bacterial infections Flashcards
botulism
neuroparalytic disease (unique from others)
produced by clostridium botulinum (anaerobic, spore-forming bacillus found in soil)
three forms of botulism:
food-borne
infant botulism
wound botulism
mechanism of action of botulinum toxin
toxin blocks release of ACH from vesicles at neurons, preventing use of muscles
botulism: clinical findings
Visual Disturbance (within 36 hours):
-Diplopia
-Loss of accommodation
-Fixed dilated pupils
-Ptosis (eyelid droop)
-Extraocular movement palsy
Dry mouth
Dysphagia/dysphonia (difficulty swallowing, not pain)
Nausea and vomiting
botulism clinical findings cont.
Acute, bilateral cranial nerve neuropathy (unique part):
-Symmetric descending weakness (only thing that will cause symmetric descending weakness)
-Paralysis progressing to respiratory failure and death
The sensory examination is normal (can feel face, just can’t move it)
-MOTOR NEURONS ONLY
note on emphasis:
stroke will knock out everything
botulism: sensory is fine, but paralysis and symmetrical descending weakness
botulism is very serious and can cause death
botulism
diagnostic findings: toxin analysis of serum, stool, vomit, food
Treatment: serum antitoxin
In most cases will make something like this a test question:
do you eat a lot of jarred or self-canned foods? Botulism!!
Campylobacter jejuni infection
One of the most frequently occurring bacterial agents of gastroenteritis
Occurs worldwide (diarrhea in children in underdeveloped countries)
Highest incidence <5 years old, especially in resource-limiting settings
Estimated 1.3 million cases annually in US
Campylobacter jejuni sources of contamination
Poultry
Unpasteurized milk
Contaminated drinking water (Traveler’s Diarrhea)
-(Traveler went (camp)ing in costa rica)
Campylobacter jejuni risk factors
International travel in the week prior to onset
Use of proton pump inhibitors and histamine-2 receptor antagonists (why?)
Campylobacter jejuni symptoms
-Arise 1-3 days after exposure; typical duration 1 week
-Watery diarrhea which may be bloody
-Abdominal pain/cramps
-Nausea
-Occasional vomiting
-Weight loss
Campylobacter jejuni Diagnosis
Gold standard: Stool culture
not usually done in clinical practice
-takes too long, symptoms only last a week
Campylobacter jejuni management
Self-limiting
Supportive therapy: Fluid and electrolyte replacement
Campylobacter jejuni: traveler’s diarrhea
Antibiotics are usually recommended
Either azithromycin, 1 g orally as single dose
Or Ciprofloxacin, 500 mg twice daily orally for 3 days
note: there are reasons why you would choose one over the other (heart issues for ex.)
rare complications of campy jejuni
-Bacteremia
-Guillain-Barre syndrome
-Reactive arthritis
GB syndrome: (“out of the blue stroke kind of” where nerves break down [ex. if they get a cold] but can regenerate back to normal [so severe patient must learn to walk again])
Chlamydia Trachomatis
Sexually transmitted disease caused by Chlamydia trachomatis
-Often asymptomatic
-Common cause of urethritis, cervicitis, and post-gonococcal urethritis.
-Occasionally causes epididymitis, prostatitis, or proctitis
Leading cause of infertility in females in the US
Symptoms causing suspect of Chlamydia
-Vaginal discharge
-Postcoital or intermenstrual bleeding or dysuria in women
-Urethral discharge, dysuria, scrotal pain or swelling in men
-dysuria: painful urination
Chlamydia: Diagnostic findings
-Highly sensitive nucleic acid amplification tests (NAAT)
-In women: Vaginal swab
-In men: Use first-void urine
-Rectal and oropharyngeal swabs may be performed, if necessary
Chlamydia: treatment (meds)
Doxycycline orally 100 mg twice daily for 7 days
-Preferred
-DO NOT USE in pregnancy
A single oral 1-g dose of azithromycin 500 mg
-Preferred for pregnancy or with concern of
adherence
levofloxacin once daily for 7 days.
Chlamydia treatment (without meds)
-Abstinence from sexual intercourse for 1 week after completion of medication
-Retesting is not recommended except in pregnancy
-Screening for reinfection is recommended in all patients 3 months after treatment
-Test and treat sexual partners (within 60 days)
Chlamydia treatment (without meds)
-Abstinence from sexual intercourse for 1 week after completion of medication
-Retesting is not recommended except in pregnancy
-Screening for reinfection is recommended in all patients 3 months after treatment
-Test and treat sexual partners (within 60 days)
Cholera (risk factors)
An acute diarrheal illness caused by Vibrio cholerae
-The disease is toxin-mediated (getting sick off the
toxin, not the bacteria)
Risk factors: Travel endemic area, contact with infected person, crowding, war, famine, refugee camps
Cholera: Clinical Findings
-The toxin produces hypersecretion of water and chloride ion in the small intestine
-Sudden onset of severe, frequent watery diarrhea(!!)
-Massive diarrhea of up to 15 L/day.
-Liquid stool is gray; turbid; and without fecal odor, blood, or pus (“rice water stool”).
-Severe dehydration may lead to hypotension and shock within hours
-Fever is rare
-Can kill you
Cholera: Diagnostic findings and treatment
Diagnostic Findings:
-Stool cultures are positive, and agglutination of vibrios with specific sera can be demonstrated
Treatment:
-Replacement of fluids
-Supportive management
Cholera: Antimicrobial treatment
Antimicrobial therapy will shorten the course of illness
Several antimicrobials are active against V cholerae, including:
Tetracycline
Ampicillin
Chloramphenicol
Fluoroquinolones
Azithromycin
Trimethoprim-sulfamethoxazole
Diphtheria
-Acute infection caused byCorynebacterium diphtheriae
-An acute infection with a toxin-producing strain of Corynebacterium diphtheriae
-Usually attacks the respiratory tract but may involve any mucous membrane or skin wound
-The organism is spread primarily by respiratory secretions
-Exotoxin produced by the organism is responsible for myocarditis and neuropathy
Diphtheria: Clinical findings (3 forms)
Three forms of diphtheria:
Nasal infection
-Nasal infection produces few symptoms other than a nasal discharge
Laryngeal infection
-Laryngeal infection may lead to upper airway and bronchial obstruction
Pharyngeal diphtheria
-In pharyngeal diphtheria, the most common form, a tenacious gray membrane covers the tonsils and pharynx
Diphtheria: Treatment
Removal of membrane (from throat)
Antitoxin
Antibiotics: Penicillin or Erythromycin
Diphtheria: Treatment
Vaccine: Booster dose of diphtheria toxoid
-Plus, active immunization if not previously immunized,
-Antitoxin prepared from horse serum
-As well as a course of penicillin or erythromycin
-Azithromycin, clarithromycin or erythromycin for
carrier state (all -mycin)
Diphtheria: Prevention
Isolation from potentially sick person
Prophylaxis for close contacts:
-Booster dose of diphtheria toxoid
-Course of penicillin or erythromycin
Women should receive Tdap with each pregnancy, preferably between 27 and 36 weeks
Diphtheria: Complications
Exotoxin produced by the organism is responsible for myocarditis and neuropathy
Gonorrhea
-Sexually transmitted infection
-Caused byNeisseria gonorrhoeae, a gram-negative
diplococcus
-Greatest incidence in the 15- to 29-year-old age group.
-The incubation period is usually 2–8 days.
-Can infect any mucocutaneous surface
-Oral, urethral, vaginal, anal
Gonorrhea: clinical findings in men
Men:
-Burning on urination and a serous or milky discharge(!)
-One to 3 days later, the urethral pain is more pronounced and the discharge becomes yellow, creamy, and profuse, sometimes blood-tinged.
-Chronic infection leads to prostatitis and urethral strictures (can also increase risk of prostate cancer)
-Rectal infection is common in men who have sex with men
-Atypical sites of primary infection (eg, the pharynx) must always be considered
-MAY PRESENT ASYMPTOMATIC
Gonorrhea: clinical findings in women
Women:
-Becomes symptomatic during menses
-Women may have dysuria, urinary frequency, and urgency, with a purulent urethral discharge
-Vaginitis and cervicitis with inflammation of Bartholin glands are common
-It can progress to involve the uterus and tubes with acute and chronic salpingitis, with scarring of tubes and sterility
-Can lead to Pelvic Inflammatory disease (PID)
-Rectal infection may result from spread of the organism from the genital tract or from anal coitus
Gonorrhea: clinical findings
Disseminated Disease: systemic complications follow the dissemination into bloodstream
Two distinct clinical syndromes:
-Either purulent arthritis or
-(possible pearl): The triad of rash, tenosynovitis (inflamed tendons), and arthralgias (join pain)
-are commonly observed in patients with
disseminated gonococcal infection, although overlap
can be seen.
Gonorrhea: Clinical findings
Conjunctivitis (eyes!)
-The most common form of eye involvement is direct inoculation of gonococci into the conjunctival sac
-In adults, this occurs by autoinoculation of a person with genital infection
-The purulent conjunctivitis may lead to loss of the eye unless treated promptly
Gonorrhea: Diagnostic Findings
-Historically gram stain & culture of discharge was performed –uncommon now
-Nucleic acid amplification testing (NAAT) of discharge or urine for men & women
-Looks for gonorrhea & chlamydia concurrently
-Excellent sensitivity & specificity
-Doesn’t preclude doing a pelvic exam!
test Q?
GC-CHL
(check gonorrhea and chlamydia together, they’re best buds)
Gonorrhea: treatment
Ceftriaxone 500mg IM X1
Conjunctivitis
A single 1-g dose ofceftriaxoneis effective
Gonorrhea: Treatment of pelvic inflammatory disease
Ceftriaxone
AND
Probenecid
AND
Doxycycline
with or withoutmetronidazole
Methicillin-Resistant Staphylococcus Aureus (MRSA)
-Any strain of S. aureus carrying gene(s) conferring resistance to penicillinase-resistant (or semi-synthetic) penicillin, such as methicillin or oxacillin.
-Prevalence is widespread
-Can be acquired in community or healthcare settings
-The incidence of infections is declining but colonization is increasing
-Can cause a wide spectrum of infections
-Prominent cause of purulent cellulitis (purulent=pus=infection)
note for exam:
take two or three main nuggets to set each bacterial infection apart when studying
MRSA: Diagnosis
Isolation of the organism from culture
Susceptibility testing will demonstrate oxacillin (a semi-synthetic penicillin) resistance
MRSA: Prevention
-Pre-operative screening for carriers
-Decolonization with chlorhexidine bathing and nasal mupirocin
-Standard infection control procedures
MRSA: Management
Management:
-Varies by clinical manifestation
-Drainage of abscess
-Prompt administration of antibiotics:
-Vancomycin- 1st line for serious infections
-Clindamycin
-Trimethoprim/sulfamethoxazole (Bactrim)
-Doxycycline
Pertussis
AKA “whooping cough”!!
Transmitted in respiratory droplets
Incubation period: 7–17 days
Half of all cases occur before age 2 years
Pertussis: clinical findings (3 stages)
Three consecutive stages:
Catarrhal (1-2 weeks)
Paroxysmal (up to 10 weeks)
Convalescent (up to 12 weeks)
Pertussis: clinical findings (3 stages)
The Catarrhal Stage (Upper Resp symptoms)
-Coryza, rhinorrhea (runny nose), mild cough, low-
grade fever
The Paroxysmal Stage
-Paroxysms of cough with inspiratory “whoop”
-May cause cyanosis (bluish discoloration of skin!!)
-Post-tussive vomiting
The Convalescent Stage
-Cough frequency and severity gradually decreases
Pertussis: Diagnostic Findings
-Nasopharyngeal culture (like covid swab)
-Elevated WBC count (!!)
Pertussis: Treatment
Antibiotics: (remember -mycin)
-Erythromycin 500 mg four times daily orally for 7 days
-Azithromycin 500 mg once 1 day, then 250 mg once daily for 4 days
-Clarithromycin 500 mg three times daily for 7 days
-Trimethoprim-sulfamethoxazole 160 mg–800 mg orally twice a day x 7d
Treatment shortens the duration of carriage and may diminish the severity of coughing paroxysms (attacks)
Pertussis: Prevention
Vaccination:
Infants (DTaP)
-diphtheria toxoid, tetanus toxoid, and acellular
pertussis vaccine
Adults (Tdap)
-tetanus toxoid, reduced diphtheria toxoid, and
acellular pertussis vaccine
Pregnant women
-Tdap between 27 - 36 weeks of every pregnancy
-Tdap administered immediately postpartum if not
done already
Zpack:
azithromycin (broad spectrum antibiotic)
Rheumatic Fever
Systemic immune process resulting from streptococcal infection of the pharynx (strept throat)
-Rheumatic carditis and valvulitis (vegetation on valves)
-May be self-limited
-May lead to slowly progressive valvular deformity
-A perivascular granulomatous reaction with valvulitis is characteristic lesion
Chronic Rheumatic Heart Disease (Rheumatic Fever pearl)
Results from single or repeated attacks of rheumatic fever that produce:
-Rigidity and deformity of valve cusps
-Fusion of the commissures
-Shortening and fusion of the chordae tendineae (parachute getting tangled)
-Valvular stenosis or regurgitation results and the two often coexist
-Affects mitral, aortic, and tricuspid valves, but the pulmonary valve only very rarely
(on a test, person has a sore throat, heart problem, pulmonary valve sounds fine, Rheumatic!!)
random side note:
repeated infections, gotta consider immunodeficiency
Rheumatic Fever: Signs and Symptoms
Categorized as:
-Major Criteria
-And Minor Criteria
(Signs of acute rheumatic fever usually commence 2–3 weeks after infection)
Major criteria:
Carditis
Carey–Coombs short mid-diastolic mitral murmur may be present due to inflammation of the mitral valve
Erythema marginatum
Subcutaneous nodules
Sydenham chorea
Polyarthritis
Minor criteria:
Fever
Polyarthralgias
Reversible prolongation of the PR interval
Elevated erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP)
Positive throat culture or rapid streptococcal antigen test and elevated or rising streptococcal antibody titer
Rheumatic Fever: Diagnosis
Rapid ESR is nonspecific evidence of inflammatory disease (erythrocyte sedimentation rate)
High or increasing titers of antistreptococcal antibodies (antistreptolysin O and anti-DNase B)
(+ strept test doesn’t necessarily mean rheumatic fever. Follow up with these two tests)
Rheumatic Fever: Treatment (meds)
Aspirin (salicylates)
-Adults may require large doses of aspirin, 0.6–0.9 g every 4 hours; children, lower doses
-Markedly reduces fever, relieve joint pain and swelling, but have no effect on the natural course of the disease
Penicillin
-Benzathine penicillin, intramuscularly
Corticosteroids
-Prednisone
-Usually causes rapid improvement of the joint symptoms
-Indicated when response to salicylates has been inadequate
Rheumatic Fever: Complications
Rheumatic valvular disease affects:
-The mitral valve most commonly
-The aortic valve second most commonly
-The tricuspid valve third most commonly
Heart failure
Arrhythmias, pericarditis with effusion, and rheumatic pneumonitis
TEST: (Doesn’t impact pulmonary, mostly impacts mitral!)
Rheumatic Fever: Prevention
-Start early treatment of streptococcal pharyngitis with penicillin
-Prevention of recurrent episodes is critical
-PREFERRED treatment regimen:
Benzathine penicillin G, 1.2 million units intramuscularly every 4 weeks
Rocky Mountain Spotted Fever
-Rickettsia rickettsia (Gram Negative)
-Spread by bite of ticks (vector, PEARL [hiking?])
-Several hours of contact between the tick and the human host are required for transmission
-Up to 40% of patients do not recall a tick bite
Rickettsia: Pathophysiology
-Rickettsia is an obligate (restricted to) intracellular bacteria that grows and multiplies in the endothelial cells in the small vessels of the body (arterioles & venules)
-The endothelium gets damaged and causes vessels to become blocked by thrombi, producing vasculitis in the skin, subcutaneous tissues, CNS, lungs, heart, kidneys, liver, and spleen
-This causes blood leakage into the surrounding tissues and the appearance of the rash on humans.
Can lead to Disseminated Intravascular Coagulation (DIC)
DIC
Your body goes way overboard and clamps everything down, starts clotting in every nook and cranny of your body
Ticks
Brown Dog Tick:
-Found worldwide
-transmits rocky mountain spotted fever
-often dogs are hosts
-Rocky mountain wood tick: Western US (not CA)
-American Dog Tick: East of Rockies and portions of pacific coast
Test:
Is it lyme disease or rocky mountain spotted fever?
will mention either hiking or tick bite
different symptoms
Which five state account for 60% of RMSF cases?
NC, Oklahoma, Arkansas, Tennessee, Missouri
RMSF: Early symptoms
Abrupt onset of high fever
Chills
Headache
Nausea and vomiting,
Myalgias
Restlessness
Insomnia
Irritability
Edema around eyes and backs of hands (note: unique to spotted fever)
Rash (occurs 2-4 days after onset of fever)
RMSF early stage symptom:
Characteristic rash: appears 2-4 days, small, flat, pink macules on wrists, forearms, and ankles and spreads centrally to trunk and palms of hands and soles of feet
(resembles eczema, but If also fever, think spotted fever)
Other symptoms
Facial flushing, conjunctival infection, hard palate lesions (roof of mouth)
Late symptoms
-Altered mental status, coma, cerebral edema
-Respiratory compromise (pulmonary edema, acute respiratory distress syndrome)
-Necrosis, often requiring amputation
-Multi-organ system damage (CNS, renal failure)
Petechial rash is sign of severe disease
RMSF: diagnosis
Laboratory Findings:
-Thrombocytopenia (low platelet count)
-Hyponatremia (diluted sodium)
-Elevated aminotransferases
-Hyperbilirubinemia (indicates poor liver function?)
Cerebral Spinal Fluid (CSF) may show:
-Hypoglycorrhachia
-Mild pleocytosis
Disseminated intravascular coagulation is observed in severe cases.
RMSF: Diagnostic method
immunohistologic or PCR demonstration ofR rickettsiiin skin biopsy specimens (or cutaneous swabs of eschars or skin lesions)
Do not delay treatment while waiting for the results!!
RMSF: treatment
doxycycline
Pregnant: NOT doxycycline
RMSF: most common cause of death
Pneumonitis with respiratory or cardiac failure
Sequelae may include:
Seizures
Encephalopathy
Peripheral neuropathy
Paraparesis
Bowel and bladder incontinence
Cerebellar and vestibular dysfunction
Hearing loss
Motor deficits
RMSF: Prevention
Protective clothing, tick-repellent chemicals containing DEET, check for ticks frequently
Salmonellosis
“Non-typhoidal salmonellosis”
Leading cause of FOODBORNE ILLNESS and mortality due to foodborne pathogens in the US and leading cause of BACTERIAL DIARRHEA worldwide
Salmonellosis: Sources
-Eggs
-Unpasteurized dairy products
-poultry
-nearly any food product can be contaminated and transmit disease
Salmonellosis: Clinical manifestations
Symptoms begin 6-72 hours after exposure and last for 3-7 days
Mild and self-limiting
Nausea
Vomiting
Abdominal cramping
Non-bloody diarrhea
Salmonellosis: Evaluation methods
Stool cultures
Blood cultures
Salmonellosis: Management
Most patients with mild symptoms:
Supportive care
Rehydration
Self-limiting
Treatment for those at risk for severe disease:
aka infants, older people, prosthetic valves or joints, severe atherosclerosis, immunocompromised?
treat with: mostly -acin
Salmonellosis: Complications
Bacteremia: May lead to hematogenous seeding of remote sites
Endovascular infections
-Aortitis or endocarditis
-Bone and Joint infections
-Visceral abscess
Shigellosis
Serogroup A: associated with epidemics, generally most severe type
Serogroup B, C: not as important
Serogroup D: most common in US
Shigellosis: Transmission and Risk Factors
Transmission:
-Fecal-oral spread
-Contaminated water, food, fomites (non-tangible vector)
Risk factors in US and Europe:
-Children in daycare
-Migrant workers
-Travelers to developing countries
-Custodians
-Men who have sex with men
Shigellosis: Clinical Presentation
-Fever, fatigue, malaise, anorexia
-Watery diarrhea (with or without blood) precedes dysentery
-Dysentery occurs within hours to days
-Frequent, small, bloody, mucoid stools with
abdominal cramps and tenesmus (diarrhea “dry
heaves”)
TEST: (only one so far that’ll give us bloody snot poop that just came back from a waterpark)
Shigellosis: Diagnosis
Stool culture
Polymerase chain reaction (PCR)
-Only available in specialized labs. Expensive and not regularly used
Shigellosis: Management
-Rehydration (oral or IV)
-Antibiotic therapy for severe cases
-Ciprofloxacin 750 mg orally twice daily for 7–10
days
or
-Levofloxacin 500 mg orally once daily for 3 days
-Ceftriaxone 1 g intravenously once daily for 5 days
Self-limiting in healthy persons
Tetanus
C tetani (spores found in soil)
Puncture wounds are more prone to become colonized
(laceration, clinically they rip open and sterilize wound, in puncture wound skin closes around bacteria)
Tetanus: Clinical Findings
-Pain, tingling, spasm near muscle
-Uncontrolled spasm, exaggerated reflexes.
-Stiff jaw, neck, hyperreflexia then trismus
-jaw spasm OR lock jaw
-Spasm glottis may cause asphyxia
Tetanus: Complications
-Airway obstruction is common.
-Urinary retention and constipation may result from spasm of the sphincters.
-Respiratory arrest and cardiac failure are late, life-threatening events
Tetanus: Prophylactic Treatment
Fully Vaccinated: nothing needed to treat wound
Unknown/not vaccinated:
-For clean, minor wounds:
-Td or Tdap vaccines
-All other wounds:
-Td or Tdap vaccine
-Human tetanus immune globulin (especially for unvaccinated) given IM
Tetanus: Prevention
Td (Tetanus diphtheria toxoid vaccine) every 10 years
-after 5 years if there is an injury
Typhus
A group of infectious diseases caused by Rickettsial pathogens transmitted by insect vectors
Also known as “Rickettsial Fever” or “Typhoid Fever”
(not same as rickettsia rickettsia)
Common Forms:
Epidemic (Louse-Borne) Typhus
Endemic (Murine) Typhus
Scrub Typhus
Endemic (Murine) typhus
Flea-borne
primary reservoir: Rats
areas of low sanitation where rats are abundant (like NY or chicago)
Endemic (Murine) typhus cont.
People become infected withR. typhiwhen they come into contact with infected flea feces via scratched or abraded skin (even like skin exfoliation)
Endemic (Murine) typhus: signs and symptoms
-Fever, headache, myalgia, and chills.
-Relative bradycardia is reported.
-Maculopapular rash occurs in around 50% of cases; it is concentrated on the trunk, mostly sparing the palms and soles, and fades rapidly
TEST: (If maculopapular rash due to rickettsia disease but is NOT in the HANDS and FEET, think typhus!!!)
The illness may be associated with maternal death, miscarriage, preterm birth, and low birth weight if acquired early during pregnancy.
Endemic (Murine) Typhus: Diagnosis/Lab findings
Diagnosis:
Serologic confirmation with specificR typhiantigens
Laboratory Findings:
Anemia, thrombocytopenia, leukopenia, hyponatremia, and elevated levels of liver enzymes commonly occur.
Endemic (Murine) Typhus: Complications
-Pulmonary, in the form of pneumonia, followed by pleural effusion and respiratory failure
-Neurologic (peripheral facial paralysis, meningismus, ataxia, seizures),
-Acute kidney injury
-Multiorgan failure
Endemic (Murine) Typhus: Treatment/Prognosis
Treatment:
Doxycycline
Ciprofloxacinandampicillinare reportedly successful in pregnant women
Prognosis:
Usually self limiting with low mortality rate
WHO antibiotic oath
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