it causes a vesicular rash.
Virus remains dormant in the cranial nerve ganglia and dorsal root ganglia. Reactivation of virus leads to Herpes zoster .
Varicella-Zoster Virus: treatment
Shingles – oral acyclovir
Immunocompromised with shingles – IV acyclovir
Aspirin contraindicated due to Reye’s syndrome
Varicella-Zoster Virus in immunocompromised
Vaccine contraindicated in hematologic malignant neoplasms, AIDS, HIV infection with CD4 count of 200/mm3 or lower, and in persons receiving high dose immunosuppressive therapy, or anti-tumor necrosis factor –a therapy.
VZIG (varicella-zoster immunoglobulin) post exposure prophylaxis of immunocompromised patients
Staphylococcus aureus
Gram positive cocci in clusters Catalase positive Coagulase positive Beta hemolytic Small yellow colonies on blood agar Ferments mannitol
Staphylococcus aureus: virulence
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
Staphylococcus aureus: 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
SA Toxin Mediated Diseases
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
Staphylococcus aureus: treatment
Gastroenteritis is self limiting
Nafcillin/Oxacillin
MRSA – Vancomicin
Pnemocystis jirovecii
Fungus
Obligate extracellular parasite
Silver stain
Opportunistic infection in HIV patients with CD4 count less than 200
Pneumocystis jerovecci: 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 sulfamethaxazole/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
Histoplama capsulatum: 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
Histoplamsa capsulatum: PE & treatment
X-ray
Acute Pneumonia with patchy lobar or multilobar infiltrate
Chronic Pneumonia with upper lobe infiltrates, multiple cavities, fibrosis of lower lobes – mimics TB
Treatmet
Itraconazole
Amphotericin B
Coccidiodes immitis
Dimorphic fungi
Inhaled arthroconidia enlarge and form spherules
Spherules undergo internal septation producing endospores
Endemic in southwest deserts
Coccidiodes immitis: 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
Coccidiodes immitis: treatment
Disseminated infection
Immunocompromised , e.g. AIDS
3rd trimester pregnancy
Skin, joints, and bones
Treatment
Itraconazole
Amphotericin B
Paramyxoviruses
Enveloped, helical nucleocapsid Negative-sense ssRNA Parainfluenza Measles Mumps RSV
Parainfluenza
Transmission by large particle fomites and close person-to-person contact
Most children exposed by start of elementary school
Coryza, rhinorrhea, pharyngitis without lymphadenopathy, and low grade fever
Symptoms usually last 3-5 days
Signs of lower tract infection present as croup
Parainfluenza: clinical
Croup
Raspy, barking cough with inspiratory stridor, dyspnea, and respiratory distress
Symptoms result from subglottic inflammation and edema
Bronchiolitis or Pneumonia
Cough, rales, wheezing, and hypoxia
Cold
Reinfection of adults with parainfluenza typically causes cold symptoms in normal adults and children
Measles – Rubeola
Highly contagious
3 C’s cough, coryza, conjunctivitis
Generalized maculopapular rash
Fever
Transmission by direct contact with large respiratory droplets
Infectious 4 days prior to rash until 4 days after onset of rash
Measles – Rubeola: clinical
Incubation 8-12 days
Prodrome of fever, cough, coryza, conjunctivitis, and Koplik spots
Malaise, myalgia, and headache
Koplik spots proceed rash by 1 day and are resolved 2 days into rash
Rash typically starts 2-6 days after the onset of catarrhal symptoms and starts on face or behind ears as individual macules. Rash coalesces, forms papules and progresses from head to trunk to extremities. Rash covers entire body by 4 days. Fades in same order.
Measles – Rubeola: complications
Diarrhea, otitis media, and pneumonia
Postinfectious encephalomyelitis
2 weeks after rash with onset of headache, recurrence of fever, vomiting, stiff neck
25% mortality
33% of survivors with neurologic sequelae
Subacute sclerosing panencephalitis
Degenerative demyelinating disease due to chronic infection.
Occurs years after the acute measles infection and is universally fatal
Measles - Rubeola: treatment
Treatment is supportive
Prevention
Live, attenuated vaccine - MMR
Mumps
Transmission droplet spread of upper respiratory secretions
Incubation 18 days
Clinical Manifestations
Parotitis
Aseptic Meningitis – common and usually mild
Encephalitis rare and severe
Orchitis
Treatment – supportive
Prevention – live, attenuated vaccine - MMR
Respiratory Syncytial Virus
Epidemics begin in late fall in southern states and peak in February and March in colder climates
60% of bronchiolitis and 25% of pneumonia in infants
Transmission
Direct contact with large-particle fomites of respiratory secretions
RSV: Clinical Manifestations - infants
Conjunctival injection, mucopurulent nasal discharge, cough, low-grade fever
Otitis Media
Lower respiratory symptoms in 25-50% of infants with cough, wheezing, tachypnea, use of accessory muscles, and cyanosis.
Expiratory wheezing, rhonchi, and fine rales on lung examination
Chest x-ray
Hyperinflation and diffuse interstitial pneumonitis
RSV: treatment
Treatment – Ribavarin
Prevention
Frequent handwashing
No vaccination available
Strongyloides stercoralis
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.
Strongyloides stercoralis: clinical
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
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
Invasive Aspergillosis: diagnosis & treatment
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 & treatment
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
Cryptococcus in immunocompromised
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
Cryptococcus: meningoencephalitis
Headaches over several weeks Nuchal rigidity Lethargy Personality changes Confusion Visual abnormalities Nausea and vomiting
Cryptococcosis: Pulmonary Infection
Risk factors include COPD, Corticosteroid use, and solid organ transplant
Fever, cough, and dyspnea
Treated with antifungals
Cryptococcosis: 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
Cryptococcosis: treatment of CNS infections
Non-AIDS Patients
Amphotericin B and flucytosine for 6 weeks
AIDS Patients
Amphotericin B and flucytososine for 2 weeks, followed by fluconazole 400 mg daily for 8 weeks, then suppressive therapy with fluconazole 200 mg daily
Cytomegalovirus
Member of herpesvirus family
Double stranded DNA genome
Latent infections
Most clinical disease caused by reactivation of latent virus in the immunocompromised host.
Hallmark pathology is large central basophilic intranuclear inclusion “Owls eye”
Cytomegalovirus: clinical
Congenital and Neonatal
Microcephaly, intracerebral calcification, hepatosplenomegaly, and rash
Mental retardation and hearing loss
Mother with primary infection during pregnancy
Immunocompetent Most asymptomatic, few with mono like illness
Cytomegalovirus in immunocompromised
Transplant Recipients Fever, neutropenia, atypical lymphocytes, and hepatosplenomegaly Hepatitis – transplanted liver Pneumonia Colitis - diarrhea AIDS CD4 counts less than 50 Retinitis Colitis
Cytomegalovirus: diagnosis, treatment, prevention
Diagnosis Culture CMV Antigen or nucleic acid detection Serology Prevention Reducing exposure to body fluids, “safe sex” Treatment Antivirals
