Infectious Disease Bacterial Flashcards
Bacterial Disease (13)
Cellulitis Erysipelas Impetigo Pertussis Acute rheumatic fever Botulism Chlamydia Cholera Diphtheria Gonococcal infections Salmonellosis Shigellosis Tetanus
Mycobacterial Disease
Atypical mycobacterial disease
Tuberculosis
Pertussis Epidemiology
United States
1980s cyclical incidence, peaking every 2-5 years
Most cases – June-September
Neither h/o disease nor vaccination provides complete or lifelong immunity
Protection after vaccination wanes in 3-5 years, esp Tdap (DTaP titer not measurable after 12 years)
Milder disease post vaccination
International
Estimated 48.5 million cases
~ 295,000 deaths per year
Case-fatality rate among infants in low-income countries ~ 4%
Pertussis Etiology
B pertussis and B parapertussis - causative agent
Highly contagious
80% of susceptible household contacts become infected after exposure
Family members or relatives suspected source of infection in 75% of cases
Diagnosis of Pertussis
Clinical case definition:
Acute cough lasting at least 14 days with one of paroxysmal cough, posttussive vomiting, or inspiratory whoop
Cough that lasts at least 14 days in an outbreak
Confirmed case
Cough in whichB pertussisis isolated and cultured
Consistent clinical case definition confirmed by polymerase chain reaction (PCR) findings or epidemiologic linkage to a laboratory-confirmed case
PCR - good sensitivity compared to culture, more rapid, may detect later than culture or after antibiotic treatment
Leukocytosis (15,000-50,000 103/µL) with absolute lymphocytosis (not in vaccinated)
Pertussis Pathogenesis
Primarily a toxin-mediated disease
Bacteria attach to cilia of respiratory epithelial cells
Inflammation occurs which interferes with clearance of pulmonary secretions
Pertussis antigens allow evasion of host defenses (lymphocytosis promoted but impaired chemotaxis-move along gradient to organism)
Pertussis Morbidity/Mortality
Complications in infants
69% of infants younger than 6 months with pertussis require hospitalization
13% develop pneumonia, either fromB pertussisinfection or 2nd infection with other pathogens
Seizures and encephalopathy–result from severe paroxysm-induced cerebral hypoxia and apnea, metabolic disturbances such ashypoglycemia, and small intracranial hemorrhage
Reported deaths due to pertussis in young infants have substantially increased over the past 20 years
Pertussis Stage 1
Incubation 3-12 days
Catarrhal phase indistinguishable from URI (nasal congestion, rhinorrhea, sneezing, low-grade fever, tearing)
Most infectious , communicable 3+ weeks after cough onset
Pertussis Stage 2
Paroxysmal phase - paroxysms of intense coughing (lasting up to several minutes)
Older infants and toddlers, paroxysms w/ or w/o whoop
Infants < 6 mo do not have the characteristic whoop, more often apnea, at risk for exhaustion
Posttussive vomiting all to common
Pertussis Stage 3
Convalescent stage - chronic cough lasting weeks to months (hence called 100 day cough in Canada)
Treatment of Pertussis
Antibiotics begun in paroxysmal stage do not affect duration & severity
Antibiotics clear Bordetella pertussiscolonization & prevent spread
1 month or older, macrolide antibiotics (erythromycin, clarithromycin, and azithromycin)
2 mo or older with macrolide allergy - trimethoprim-sulfamethoxazole
Erythromycin and clarithromycin not recommended in infants < 1 mo (increased risk for infantile hypertrophic pyloric stenosis - IHPS)
Azithromycin (less risk for IHPS) < 1 mo
Hospitalization appropriate for Pertussis when?
Infants younger than 3 months
Infants aged 3-6 months, unless observed paroxysms are not severe
Premature young infants; and infants
Children with underlying pulmonary, cardiac, or neuromuscular disease
Droplet precautions are recommended for 5 days after initiation of effective therapy or until 3 weeks after the onset of paroxysms if appropriate antimicrobial therapy is not given
Diagnosis for Acute Rheumatic Fever
combination of clinical manifestations that can develop in relation to group A streptococcal pharyngitis Chorea Carditis Subcutaneous nodules Erythema marginatum Migratory polyarthritis
Acute Rheumatic Fever (ARF)
Incidence of acute rheumatic fever (ARF) has declined in most developed countries
Most clinicians have little or no practical experience with the diagnosis & management of ARF
Etiology of Acute Rheumatic Fever
Heavily encapsulated strains of group A streptococci with rich M protein (a sign of virulence) associated with ARF
Group AStreptococcuscause the myriad of clinical diseases with cross reaction of bacterial antigens with target organs (molecular mimicry)
Autoantibodies reactive against the heart found with rheumatic carditis
Antibody can cross-react with brain and cardiac antigens, and immune complexes are present in the serum (uncertain whether antibodies cause or result of myocardial injury)
ARF Pathophysiology
Migratory arthritis
80% of cases
Large joints - knees, ankles, elbows, or shoulders
Sydenham chorea (St Vitus’ Dance) once common late-onset finding is now rare
Carditis
Progressive CHF, new murmur or pericarditis
May be the presenting sign of unrecognized ARF
Most lethal manifestation
Genetics - increase in family incidence
Associated with class II HLA
Elevated immune-complex levels in patients with ARF associated with HLA-B5
Presentation of ARF
Nonspecific symptoms initially (latent period ~ 18 days (range 1-5 weeks)
Consider carditis if:
New/changing valvular murmurs
Cardiomegaly
Congestive heart failure
Pericarditis
60% with carditis - isolated mitral valve disease, less commonly mitral and aortic valve disease
Sydenham chorea is seldom seen at initial presentation
Erythema marginatum and subcutaneous nodules - < 10% of patients
Arthritis 80% - usually involves multiple large joints: knees, ankles, elbows, and wrists; less often hips and smaller joints of hands and feet
Migratory polyarthritis seen usually when febrile; rarely causes permanent joint deformity
T. Duckett Jones guide to determine high risk
Preceding history of group A strep infection helpful, not required
2 major manifestations or 1 major and 2 minor manifestations
Major manifestations : carditis, polyarthritis, chorea, erythema marginatum & subcutaneous nodules
Minor manifestations include arthralgias & fever
Laboratory –
Elevated ESR and CRP (C-reactive protein)
Prolonged PR interval (not specific/predictive of cardiac sequela
Exceptions to Jones criteria are chorea or possibly indolent carditis
Positive TC for Streptococcus in 25% of patients at the time of presentation
Work up of ARF
– Group A streptococcal antigen detection tests are specific but not very sensitive (90%)
–ASO (antistreptolysin O) – peak titer at onset of rheumatic fever (but not diagnostic of ARF)
– Antistreptococcal antibodies support d/o ARF
– Antibodies target extracellular streptococal products (ASO, antideoxyribonuclease B (anti-DNAse B), antistreptokinase, antihyaluronidase, and anti-DNAase (anti-DNPase))
— Elevated titer of at least one of these antibodies indicates streptococcal infection in 95%
ASO is found in 80-85% of patients with ARF
— Throat culture – sensitivity 25-40% (compared with sensitivity of ASO titer of 80%
— ASO elevated with anti-DNAse B or antihyaluronidase has sensitivity of 90%
— Acute-phase reactants such as C-reactive protein (CRP) and ESR usually elevated; useful monitoring disease
— Synovial fluid analysis reveals a sterile inflammatory reaction, usually with fewer than 20,000 cells/μL (mainly polymorphonuclear) without crystals
ARF – CXR, Echo, ECG
Echocardiography is more sensitive than standard auscultation - detect regurgitant lesions (prognostic significance unclear)
Standard auscultation is however favored for detecting carditis (findings of mitral regurgitation 80%)
Chest radiograph – r/o cardiomegaly
ECG may reveal a prolonged PR interval (not always associated with later cardiac sequelae)
TC may be positive streptococcus
ARF Treatment
Primary goal of treatment is eradicating streptococcal antigens from the pharynx
Penicillin is the drug of choice, parenteral benzathine benzylpenicillin assures compliance
Oral cephalosporins, rather than erythromycin, recommended if allergic to PCN (however 20% cross-reactivity)
Antibiotics do not affect the course an acute attack
Prompt treatment of recurrent strep pharyngitis reduces reactive antigen exposure
Antimicrobial therapy does not alter course/frequency/severity of cardiac disease
Salicylate effective for analgesia (esp high dose–dosage increased until N/V, tinnitus, headache, hyperpnea)
Corticosteroids reserved for severe carditis (tapered after 2-3 weeks)
Mild heart failure treated with rest and corticosteroids
Digoxin in severe carditis (patient may develop heart block, use monitored closely due to potential block)
Nocturnal tachycardia (a sign of cardiac disease) may respond to digoxin, vasodilators or diuretics
Sydenham chorea – haloperidol, also long-term antimicrobial prophylaxis, rest and sedation (chorea disappears with sleep)
AHA Committee on Acute Rheumatic Fever recommends
benzathine benzylpenicillin at 1.2 million units intramuscularly every 4 weeks, every 3 weeks if high-risk
Oral prophylaxis (less reliable) - phenoxymethylpenicillin (penicillin V) or sulfadiazine
Oral cephalosporins recommended if PCN allergic
No consensus on the required duration of antibacterial prophylaxis, AHA recommends:
Risk of recurrence greatest 3-5 years after acute episode
Prophylaxis for at least 10 years after the last episode of rheumatic fever or adult patient
Longer or indefinite prophylaxis if heart disease
Indefinite prophylaxis if high risk for exposure to strep or patients difficult to get follow-up
Botulism Etiology
Acute neuroparalysis due to a neurotoxin produced byClostridium botulinum
C botulinum - gram negative rod survives in soil & water by sporulating, anaerobic conditions allow germination
Toxin binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions (blocks acetylcholine release with weakness, flaccid paralysis)
Cure only occurs following sprouting of new nerve terminals
Different Types of Botulism
Infant botulism(IB) - ingested spores, germinate in intestine producing toxin , bee honey as a source (mortality < 1% with supportive care) Foodborne botulism (FBB) – most often improper canning or home-preparation of foods, more common in adults, 12-36 hours after ingestion develop GI symptoms from gut paralysis then later cranial nerves Wound botulism (WB) – wound contamination with C bolulinum with toxin release (incubation 4-14 days, average 10), typically no GI symptoms (one cause is injection of black-tar heroine) Due to the potency of the toxin, possible use as biological weapon (CBRNE – Botulism)