Exam VI - Respiratory & Genital Infections Flashcards

(94 cards)

1
Q

Pharyngitis

A
Streptococcus pyogenes
Group A beta-hemolytic strep, GAbS
Transmission: Respiratory droplets 
Incubation 2-4 days
Symptoms: Abrupt onset fever, sore throat with exudate (suppurative = pus generating), may have abdominal pain, nausea, vomiting
Diagnosis: rapid strep test
At risk population: children
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2
Q

Streptococcus pyogenes

A

Gram-positive cocci in pairs or chains
Catalase negative
Beta-hemolytic on blood agar plate
M Protein: antiphagocytic and antigenic variation
SPE: Streptococcal pyrogenic exotoxins; encoded by phage with many enzymes; pyro = fever causing

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3
Q

Scarlet Fever

A

caused by streptococcus pyogenes
Potential complication of strep throat due to pyrogenic exotoxin with symptoms 1-2 days after pharyngitis
Sandpaper rash
Starts on face spreads to body, not on palms or soles
1 week duration then desquamation
Strawberry tongue

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4
Q

Rheumatic Fever

A

caused by streptococcus pyogenes
Potential complication of strep throat
Antibodies made against the S. pyogenes M protein (during original pharyngitis infection) cross react with
protein on heart valves and joints
Damage heart valves over time causing endocarditis leading to scarring of heart valves, stenosis, regurgitation, and rheumatic heart disease (RHD)
Polyarthritis - multiple joints affected

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5
Q

Corynebacterium diphtheria

A

Gram positive, club shaped (rod), non-motile
Catalase positive
Humans are the only reservoir
Respiratory: transmission respiratory aerosols
Cutaneous: transmission skin contact

Virulence Factor
Diphtheria toxin: phage mediated produced at site of infection that disseminates through the blood and binds to receptors on heart, throat, and nerve cells

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6
Q

Mechanism of Action: diphtheria

A

Same as P. aeruginosa Exotoxin A (AB toxin)
ADP-ribosyl transferase
Inactivates elongation factor 2
Inhibits host protein synthesis

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7
Q

Respiratory diphtheria

A

Incubation 2-4 days
Attach and multiply in the pharynx- location of infection
Exotoxin causes tissue damage
Formation of thick gray pseudomembrane exudate - will bleed if tested with swab
Malaise, sore throat, fever, exudative pharyngitis, bill neck
Potential complications: myocarditis and neurotoxicity

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8
Q

Cutaneous diphtheria

A

Gains entry to subcutaneous tissue through break in the skin - immunocompromised
Chronic, non-healing ulcer - necrosis due to toxin

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9
Q

Diagnosis of diphtheria

A

Selective agar: cysteine tellurite blood agar
Tinsdale agar
Tellurite: grayish black colonies
Cysteine: brown halos surrounding colonies
PCR

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10
Q

Bordetella pertussis

A

Gram negative (has LPS) coccobacillus (rod), aerobic
Disease: pertussis
highly contagious disease with uncontrolled violent coughing
High Risk Population: unvaccinated children and vaccinated teens (middle school, high school age)

Virulence factors:
Attachment: bind to ciliated epithelial cells = pertactin and filamentous hemagglutinin
Tissue damage caused by pertussis toxin
ADP ribosylating activity of G proteins, increased cAMP, increased resp. mucus
tracheal cytotoxin has a high affinity for cilia causing ciliostasis or death of cells leading to characteristic cough; also stimulates IL-1 resulting in fever via T cells

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11
Q

Pathogenesis of Bordetella pertussis (4)

A
  1. Exposure: aerosol droplet inhalation
    needs human reservoir
  2. Attachment to ciliated epithelial cells via pertactin and filamentous hemagglutinin
  3. Proliferation
  4. Tissue damage via pertussis toxin and tracheal cytotoxin
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12
Q

Pertussis: 3 stages

A

7 to 14 day incubation

  1. Catarrhal: coldlike symptoms, runny nose, sneezing, malaise, low fever, loss of appetite; highly transmissible, large # of bacteria
  2. Paroxysmal: damage ciliated cells, impaired mucus clearance; prolonged coughing fits with inspiratory whoop, 40-50/day, vomiting exhaustion, ruptured blood vessels in the eyes
  3. Convalescence: recovery
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13
Q

Diagnosis of Pertussis

A
Nasopharyngeal aspirate best
Classic: Bordet-Gengou medium
Current: Regan-Lowe agar 
Inoculate at bedside
7-12 days incubation
PCR – best if available
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14
Q

Treatment of Pertussis, Tetanus, and Diphtheria

A

Acellular Vaccine - currently recommended
Inactivated pertussis toxin + Filamentous hemagglutinin + pertactin
Part of DTaP for children

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15
Q

Pneumonia

A

Inflammation of the lungs accompanied by fluid filled alveoli and bronchioles
May involve: hemoptysis (coughing blood)
Caused by inhalation of aerosols, aspiration of normal flora (URT and GI), or hematogenous spread from another site of infection
nosocomial or community acquired
Types: typical vs. atypical

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16
Q

Typical Pneumonia

A

streptococcus pneumonia
Abrupt onset, fever, chills, congestion, shortness of breath (dyspnea), chest pain
**Productive cough
Streptococcus pneumoniae, Klebsiella pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus

Characteristics of bacteria: also known as pneumococcus, lobar pneumonia, gram positive, pairs or chains, alpha hemolytic, blood agar, CAPSULE, adhesin, IgA protease, pneumolysin: lyses ciliated epithelial cells

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17
Q

Typical Pneumonia: Causes, Dx, and Tx

A

Fall & winter, CAP (community acquired pneumonia)
Predisposing factors: viral infection, influenza, HIV, alcoholism, children, elderly, splenectomy

Diagnosis: sputum sample - rust colored
Microscopy - gram positive cocci and numerous PMNs, antigen agglutination (secreted in urine as well as sputum)
Alpha hemolysis
Optochin sensitive

Vaccines:
Pneumovax: 23 most common capsule serotypes, PPSV23; adult
Pneumococcal conjugate vaccine: PCV13, children

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18
Q

Atypical Pneumonia

A

Organisms not seen with Gram stain (except Lp)
fever, headache, malaise, myalgia, nausea, diarrhea, many neutrophils, dry hacking cough
***Nonproductive cough (no sputum)

Mycoplasma pneumoniae
Chlamydophila spp.
Legionella pneumophila
Coxiella burnetii

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19
Q

Mycoplasma pneumoniae

A

Primary atypical pneumonia, community acquired
Symptoms: atypical pneumonia; persistent nonproductive cough, excessive sweating
May last several weeks to months; lack of seasonality
“walking pneumonia”
Characteristics: smallest free living microbe, no cell wall, capsule, adhesin (attachment to the base of the cilia)
Transmission: inhalation of aerosols

Dx: usually can not see the bacteria with microscopy, large number of PMNs, grows very slowly in culture, 2-6 weeks, cold agglutinins
PCR

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20
Q

Chlamydophila pneumonias

A

Characteristics: gram negative, CAP, obligate intracellular bacteria; mild infection
TWAR: Taiwan Acute Respiratory Agent
Transmission: respiratory droplets
Symptoms: mild fever, sore throat, malaise, persistent cough; atypical pneumonia

Diagnostics: Microscopy/Gram stain: no organisms seen
large number of PMNs
ELISA
Elementary body: body that gains entry to the cell and survive; most active
Reticulate body: when ready to multiply it starts the second stage

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21
Q

Psittacosis

A

Chlamydophila psittaci
Parrot fever
Disease of birds can be transmitted to humans

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22
Q

Legionnaires’ Disease

A

Legionella pneumophila; atypical pneumonia
Characteristics: gram negative, does not Gram stain well, intracellular
Water cooling towers and air conditioning units
Environment: amoeba
Human: alveolar macrophages
Transmission: inhalation of aerosolized droplets
Symptoms: abrupt onset of fever, headache, pleurisy, chills, myalgia, dry cough; complications involving GI tract, CNS, liver and kidneys are common
Pontiac Fever: strong immune system means that this infection will probably go away on its own

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23
Q

Legionnaires’ Disease: Risk and Dx

A

Risk factors: smokers, COPD, high alcohol consumption, elderly, immunosuppressed, renal transplant patients, or patients on dialysis

Diagnosis:
Culture: fastidious (picky) - buffered charcoal yeast extract agar (BYCE) with iron salts and cysteine
Fluorescent antibody staining
Antigen can be detected in urine

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24
Q

Common Causes of Nosocomial Pneumonia

A

Pseudomonas aeruginosa, S. aureus, H. influenza
Enterics: Enterobacter , Klebsiella, E. coli, Serratia marcescens - if they go anywhere else other than GI via vomiting = problems

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25
Pseudomonas aeruginosa
Gram-negative rod, ubiquitous, capable of growing on many substrates and temperatures ranging 4-42 C, aerobic, and forms a biofilm - Alginate capsule Motile: flagella and pili Opportunistic and nosocomial infections; highly antibiotic resistant Characteristic color and sweet grape like odor Oxidase positive
26
P. aeruginosa: CF
Risk factors: cystic fibrosis - colonized by S. aureus first then with P.aeruginosa by 5 yrs old - lifelong Burkholderia cepacia is also another lung bacteria that affects those with CF These bacteria cause the immune system to cause the damage (indirectly) Most CF patients die from P. aeruginosa lung associated infections (90%) Research very hard because alginate in P. aeruginosa contributes to the biofilm formation Fresh isolates of P. aeruginosa from CF patients are mucoidy, but in vivo and in vitro switching in the mucoidy phenotype via quorum sensing in culture Hospitalized on ventilation- high risk
27
Anaerobes
Aspiration of respiratory or gastric material Risk factors: dental work and loss of consciousness mixture of Bacteroides and Fusobacterium - necrotizing, lung abscesses, empyema (formation of pus in pleural cavity) ***copious amounts of foul smelling sputum
28
Potential Bioterrorism Agents
``` Anthrax Plague Q fever Tularemia Brucellosis ```
29
Bacillus anthracis
Gram positive rods occurring in chains Aerobic, non-motile, forms resistant endospores Spores remain viable for years in soil, dried or processed hides; present in air, water, soil and vegetation Three types: cutaneous, inhalation, and GI Inhalation: capsule (polyglutamic acid capsule (AA)) + anthrax toxin Transmission: inhalation of endospores (spores have no taste or smell) Symptoms: Initial - sore throat, mild fever, myalgia, cough After several days - severe coughing, nausea/vomiting, lethargy, confusion, shock, death
30
Anthrax Toxin
Major virulence factor secreted by B. anthracis Encoded by plasmid pXO1 carrying three toxin genes A/B toxin Three component proteins: Protective antigen (PA) Edema factor (EF) Lethal factor (LF) *these cause tissue damage, edema, and cell death High mortality rate
31
Anthrax Vaccine
Diagnosis: microscopy/Gram stain of sputum Treatment: penicillin, doxycycline, ciprofloxacin Vaccine available for military and researchers decontamination is costly and time consuming
32
Mycobacterium tuberculosis: General Information
Aerobic, acid fast rods, intracellular Cell wall contains mycolic acid, which areresistant to detergents and common antibiotics and provide protection from desiccation Grows very slowly on culture Due to the high lipid content of the cell walls acid-fast bacteria retain the carbolfuchsin and will appear fuchsia
33
TB: Transmission, Symptoms, Risk Factors, and Virulence
Transmission: inhalation Incubation: 4-12 weeks Virulence: cord factor (not a toxin) causing a characteristic serpentine arrangement due to aggregation of the cells Tissue necrosis is due to immune response (indirect) Symptoms: productive cough (sputum may be bloody), mild fever, fatigue, malaise, weight loss, sweating Risk factors: poor nutrition, drug users, alcoholics, crowded living conditions (prisons), immunocompromised Endemic areas: Southeast Asia, Sub-Saharan Africa, Eastern Europe
34
Three types of Tuberculosis
1. Primary tuberculosis – initial case of tuberculosis disease 2. Secondary tuberculosis – reactivated tuberculosis 3. Disseminated tuberculosis – tuberculosis involving multiple systems (poor prognosis)
35
Mechanism of TB
Inhalation of bacteria and then engulfed by alveolar macrophages, but not killed (intracellular) Survive and multiply and attract and activate more macrophages to form tubercle/granulomas to hide from immune system Can remain dormant for years to decades, but immunosuppressed individuals become infected
36
Change in TB Over Time
1. Caseous lesion- cheese-like consistency 2. Ghon complexes -calcified caseous lesion; show up prominently in chest X-rays (in lungs and lymph nodes) 3. Tuberculous cavities- tubercle that has liquefied and formed an air-filled cavity from which bacteria can spread (reactivation and miliary tuberculosis)
37
TB Dx
Screening: tuberculin skin test, Mantoux test, PPD test (same thing just different names) Intradermal injection of purified protein derivative, then check site in 48-72 hours CMI - cell mediated immunity Positive indicates exposure not an active infection, so must get a chest X-ray to look for signs of tubercles Microscopy sputum, acid fast stain, fluorescent auramine stain, Lowenstein-Jensen agar Grows very slowly -6-8 weeks
38
TB Resistant Strains and Tx
MDR-TB: multidrug resistant - resistant to isoniazid and rifampin XDR-TB: extremely drug resistant- resistant to isoniazid, rifampin, and at least one of the 2nd line drugs DOTS: Directly Observed Treatment Short course recommended by the WHO and CDC; ensures patient compliance or jail Treatment: combination therapy of isoniazid and rifampin or ethambutol and pyramindole (RIPE) 6-9 months Potential exposure: isoniazid treatment BCG Vaccine: Bacille Calmette-Guerin Live, attenuated M. bovis not used in the U.S. because screening would not be as cheap as it is now and anyone with suspected TB would need a chest X-ray and other tests
39
Lactobacillus sp.
Facultative or strict anaerobic gram positive rod NF of mouth, stomach, GI track, GU tract Can cause opportunistic infections
40
Bacterial Vaginosis (BV)
1. Discharge – watery /milky adherence to the vaginal wall 2. pH – raised 3. Specific tests – Amine test: KOH + vaginal fluid; fishy odor =“Whiff test”; BV – Positive Amine Test 4. Gram stain results – clue cell; gram variable Clue cell: overgrowth of bacteria present; gram negatives and positives; epithelial cells is covered with growth No itchiness, no painful urination; not a lot of discomfort There are no white cells (PMNs); neutrophils; aka your body is not reacting to it and your immune system isn’t activated Very bad odor and vaginal discharge due to putrescine, cadaverine, trimethylamine (product of bacterial metabolism)
41
BV Causative Agents
Gardnerella vaginalis – most associated Mycoplasmas Anaerobes – Peptostreptococci, Bacteroides spp., and Mobiluncus spp.
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Garnerella vaginalis
``` causative agent of BV Gram-variable bacillus Member of endogenous vaginal flora Major organism associated with BV Culture not really very useful for dxs Seen on gram stain – clue cells Gardnerella has been isolated from sexually inexperienced girls A disturbance of the vaginal microbial ecosystem ```
43
Mycoplasma
causative agent of BV Gram stain: no gram stain because no cell wall Cell membrane characteristic: has sterols Why are these characteristics important: cannot treat it with beta lactams because they target the cell wall, which is does not have Other Members of Species: M. genitalium: non-gonococcal urethritis (NGU) and Pelvic Inflammatory Diseases (PID) Ureaplasma urealyticum: NGU, pyelonephritis, spontaneous abortion M. hominis: Pyelonephritis and postpartum fevers
44
Mobiluncus species
causative agent of BV Obligate anaerobic gram variable curved rod with tapered ends Classified as gram positives: have gram-positive thick cell wall, lack endotoxin, and is susceptible to vancomycin, etc.; doesn't stain well Mobiluncus curtisii Abundant in women with BV Role in pathogenesis vague
45
Streptococcus agalactiae
Gram positive cocci in chains Beta hemolytic; small zone of hemolysis compared to strep pyogenes Lancefield: group B Capsule: polysaccharide and antibody protective Vaginal colonization: causes bladder infections, premature delivery, prolonged membrane rupture, and postpartum fever Transmitted to infants during birth leading to neonatal disease Can cause neonatal meningitis if capsule present
46
Neonatal Disease: Streptococcus agalactiae
``` Early onset (<7 days old): bacteremia, pneumonia, meningitis, severe consequences Late onset (1 week to 3 mos.): bacteremia with meningitis if capsule present ```
47
Vulvovaginal candidiasis (VVC)
Second most common vaginal infection in US primary source - endogenous opportunistic pathogens (when taking antibiotics and normal flora decreases allowing its population to grow) Fungal Species: Candida albicans and Candida spp. Three groups of females 1. never had an episode 2. infrequent, isolated episodes 3. repeated, recurrent, chronic infections 75% of women will have at least one episode some are more prone than others
48
Candida Characteristics
1. Discharge - Cottage cheese appearance, discrete pustulopapular lesions 2. pH – 4.5 3. Specific tests – germ tubes from yeast; grows on Sarbouraud Dextrose agar 4. Gram stain results - positive
49
VVC Symptoms, Dx, and Tx
chief complaint - itching burning sensation when urinating cervix normal erythema, swelling of labia and vulva Dx: microscopic finding - yeast cells, budding hyphae, few PMN’s (neutrophils) laboratory identification **germ tubes for Candida albicans pseudohyphae on cornmeal agar biochemical tests for other species Grows on routine lab media, but to culture would use ***Sabouraud dextrose agar Tx: hard to treat because they are eukaryotic
50
Other Candida Infection Symptoms
``` Esophagitis – HIV/immunocompromised Diaper rash – infants and elderly Thrush – HIV/immunocompromised Nail infections – occupation with hands in water like dishwashers/artificial nails Systemic - immunocompromised ```
51
Trichomoniasis
anaerobic flagellated protozoan: life cycle is simplest for protozoa; binary fission, no cyst stage requires preformed purines, pyrimidines, fatty acids, and sterols Survives on fomites for approx. 30 minutes - needs human host 1. Discharge - frothy yellowish, green; large amount of discharge 2. pH – 4.7 3. Specific tests – wet prep, see protozoan; large number of PMNs; positive whiff test 4. Gram stain - will NOT show up on a gram stain because not bacteria
52
Trichomoniasis: At Risk
At risk: lower socioeconomic populations, multiple sexual partners, previous history of STD, coexistent infection, non-use of barrier or hormonal contraceptives
53
Trichomoniasis: Signs and Symptoms
Vaginitis, urethritis Chief complaint – frothy yellowish, green discharge Strawberry cervix - localized hemorrhages on cervix and vagina (dark spots) Other signs/symptoms: bad odor, vulvar pruritus (itching), dysuria (painful urination) Vaginal soreness, dyspareunia (pain during sex) Males - slight urethral discharge control depends on treating partners: evaluate for other STD’s and evaluate for candidiasis, BV
54
Cervicitis and Urethritis in Females
Cervicitis: most common STD syndrome Often “Silent partner” to male urethritis Inflammation of columnar and subepithelium of endocervix is greatest in adolescent girls so they are very susceptible compared to older women Cervicitis and Urethritis: up to 70% of women are asymptomatic Serves as reservoir Dysuria, vaginal discharge, vaginal pruritus (itching and discharge) Mucopurulent watery discharge Easily induced bleeding of the cervix
55
Neisseria species
Neisseria gonorrhoeae- pathogenic Neisseria meningitides - pathogenic Neisseria species- normal flora and non-pathogenic Gram negative diplococci/ kidney bean shaped Neisseria gonorrhea - have many PMNs Capnophilic- thrive in high CO2 environment Growth on routine media N. gonorroheae- chocolate agar but not blood agar N. meningitidis- both chocolate agar and blood agar All oxidase positive N. gonorrhoeae – glucose only N. meningitidis – glucose + maltose
56
Neisseria Virulence Factors
Pili - attachment to non-cilated epithelial mucosal cells, resist phagocytosis by neutrophils, and antigenic variation to hide from immune system Por protein: PorA- silent in N. gonorrhoeae but on in N. meningitidis PorB- on in both Neisseria gonorrhoeae and meningitidis, must be functionally active, antigenic variation, prevents phagolysosomal fusion Transferrin-binding proteins (also lactoferrin BPs)- acquisition of iron for growth restricting hosts to humans LOS- like LPS, but oligosaccharide (shorter); still has Lipid A portion serving as the endotoxin causing pelvic inflammatory disease IgA protease Beta lactamase
57
Primary Disease in Neisseria and Epidemiology
acute urethritis, proctitis, pharyngitis, ophthalmia neonatorum, acute cervicitis or vulvovaginitis Epidemiology: US higher than most other developing countries Poverty, inner city African-American Multiple sex partners, recent new partner females more affected than males; females = reservoir
58
Neisseria gonorrhea: Characteristics
1. Discharge - mucourulent, creamy yellow discharge 2. Gram stain results – negative in pairs within PMNs 3. Other tests – NA amplification, oxidase positive, and glucose oxidized 4. Signs and symptoms & Complications- Sterility from complications adhere to stratified columnar epithelial cells penetrate to subepithelial connective tissue and multiply severe acute inflammatory response
59
Neisseria gonorrhea in Males vs. Females
Males: from anterior to posterior urethra and Cowper’s glands; fibrosis - urethral strictures; prostatitis, epididymitis; permanent sterility may develop Females: burning and frequency of urination, mucopurulent discharge, fever and abdominal pain from primary foci to fallopian tubes, pelvic peritoneum salpingitis, tubo-ovarian abcesses,PID permanent sterility or ectopic pregnancy may result
60
Disseminated Gonococcal Infection - Gonococcemia
Sometimes the infection gets into the blood and spreads throughout the body about 1% of male or female patients, usually w/ asym. genital infection, septicemia LOS toxicity - chills, fever, malaise, petechial skin lesions Migratory arthralgia, suppurative arthritis of wrists, knees, ankles, pustular rash on erythematous base on extremities but NOT on head/trunk Dx: male urethral exudate - gram stain females - culture and ID other sites males, females - culture and ID
61
Gonococcemia: Culture
inoculate immediately onto appropriate media Thayer Martin, NYC media Transgrow, Jembec Plate does NOT grow on blood agar, only on chocolate atmosphere (enriched CO2) and temperature important Nucleic acid amplification assay: test for Gonorrhoea and Chlamydia both Culture Media: chocolate agar, Thayer-Martin agar, NYC medium Biochemical testing: glucose oxidized
62
Treatment of N. Gonorrhea and Chlamydia
ceftriaxone single dose treat w/doxcycline for co-infection w/Chlamydia neonates - drops at birth required by law 0.5% erythromycin 1% tetracycline or 1% silver nitrate (won’t effect Chlamydia)
63
Chlamydia trachomatis
obligate intracellular bacterium cell wall lacks peptidoglycan life cycle contains elementary bodies, reticulate bodies require source of ATP from host; will not grow on culture Elementary Bodies: Infectious form, cannot replicate, bind to receptors on host cells, metabolically inactive Reticulate Bodies: Metabolically active form, replicating form, non-infectious form
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Types of Chlamydia
Chlamydophila pneumoniae Chlamydophila psittaci Chlamydia trachomatis
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Chlamydia Serovars
A, B, Ba, C – Endemic trachoma- eye infection that can lead to blindness is untreated; discharge B, D-K – Genitourinary disease; discharge L1, L2, L3 – Lymphogranuloma venereum; ulcerative
66
Chlamydia: General Information
Most prevalent STD in US, many are co-infected w/gonorrhea, only source is humans Other infections: pharyngitis, conjunctivitis, PID (pelvic inflammatory disease), perihepatitis 1. Discharge – scant and watery 2. Gram stain results – PMNs with no gram stain 3. Other tests – NA amplification 4. Signs and symptoms: infection asymptomatic initially host develops acute inflammatory response - PMN’s “watery” discharge
67
Urethritis in Men
Most are symptomatic Reiter syndrome: urethritis, conjunctivitis, polyarthritis, mucocutaneous lesions, EB found in specimens with arthritis caused by chlamydia
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Pathogenesis of Chlamydia in Males, Females, and Newborns
males - disseminate into epididymis - epididymitis female - travel up fallopian tubes into peritoneal cavity - salpingitis, PID newborns – mucopurulent conjunctivitis 1-2 wks after delivery; pneumonia, pneumonitis
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Salpingitis and perihepatitis
``` Most serious – salpingitis Range from silent infection to severe Fever, lower abdominal pain, tenderness of uterus, adnexae (structures related to the uterus) Severe inflammatory response caused by chlamydia ```
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Lab Dx: Chlamydia
Fluorescent antibody staining of genital specimens, conjunctival scrapings Culture – most specific and requires tissue culture can do ELISA, genetic probes Nucleic acid amplification test
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Lymphogranuloma venereum
caused by Chlamydia trachomatis (not the same as genital chlamydia); L serovars cause Rare in US, common in developing countries STD, often co-infection Would be in differential for ulcer diseases People who travel out of the country are more likely Dx: cannot gram stain chlamydia so use NAAT, serology Isolation of Chlamydia from infected tissues, secretions
72
STDs: Mucupurulent Discharge vs. Ulcerative
Ulcerative: Granuloma inguinale, Chancroid, Syphilis, LGV (covered with chlamydia) Mucopurulent: Chlamydia, Gonorrhea, Trichomonas
73
Painless vs. Painful
Painless: Syphilis, LGV, granuloma inguinale, Painful: Chancroid, HSV
74
Lymphogranuloma venereum (LGV) Stages
Primary lesion- generally painless papule that ulcerates, non-indurated herpetiform ulcer Secondary stage - acute lymphadenitis with bubo formation (painful), acute hemorrhagic proctitis following rectal intercourse, fever, other symptoms of systemic infection Tertiary stage - rare Development of genital ulcers, fistulas, rectal strictures, genital elephantiasis – result of inflammatory response
75
Klebsiella granulomatis
Disease - Granuloma inguinale aka Donovania granulomatis until recently Causative agent: gram-negative rod Pathognomonic feature: Donovan bodies - vacuole w/i PMN or plasma cell where organism multiplies
76
Donovanosis
Four classic forms of presentation 1. ulcerogranulomatous 2. hypertrophic or verrucous (cauliflower growth) 3. necrotic – foul smelling ulcer 4. sclerotic – formation of fibrous and scar tissue; walled off and thick Firm subcutaneous nodule progresses to beefy-red, granulomatous heaped ulcer, ulcers generally painless multiple lesions form; bleed on contact
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Differential Dx for Granuloma inguinale (Donovania)
Carcinoma - esp. with advanced lesions Syphilis - condylomata lata Large herpetic ulcers Amebiasis
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Haemophilus ducryei
Chancroid: aka soft chancre caused by Haemophilus ducreyi; predominantly male disease; has irregular border Haemophilus ducreyi: gram negative rod with“school of fish” appearance Reservoir: genital tract of humans Culture: requires specific media, requires X factor only Oxidase positive (like gonorrhea and aeruginosa)
79
H. ducryei: Chancroid Pathogenesis
Small erythematous papule, not painful initially Patients seek attention after having ulcers from 3-5 weeks since it is painful at that point Range from 1-4 ulcers typically Very painful, friable ulcer with ragged borders develops Ulcer base may be covered with yellow or grey necrotic purulent exudate Lymphadenopathy from spread to inguinal lymph nodes may rupture, exudates highly contagious
80
Dx and Epidemiology: Chancroid/ H. ducryei
Definite – isolation of H. ducreyi from lesion Probable – clinical findings compatible, negative darkfield, negative syphilis serology, negative HSV culture Epidemiology: Probably underreported, mostly minority populations, African-American, Hispanics, Heterosexuals Female prostitutes and clients
81
Treponema palllidum: Syphilis
Ulcer description: hard chancre, indurated, well circumscribed; painless; regular border spirochete- thin and cannot gram stain so use silver stain or darkfield microscopy (+ = disease) corkscrew type motility with axial filaments Bundles of periplasmic flagella cannot culture on artificial media Lack TCA cycle – need host to survive Sensitive to oxygen
82
Syphilis Transmission
sexual contact - abraded skin or mucous membranes oral, anal sex congenital secondary disease w/latent infection Primary, secondary, tertiary, latent, and neonatal phases
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Primary Phase of Syphilis
Men having sex with other men are at high risk Located at site of inoculation 3 weeks incubation Chancre (hard): painless, indurated, well circumscribed ulcer Regional lymphadenopathy Heal in 1-6 weeks
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Secondary Phase of Syphilis
``` Enter blood from infected foci Flu-like symptoms Disseminated rash few days later Highly infectious Resolves spontaneously within few weeks ``` ``` Rash: Unique – found on soles of feet, palms of hands May be over entire body, in mouth Copper penny macules or papules Resolves on own within a few weeks Patient has then entered latent stage ```
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Secondary Phase of Syphilis Symptoms
Generalized lymphadenopathy (large lymph nodes) Generalized maculopapular rash Condyloma lata - soft, fleshy papules in genital region Moth-eaten alopecia (chunks of hair falls out)
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Latent Phase of Syphilis
3 weeks to 3 mos. after secondary stage Early latent - 1 year duration Can transmit to fetus May last 3 to 30 years
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Tertiary Phase of Syphilis
Waning of immunity - w/i mos. to 50 yrs. later Treponemes invade CNS, CV system, eye, skin, other internal organs Delayed Type Hypersensitivity reaction or reaction to invasive properties At this point the organism is no longer responsible, but the immune system attacks Transmission does not occur Congenital transmission rare
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Neurosyphilis
Destruction of brain parenchyma (paresis) - dementia dorsal roots of spinal cord (tabes) Tabes dorsalis – demyelination of posterior columns of dorsal columns and dorsal roots or both (taboparesis) Meningitis – classic aseptic optic atrophy meningovascular damage Cardiovascular Symptoms: thoracic aortic aneurysm aortitis, aortic endocarditis, on x-ray see ascending aortic calcifications Skin Manifestations: Gummas =destructive, granulomatous, non-progressive lesions treponemes rarely found in the lesions In bones, skin, other tissues
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AIDS and HIV+ patients: Syphilis
higher prevalence of recurrent secondary syphilis | more rapid progression to CNS
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Congenital Syphilis
Sequelae: latent infections, multiorgan malformations, death of fetus Majority: born without clinical evidence, but shows up shortly after birth Early (birth to age 2): Extensive cutaneous lesions, rhinitis or “snuffles”, teeth, bone malformations, anemia, hepatosplenomegaly, CNS disease Late: interstitial keratitis, 8th nerve deafness, notched and spaced incisors (Hutchinsons incisors), “raspberry molars”, sabre shins, saddle nose, cutaneous gummas (granulomas)
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Lab Dx: Syphilis
darkfield microscopy nontreponemal tests - RPR, VDRL treponemal test - FTA-ABS, MHA-TP CSF (acquired and congenital neurosyphilis) -VDRL increased cell count, elevated total protein
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Nontreponemal Tests
They are general screening procedures for syphilis RPR (Rapid Plasma Reagin)/circle card test – positive if agglutination; many other things that can give positives; quick and easy to do and cheap **if positive you would have to confirm them VDRL – Venereal Disease Research Laboratory: slide flocculation test Test for cardiolipin- in mitochondrial membrane because the spirochete will destroy cells IgG or IgM Some false negative False positives: autoimmune diseases; Esp. disem. LE Can use for early syphilis cure following therapy
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Treponemal Tests
for syphilis Utilize as antigen T. pallidum subsp. pallidum Fluorescent or microhemagglutination Measure IgG or IgM Positive – not an indication of active disease because positive test could signify someone who had the disease in the past Cannot use to monitor therapy Specificity 99% False +: AIDS, HIV+, Pregnant females, Narcotic addicts, Lyme disease, Neonate of infected mother
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Treatment/Prevention of Syphilis
``` Penicillin – any stage IM benzathine penicilllin G Some recommend 2 or 3 doses 1 week apart Penicillin allergic – doxycycline or tetracycline reportable, trace contacts ```