Micro TB/URTI Flashcards
Pathogen that causes the most death worldwide
MTB
Reservoir and transmission of MTB
humans are the natural reservoir and spread is person-to-person via aerosols from coughing; 90% of people who are infected do not develop the disease
MTB staining properties
does not gram stain, stains with Acid-fast because of mycolic acid within cell wall
MTB cell wall
contains many waxy-like substances that make the cell wall impermeable to many host defense systems including: mycolic acid, glycolipids, arabinogalactans, free lipids
Risk factors for TB
prison (crowded conditions), immigration from high burden country, malnourished, alcoholism, poverty, debilitating illness, AIDS, elderly, DM, Hodgkin lymphoma, CKD, malnutrition, immunosuppression; RA on TNF alpha antagonists
Primary TB
usually asymptomatic; only evidence may be a calcified lung nodule at site of initial infection; the organisms remain dormant until immune defenses are lowered
Secondary infection TB
usually involves apices of lungs due to high oxygen content; cavitation frequently occurs; erosion of cavities into airway is source of infection - person is expectorating organisms
MTB steps of initial pathogenesis
enters macrophages by phagocytosis, inhibits the formation of phagolysosome, allowing the bacteria to replicate, IL-12 is produced stimulating a T-helper response, IFNgamma is then produced by TH-1 cells and enables macrophages to contain infection
MTB and Macrophages
MTB can grow within macrophages, allowing it to avoid antibodies and complement; once phagocytksed it can inhibit phagosome-lysosome fusion via PknG protein
IFN gamma and TB
critical mediator allowing macrophages to contain the infection
TH1 and TB
Th1 response leads to granuloma formation and caseous necrosis
Activated macrophages and TB
macrophages secrete TNF and cytokines which recruit more monocytes (TNF alpha is extremely important)
Erythema Nodosum
painful rash on legs in a TB patient that indicate the body is fighting the infection
Diagnostic methods for TB
acid fast stain of sputum, nucleic acid amplification test on sputum, culture on Lowenstein-Jensen solid agar, culture in liquid media
Initial treatment of TB
Isoniazid, Rifampin, Ethambutol. Pyrazinamide
MDR TB
resistance to INH and RIF is most common; seen in AIDS patients
XDR TB
resistance to INH, RIF, fluoroquinolone and one more drug.
Risk factors for development of resistance in TB
noncompliance - use directly observed therapy to combat
Why is the TB therapy so long?
slow growth of the organism, caseous material blocks penetration by drugs, organisms is intracellular, metabolically inactive organisms in the lesion
Progressive primary TB
initially looks like acute bacterial pneumonia with lobar consolidation, infiltrates, adenopathy; the tubercle can erode into a bronchus, spill its content and the infection will disseminate
Miliary TB
caused by dissemination of infection; meningitis, Pott’s dsisease/vertebral osteomyelitis, GI involvement, urinary tract involvement with sterile pyuria, lymphadenitis most common manifestation of extra pulmonary TB
Typical treatment length for disseminated TB
9-12 months using all 4 drugs
TB and HIV
low CD4 count is an important risk factor; the pulmonary manifestations are variable with false negative common and absence of granulomas; no bronchial damage and few AFB in sputum
Difference in purified protein derivative test and the interferon gamma release assay when testing for TB?
the PPD can be false positive if the patient has been exposed to other Mycobacterial species; the IGRA is specific only to MTB
Typical treatment following a positive TB test
INH for 6-9months or INH and Rifapentine for 3 months
The Bacillus Calmette Guerin vaccine
TB vaccine used in high incidence areas, contains live attenuated mycobacterium bovid; used in US for young children with close contact to someone with TB and military personnel; contra in immunocompromised
What is a positive PPD
If no risk factors: >15mm
If homeless, IVDU, nursing home resident, recent immigrant, children under 4yo: 10-15mm
If HIV, recent contact with TB, fibrotic change oN CXR consistent with prior TB, organ transplants, immunosuppressed: 5-10 mm
TB prevention
prompt identification and treatment; use masks and respiratory isolation; treat latent converters; screen those at high risk
Viruses that cause common cold
Coronavirus and Rhinovirus
Rhinovirus structure
Picornavirus family; icosohedral, non-enveloped, positive sense single stranded linear RNA
Coronavirus structure
Helical, enveloped, positive sense single-stranded linear RNA
Rhinovirus and Coronavirus role in LRTI
they do not cause LRTI except for 2 coronaviruses (SARS and MERS)
GI issues and Rhinovirus and Coronavirus
Rhinovirus is acid-labile so it will be killed by gastric acid rather than cause gastroenteritis; coronavirus can cause GI illness
Most effective prevention of Rhinovirus
handwashing; no vaccine and no treatment due to limited course of infection and number of antigenic types; spread by direct contact and aerosols
Rhinovirus facts
2-3 day incubation period, resolves in 1 week; causes minimal pathology to respiratory epithelium; pathogenesis associated with chemical mediators of inflammation that cause vasodilation, mucous secretion, stimulation of sneeze and cough reflexes
Common complication of viral URTI
acute bacterial sinusitis
Organisms that cause otitis media
H. influenza, S. pneumonia, M. catarrhalis
Primary therapy for otitis media
Amoxicillin; if purulent conjunctivitis (H. flu) give Augmentin due to beta lactam resistance
Diphtheria pathogenesis
A-B toxin blocks protein synthesis by inactivating EF-2 by ADP ribosylation, resulting in decreased protein synthesis
Pertussis pathogenesis
A-B toxin stimulates adenylate cyclase by catalyzing the addition of ADP ribosylation to the inhibitory subunit of the G protein complex (inhibiting it), resulting in overactive cAMP-dependent protein kinase activity; causes decreased cilia activity
H. flu pathogenesis
Produces IgA protease facilitating attachment to the mucosa; also is encapsulated and evades phagocytosis
Rhinovirus pathogenesis
binds to intercellular adhesion molecule 1 (ICAM-1)
Pseudomembrane
graying membrane in the throat of someone infected with diphtheria; composed of fibrinous exudate and necrotic cells; serves as platform for bacterial growth and toxin production; can extend and cause mechanical obstruction
3 complications of diphtheria
mechanical obstruction, myocarditis accompanied by arrhythmias and circulatory collapse, and nerve weakness or paralysis, esp of cranial nerves
Micro characteristics of diphtheria
gram positive bacillus, pleomorphic, club shaped, arranged in palisades, beaded appearance
Diagnosis of Diphtheria
throat swab cultures on Loeffler’s medium, tellurite plate and blood agar; then check for toxin with antibody inoculation, antibody-based gel diffusion precipitin test, or PCR; smears of throat swab should be stained with gram stain and methylene blue (reveals typical metachromatic granules)
Treatment for Diphtheria
Antitoxin administration and either penicillin or erythromycin
Diphtheria prevention
vaccine (inactivated toxin) at 2,4,6 15-18 months and 4-6 years with booster at 11 and 20
Pertussis symptoms
“Whooping cough,” severe cough, runny nose, malaise, hacking cough with mucus production; coughing can lead to vomiting; contagious; CBC will have lyphocytosis
Treatment for Pertussis
Azithromycin can help very early in the illness to shorten duration of damage and decrease risk of transmission, but toxins damage respiratory mucosa very early
Stages of Pertussis infection
Cararrhal: 2 weeks of mild URT symptoms; Paroxysmal (2-3 months): cough stage; Convalescent phase: reduction in coughing (1-2 weeks)
Pertussis diagnosis
NP swab: DFA or PCR
Pertussis toxin effects
causes striking lymphocytosis; inhibits signal transduction by chemokine receptors, resulting in failure of lymphocytes to enter lymphoid tissue such as spleen and lymph nodes
Epiglottitis
acute inflammation in the supraglottic region of the oropharynx with inflammation of epiglottis, valleculam and arytenoids
Causes of epiglottitis
H. flu usually; also H. parainfluenza, S. pneumonia, and GAS
Typical presentation of epiglottitis
urban 40yo male with sore throat, odynophagia/dysphagia, muffled voice all with rapid onset
