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330 Cards in this Set
- Front
- Back
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Treponema pallidum causes
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veneral syphilis
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Treponema pertenue causes
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yaws
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Treponema endemicum causes
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bejel
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treponema carateum causes
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pinta
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Characteristics of disease caused by non-venereal treponemas
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The course of the disease is similar among species: Primary stage that is self limited. Self limited secondary stage that usually represents dissemination. Secondary phase is followed by a latent period, after which there is a tertiary destructive phase that is not self limited.
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Yaws occurs in what areas
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warm humid, africa, samerica, se asia
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Hows is yaws aquired
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skin contact usually in childhood
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Yaws clinical manifestations
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papules that heal spontaneously
secondary phase - more papules, osteitis late phase - cutaneous plaques, GUMMMATOUS lesions, hyperkeratosis of the palms and soles |
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Where does Pinta occur
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Arid regions
Mexico, Central America and Columbia |
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Pinta is aquired via
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skin contact
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Pinta clinical manifestations
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small pruritic erthematous papules on face and neck
2nd phase, pigmentation late phase DEPIGMENTATION on wrists elbows and ankles |
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Where does Bejel occur
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Africa and W. Asia
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Clinical manifestations of Bejel
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oral mucosal lesion
2nd phase - mucous patches, periositis and adenopathy late phase - gummatous lesions |
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how can non-veneral treponamas be diagnosed
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dark-field microscopy
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How is bejel transmittied
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skin contact and sharing and eating drinking utensils
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Louse-Borne disease is caused by?
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Borrelia recurrentis
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Borrelia recurrentis causes epidemics in what cases
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after catastrophic events
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Describe Borrielas antigenicity
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in the blood during febrile periods
hides out in organs during afebrile periods returns antigentically different |
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Clinical manifestations of Borriela
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fevers, chills, headache, myalgia, rash
death from myocarditis intensity of symptoms decreases with each relapse single relapse in louse bourne disease |
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Diagnosis of Borriela
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organism in blood
dark field miroscopy Giemsa/Wright stain |
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Treatment of Borriela
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single dose of tetracycline or erthromycin for louse borne
longer course for tick borne |
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Lyme disease is caused by
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Borrelia burgdorferi
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When is an IgM response seen in lymes
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3-6 weeks
IgG response follows gradually |
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Lyme disease stage 1
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erythema chronicum migrans (ECM)
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Lyme disease stage 2
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disseminated infection
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Lyme disease stage 3
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persistant infection months to yrs after intial infection
may follow a long latent period |
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Lyme disease cutaneous manifestations
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ECM - outer red border, central clearing
days later multiple sites of ECM |
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Musculoskeletal manifestations of Lyme disease
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2 weeks to yrs after infection
joint pain intermittent arthritis can lead to chronic arthritis |
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Neurological manifestations of Lyme disease
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meningeal irritation with ECM, no csf abnormalities, WBC are mostly LYMPHOCYTES
untreated - cranial nerve palsies, meningitis |
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Cardiac manifestations of Lyme disease
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5% of untreated patients have heart block, ekg changes
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Lyme disease diagnostic tests
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Western blot is used for confirmation. 3 bands for IgM, numerous bands for IgG.
PCR important for meningitis and arthritis- send CSF or synovial fluid for PCR C6 antibody measures immune response. Specific and sensitive |
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Transmission of Leptospira occurs via
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water or soil contaminated with animal urine
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Leptospira pathophysiology (effects 4 organs)
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heptaocellular damage - jaundice
renal failure meningitis chronic uveitis Liver and kidney involvement with fever- think leptospirosis |
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Milder form of leptospira
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Anicteric
fever headache SEVERE muscle pain clinical signs of meningitis. |
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Worse form of leptospira
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Icteric form (weils disease)
impaired renal and hepatic function hemmorrhage, shock |
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Leptospira treatment
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IV penicillin, ampicillin in ill patients
oral in others |
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Which organisms are spirochetes?
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Borrelia, Leptospira, and Treponema
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What are the three stages of Lyme dz?
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1: erythema chronicum migrans and flu sx, 2: neurologic and cardiac manifestations, 3: autoimmune migratory polyarthritis
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Signs and symptoms of Lyme disease
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1. Bell's palsy (and other CNS manifestations in Stage 2)
2. Arthritis (Autoimmune migratory in Stage 3) 3. Kardiac block (Stage 2) 4. Erythema chronicum migrans (Stage 1) |
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What part of the GI tract are anaerobes more prominent
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distal illeum and colon
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How is the enviorment for an anaerobic infection created
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tissue destruction and necrosis leads to low oxygen tension
Anaerobic infection usually occurs due to a secondary invasion from normal anaerobic flora |
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A breach in the colon will lead to
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intrabdominal sepsis, very common cause for anaerobic infection
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Two most common organisms in an intraabdominal absess
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Bacteroides fragilis and E Coli
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What are the two stages to intraabdominal abcess formation
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1 - E.Coli sepsis
2 - B. Fragilis abscess |
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Common site in head/neck for anaerobic organisms
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gingival sulcus
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Predominant organisms in head/neck
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anaerobic streptococci, prevotella, fusobacterium
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What is ludwigs angina
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infection of the floor of the mouth
Ludwig’s Angina is an infection of the submandibular space (consisting of sublingual and submylohyoid spaces as well). Predisposing factors include odontogenic infection (70-85%), trauma, mandibular fracture, foreign bodies, and neoplasm. This is usually a polymicrobial infection of oral aerobes, anaerobes, and occasionally S. aureus. Notice the swollen submandibular space in slide 20. The flowing are clinical features of this infection: • Mouth pain, drooling, dysphagia, respiratory distress, “hot potato” voice • Edema of the floor of the mouth with swelling and displacement of the tongue posteriorly and superiorly • Woody, tender swelling in suprahyoid region of the neck |
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What is aspiration pneumonia
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aspiration of oral pharyngeal bacteria and the development of a pneumonia
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Describe the sputum in aspiration pneumonia
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foul smelling
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Most common predisposition to aspiration pneumonia and why
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alcohol
suppresses cough and gets cillia drunk also anesthesia, poor oral hygiene, drug overdose, gingival disease patients w/o teeth are not likely to get aspiration pneumonioa |
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Why arent sputum samples for asp. pneumonia reliable
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mouth is full of anaerobes
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Aspiration pneumonia is a common precursor for....
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lung abscesses
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lung abscesses are a common precursor for
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brain abscesses
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brain abscesses symptoms
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subacute
fever, headache altered sensorium, focal neurologic deficits papilledema |
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Why is lumbar puncture contraindicated in patients with brain abscesses
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risk for herniation
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Why are diabetics at risk for anaerobic infections (3)
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decreased blood flow
decreased sensation high glucose decreases wbc activity |
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Hallmark of anaerobic soft tissue infection is...
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the presence of gas in tissue
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When can aerobic gram negatives produce gas?
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when there is high glucose concentrations
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Gas gangrene is cause by what organism
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C. Perfringens when there is traumatic GI injury
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Infection with this organism causes non-traumatic gas gangrene and is associated with colonic carcinoma
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C. septicum
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C perfringens causes this via enterotoxin
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food poisoning
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Toxins released by C. difficile
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toxin A which increases fluid secretion
cytotoxin b which destroys cytoskeleton |
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Three forms of botulism
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Food borne
infant - honey ingestion wound - iv drug use |
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C. difficile causes what when normal flora is destroyed
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psuedomebranous colitis
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psuedomebranous colitis treated with?
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vancomycin and metronidazle
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Leading Killer of HIV+ individuals and Women worldwide
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TB
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Mycobacterium morphology
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aerobic, non-spore forming, non-motile, acid fast (long chain mycolic acids)
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3 myobacteriums that can cause TB
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M. tuberculosis
M africanum M. Bovis |
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tb transmission
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inhalation of droplet nuclei
TB is essentially always transmitted by someone |
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amount of exposure for tb tranmissions
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prolonged >4hrs
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1st 8 weeks pathogenesis
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inhalation
macrophage ingestion local focus (ghon focus) lymphatic spread to hilar nodes hematogenous dissemination dev of cell mediated hypersen descruction of macrophage killing of mycobacteria caseous necrosis |
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Primary TB is mostly seen in
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HIV + children
Primary TB in kids. Latent reactivation TB in adults. |
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limitations to tuberculin skin test
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not sensitive and not specific
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Can TB patient without active infection spread TB
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no
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TB cxr
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apical or posterior segments of upper lobe, superior segments of lower lobe
unusual appearance in HIV |
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two acid fast stains
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Ziehl-Neelsen
Kinyoun (does not require heating) need 10^4 organisms |
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time for TB growth in liquid media
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5days-2weeks
solid is 3-6 weeks |
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MDR Tb implies resistance to what drugs
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INH, Rifampin
associated with HIV+ use 4-5 drugs, always use an aminoglycoside |
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What is immune reconstitution inflammatory syndrome
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seen in TB/HIV patients when they begin HIV treatment
fever, lymph node swelling maybe due to improved immune function and exaggerated host response |
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drug used for preventative therapy and latent TB
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isoniazid
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What does a positive PPD indicate?
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1. Current infection
2. Past exposure 3. BCG vaccination |
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What does a negative PPD indicate?
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1. No infection
2. Anergy (due to: steroids, immunocompromise, malnutrition), inject candida/mumps vaccine into other arm. If still negative, anergic. |
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Mechanism of asymptomatic primary TB
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1. Cell-mediated defense walls off foci of bacteria in caseous granulomas
2. Granulomas heal with fibrosis, calcification and scar formation |
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Mechanism of symptomatic primary TB
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1. Large caseous granulomas develop in the lungs/other organs.
2. In the lungs, caseous material liquifies, is extruded out the bronchi and leaves cavitary lesions behind. |
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Mechanism of secondary Pulmonary TB
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1. Infection occurs at apical areas of lung around the clavicles due to highest oxygen tension caused by decreased pulmonary circulation.
2. Infected areas grow, caseate, liquify and cavitate. |
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TB reactivation sites
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1. Pulmonary (Lung parenchyma)
2. Pleura 3. Pericardium 4. Scrofula (Cervical lymph nodes: most common extrapulmonary site worldwide) 5. Kidney (Sterile pyuria) 6. Thoracic and lumbar spine (Pott's disease) 7. Chronic monoarthritis 8. CNS (subacute meningitis or parenchymal tuberculoma) 9. Miliary TB (Millet sized tubercles all over the body) |
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Tuberculosis rule of 5s
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1. Droplet nuclei are 5 micrometers and contain 5 mycobacteria
2. 5% risk of reactivation in first 2 years and then 5% lifetime risk 3. Patients with HIV ("High five") have 5+5% yearly reactivation risk. 4. Induration measurements a. HIV: >5 mm b. High risk: >5+5 mm c. Everyone else: >5+5+5 mm |
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Cause of Miliary tuberculosis
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Severe bacteremia
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NTM live in?
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water/soil
There is no evidence of human-human transmission, so infected people have no need for special infection control precautions or isolation |
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M. Avium common in
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COPD men
old women CF patients hot tub lung aids |
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Manifestations of MAC in females
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slowly progressive
low grade symptoms cough, weight loss |
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what is hot tub lung
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inflammatory response to MAC
patients are young and immunocompetent |
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tx of MAC
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12 months
many drugs don't always have to treat weight impact of disease and likelihood of cure |
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All patients w/ >50 CD4 cells should be placed on MAC prophylaxis
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M. Kansasii
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similar to tb
common in midwest/south pulmonary and disseminated |
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NTM lymphadenitis
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mostly in children
MAC most common cause M. scrofulaceum next common |
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NTM lymphadenitis tx
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remove node
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associated with water and fish, 1-2 month incubation followed by granulomatous hand lesion
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M. marinum
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3 rapid growers
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M. fortuitum M abscessus, M. chelonae
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Rapid growers cause
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skin/soft tissue infection
pulmonary abscessus>fortuitum indolent, progressive, mild systemic symptoms |
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healthcare outbreaks of mycobacteria mostly due to which 2
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fortuitum and abscessus
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footbaths at a nail saloon and ear piercings think
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M. Fortuitum furunculosis
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most difficult rapid grower to cure
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M. abscessus
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Characterization and reservoir of Mycobacterium Leprae
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Mycobacterium Leprae
1. Acid fast bacillus 2. Likes cool temperatures 3. Infects skin and superficial nerves 4. Cannot be grown invitro 5. Reservoir: Armadillos |
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Presentation of lepromatous leprosy
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"Leonine facies"
1. Loss of eyebrows 2. Nasal collapse 3. Lumpy earlobe |
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2 forms of leprosy
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1. Lepromatous (Due to failed cell-mediated immunity. Lep. is Lethal)
2. Tuberculoid (self=limiting) |
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Treatment for leprosy
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Long-term oral dapsone
Alternative: Rifampin, clofazimine, and dapsone |
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List of spirochetes
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1. Borrelia (Big!)
2. Leptospira 3. Treponema |
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Visualization of Borrelia
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Light microscopy with choice of aniline dye:
1. Wright's stain 2. Giemsa's stain |
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Signs and symptoms of Lyme disease
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1. Bell's palsy (and other CNS manifestations in Stage 2)
2. Arthritis (Autoimmune migratory in Stage 3) 3. Kardiac block (Stage 2) 4. Erythema chronicum migrans (Stage 1) |
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What is an ectoparasite?
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Its a parasite that lives on the skin. Does not cause serious disease
Elicits strong immune response |
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scabies transmission
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person to person or inanimate object, sexually
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scabies type of hypersensitivity reaction
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Method: The female burrows her self into the skin, lays eggs and when they hatch, it caused a Type IV delayed type hypersensitivity reaction.
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groups of people effected by scabies
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are infants, homeless people or those that live in crowded places
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Symptoms of Scabies
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you get a pruitic, inflamed response that can last 3-4 weeks. This is cell-mediated so
there is no histamine involved. But if you get another exposure, the symptoms are quick to come back because we have been sensitized to it. And you get these “wiggely” burrows usually on the hands, between the hands and feet. |
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How do you treat scabies
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• You need to treat twice, a week later. The reason is because the cream kills the adult bugs
but not the eggs. So after a week, the eggs will hatch and that’s when you have to apply the cream again, a week later |
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Two variants of scabies
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Norweigan - immunocomprimised, uncontrolled replication in the skin. There can be literally thousands of these mites on the skin and it can get hypertrophic. It can be so bad that they will be falling off
nodular - nodules form |
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What are Pediculoses?
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Lice
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Pediculus humanus capitis is?
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head lice
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head lice transmission
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person to person
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clinical manifestation of head lice
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hypersentivity, itching due to saliva, sleep disturbances
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treatment of head lice, cream or shampoo
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cream, also dry clothes on hot
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What is Pediculus humanus corpis
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body lice
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what is Pediculus humanus corpis a vector for
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typhus and relapsing fever
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Cimex lectularius is?
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the common bed bug
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bed bugs are attracted to?
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heat and carbon dioxide.
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how does a bed bug bite appear
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linear or clusters of bites. Some can become hemorrhagic clusters
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What causes Tungiasis
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a very small flea also called a Jigger
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Where is Tungiasis found and what parts of the body does it affect
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. They are found in sandy areas and again affect mostly the feet since fleas dont fly. It is endemic in African and mostly on the beaches.
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• Travelers get it
• Sandy regions • Feet think |
Tungiasis
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Tungiasis clinical manifiestation
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Usually it causes a papule or vesicle with a central black dot. This dot is the rear part of the female flea. The pregnant flea grows and an inflammatory response results. It can be painful and itchy and between 2-21 days later, she will excrude. Eventually she will die and you can use a sterile needle to extract here. But be careful because you can get a secondary infection with this method.
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Myiasis is
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maggots in the skin
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common with a boil forming that usually doesn’t heal. It occurs in the subcutaneous skin layer and sometimes you can feel the larvae wiggling around.
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furuncular
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what do the larva need to grow
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O2
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How does one get maggots
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Maggots can infest the skin and mainly the mucus membranes on the body. They are found in the tropics in two different types of flys. For some reason they are found in Belize in high numbers.
- The first type is the Tumbu fly found in Southern Africa. It lays eggs on damp clothing and then when you wear the damp clothes, the eggs hatch and larva can burrow into your skin. - The second type is the Botfly which is found mostly in South America. This is interesting because it will capture a mosquito in midair, lay its eggs on the abdomen of the mosquito and then the maggot will get delivered to the human skin during a mosquito bite. Craziness. |
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Characteristics of Rickettisia/Ehrlichia/Coxiella
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intracellular (except Coxiella)
fastidious gram neg pleomorphic coccobacilli zoonoses |
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Rickettisia infects
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endothelial cells
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Ehrlirichia infects
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WBC
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Coxiella infects
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macrophages
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The hallmark is infection of endothelial cells by Rickettisia causes
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vasculitis
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Responsible for Q fever
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Coxiella
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How can coxiella survive outside host
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spore forming
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What are morulae
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intracytoplasmic clumps of bacteria formed by Ehrlichia and Anaplasma
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Rocky Mountain Spotted Fever (RMSF) caused by?
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▫ R. rickettsii
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▫ R. prowazekii causes
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epidemic or louse-borne typhus
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▫ R. typhi causes
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endemic or murine typhus
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Natural history of Rickettsial Infections
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grace period (up to 2days)
eschar (presymptomatic) bacteremia (symptomatic) immune response (4wks) |
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Tick causing RMSF
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Dermacentor spp dog tick (only adult)
Summer months ticks are not painful, so it goes undetected |
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RMSF location in US
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southeast
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RMSF targets the vascular endothelial cells by attaching via
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Outer Membrane Protein A (OmpA).
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RMSF clinical manifestations
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DIC leading to thrombocytopenia
fever, headache, rash |
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describe RMSF rash
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begins peripherally and moves centrally
rash can become petechial due to coagulopathy, or hemmoragic Eschar is usually NOT seen at site of tick bite. |
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RMSF lab findings
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leucopenia, thrombocytopenia
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▫ Higher risk groups for RMSF includes?
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black males with G6PD deficiency, elderly, and chronic alcoholism.
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RMSF multiple organ manifestations
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eyes, gi, liver, spleen, brain, lungs
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Fièvre Boutonneuse or also known as “Mediterranean Spotted Fever”, “Kenya tick typhus” and “Israeli typhus.” It is typically found in Africa, Mediterranean and Middle East. Think
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• R. conorii
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African Tick Bite Fever and is found in Southern Africa.
• The typical onset includes fever, myalgias & headache. “Tache noire” (or black spot) is very common at tick bite, which is an eschar with surrounding erythema +/- regional lymphadenopathy. |
R. Africae
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Rickettsialpox • It is transmitted to humans by mites, and bites are usually painless.
• The population affected usually includes the homeless in urban areas. • There is an eschar at mite bite that appears before systemic symptoms. It is followed by abrupt onset of fever, chills & headache, then generalized vesiculopapular rash (instead of pettichae). • Complications and death are rare. |
R. akari
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• This is transmitted person to person via body louse (vector), Pediculus humanus.
• Humans are the most common reservoir, but this is also found less commonly in the flying squirrel (eastern USA). **Know this animal, it is an exam question! |
R. prowazekii, Typhus group
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R. prowazekii clinical manifestation
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prolonged fever and fatigue
Fever usually lasts 2 weeks, but it can take 2-3 months to regain strength |
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Describe the rash in louse borne typhus (R. prowazekki)
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starting centrally in the axillae/truncal (spares face, palms, soles) and spreads peripherally to the extremities. There is no eschar, and the rash becomes petechial over time.
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Brill-Zinsser Disease
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• R. prowazekii can establish latent infection, especially in people that were in concentration camps during WWII. These individuals can relapse and have a reappearance of symptoms after many years or decades later, especially with waning immunity or immunosuppression
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Endemic Murine typhus causes by
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R. typhi
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R. typhi transmission
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from rats to fleas
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Where is R. Typhi endemic in the US
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Southern California and Texas (summer/early fall) because cats and opossums are also reservoirs in these areas. Otherwise, this is a disease of travelers
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. In Poland, they made a vaccine for R. Typhi with _____ to vaccinate people with the killed organism so that they would have a positive test. Then the soldiers wouldn’t set up camp in the community
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Proteus vulgaris
felix weil agglutinatiion |
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Orienta tsutsugamushi causes
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scrub typhus
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vector for scrub typhus
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chigger (mite)
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Scrub typhus clinical features
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fever, myalgia, and headache.
regional lymphadenopathy, eschar truncal rash rare cns symptoms (deafness, delerium) symptoms resolve spontaneously |
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What does Coxiella survive intracellularly
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it likes acidic pH so it survives phagolysosome fusion
only takes 1 organism to cause disease |
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Coxiella transmission to humans
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inhalation of aerosol or contact with placenta of infected animals
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Acute manifestions of Coxiella
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▫ The acute is a self-limited febrile illness (<2 weeks) with an atypical pneumonia that shows diffuse infiltrates on a chest xray and a nonproductive cough. It can also infect the liver, causing hepatitis. Rarely, it can cause encephalitis, aseptic meningitis, and pericarditis
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Chronic manifestations of Coxiella
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▫ The chronic (>6 months) infection is more troublesome. The main manifestations include endocarditis with negative blood cultures and subacute presentation, as well as osteomyelitis. This is more common in the immunocompromised
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Three species of Ehrlichioses that cause most disease
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Ehrlichia chaffeensis, Anaplasma phagocytophilum and Ehrlichia ewingii
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peak months for EHRLICHIOSES
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summer
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HUMAN MONOCYTIC EHRLICHIOSIS
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▫ This is due to E. chaffeensis, which invades monocytes. The white-tailed deer are the normal reservoir for this infection, and humans are generally infected incidentally. This is transmitted by ticks, specifically Amblyomma americanum (Lone Star tick). It is mainly in south-central, southeastern and the mid-Atlantic states.
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HUMAN GRANULOCYTIC ANAPLASMOSIS
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▫ The causative organism is the A. phagocytophilum group. Rodents and small mammals are the main reservoir. This is transmitted by the Ixodes spp. tick (Prof’s memory trick = anaplasmosis is transmitted by the one that does not start with an A). Ixodes may also carry Lyme and Babesia.
▫ The distribution is in the US, Europe and Asia. In the US, it is found in northeastern & mid-Atlantic, upper Midwest, and Pacific Northwest areas. |
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RMSF vector
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dog tick
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RMSF type of rash
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periphery to central
maculapapular |
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R. Prowazekii vector and resovior
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louse borne
humans and squirils |
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R Typhii vector and res
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fleas from rats
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R. Prowazekii rash
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central to periphery
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R. Typhi rash
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distritubted equally,
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O tstsugamushi vector
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mite/chigger
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E. chaffeensis vector
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Amblyomma americanum lone star tick
monoctyes |
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Human Granuloctyic anaplasmosis vector
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Ixodes tick (doesnt begin with A)
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Norcardia is acquired via
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inhalation
cutaneous inoculation |
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Norcardia structure
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strict aerobic bacilli with branched filaments
aerobic gram + slightly acid fast catalase + |
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Norcardia occurs in what type of patients
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leukemia
solid organ transplant corticosteroids AIDS |
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Norcardia disease manifestations
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pulmonary disease
central nervous system infection skin infections ocular infections |
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Norcardia pulmonary disease presents most commonly as?
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In general, Nocardia Asteroides give most lung infections in the form of pneumonia (lobar); could also have cavities and nodules
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seen in 1/3 of patients with norcardia...
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single or multiple brain abscesses chronic meningitis
but it is most common to start in the lungs through inhalation and then disseminate |
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gram + branching organism think...
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Norcardia
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Norcardia cutaneous manifestations
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mycetoma
lymphocutaneous-subcutaneous abscess cellulitis hematogenous spread |
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ACTINOMYCES colonizes...
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upper respiratory tract
gastrointestinal tract female genital tract |
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When can actinomyces lead to disease?
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if the mucosal barrier is disrupted
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How does actinomycosis differ from norcardia in terms of morphology
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isnt beaded, still gram +
its a facultative anaerobe its not acid fast |
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Actinomycosis clinical manifestions
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cervicofacial
abdominal pelvic central nervous system |
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She emphasized that Actinomycosis can move through ANY TISSUE (helps for rapid diagnosis)
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Actinomycosis Diagnosis
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sulfur granules
thin, gram-positive branching bacilli fastidious and grows slowly under anaerobic conditions may take >2 weeks for culture growth “molar” colony appearance on agar |
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molar tooth colonies (This is apparently classic for Actinomyces)
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Describe Actinomyces pathology
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characterized by multiple abscesses connected by sinus tracts with macroscopic sulfur granules
suppurative areas are surrounded by fibrosing granulation, causing hard or woody induration Actinomyces, if it invades, creates multiple abscesses by tunneling through most tissues. These abscesses are often connected by sinus tracts and are often filled with sulfur granules. some woody indurations from fibrosing granulation (swelling is very firm; like wood) |
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What is the main risk factor for enteric infections?
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Lack of access to clean water
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Hemolytic-remic syndrome caused by
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Shiga toxin
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Guillen Barre caused by
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Campylobacter
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group A blood type more suspectible to
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Giaradia
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Group O blood type more suseptible to
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Cholera
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Diarrhea daycare organisms
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rotovirus, norovirus
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hospital diarrhea organisms
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C. Difficile
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linked to environmental or social disasters
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Vibrio cholerae
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mechanism of enterotoxin
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Here, the toxin has a direct effect on intestinal mucosa via increased secretion of ions into the lumen: electrolytes are pushed out into the lumen followed by water. You get a watery diarrhea. The classic one for this is cholera toxin
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Mechanism of cytotoxin
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Cause cell death. We see mucosal destruction.
bloody diarrhea |
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What are neurotoxins
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You actually don’t have an infection in your GI system, but you ingest the food toxins and this leads to an acute disease. These are preformed toxins (food toxins) which act on our autonomic nervous system. The big ones to remember are Staph aureus, B. cereus, and C. botulinum.
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Cruise ship outbreak of watery diarrhea is always a question on exams. Answer is always
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Norovirus
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Major worldwide cause of infant morbidity & mortality
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Rotavirus
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Virbrio morphology
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Curved, Gram Negative Rod
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is profuse, intense, seriously watery diarrhea with little rice grains floating in it. This is called rice water stool.
Hallmark symtomps for what organisms |
Vibrio Cholera
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Diarrhea illness Acquired from raw/undercooked shellfish
Gulf coast |
Vibrio Parahemolyticus
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Main cause of travelers diarrhea
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Enterotoxigenic E. coli
watery diarrhea |
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Two main toxins in ETEC
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heat labile - similar to AB increases camp
heat stabile- increases cGMP both lead to increases in ion secretion |
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Species causing Shigellosis
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S. dysenteriae (worst), S. flexneri, S. boydii, S. sonnei
No flagella, so no H antigen Have O antigen |
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Mechanism of Shiga toxin
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Enters cells via receptor-mediated endocytosis
Binds 60S ribosome: inhibits protein synthesis Cytotoxin S. dysenteriae only |
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Shiga toxin complications
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hemolytic-uremic syndrome (HUS), febrile seizures, reactive arthritis
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Two major pathogens of campylobacter
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C. jejuni: reservoir = poultry
Grows at 42oC Enterocolitis: watery, bloody, foul-smelling diarrhea All ages affected; normal hosts Usually self-limited illness C. fetus: reservoir = cattle, sheep Grows at 25oC Systemic disease: bacteremia, meningitis, abscesses Gastroenteritis less common May be fatal in immunocompromised |
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What strain of Ecoli produces shiga toxin
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O157:H7
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Shiga toxin producing E. Coli found in
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Ground beef, salami, spinach, apple cider, yogurt
Municipal water, swimming pools |
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STEC complications
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HUS, renal failure
DONT GIVE ANTIBIOTICS |
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Exotic pet and diarrhea could be
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Salmonella
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Who is at risk for NTS enterocolitis
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At risk: neonates, elderly, lymphoreticular disorders & AIDS
Invasive disease due to NTS is emerging problem in HIV/AIDS |
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Why is a gallstone a complication in NTS enterocolitis
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may produce a chronic carrier state
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organisms causing enteric fever
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Salmonella enterica serovar Typhi & Paratyphi
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Hallmark of enteric fever
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prolonged fever and bacteremia
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clinical features of typhoid fever
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Rose spots "salmon colored" maculopapular rash
get constipation instead of diarrhea |
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typhoid fever course
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Intestinal perforation or hemorrhage
Endocarditis, pericarditis Splenic or liver abscess diagnosis made with bone marrow |
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gold standard for diagnosing enteric infection
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stool culture
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two agars used for stool culture
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Mackonkey, Hektoen
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Always remember to not give antibiotics for O157:H7
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What supplements can children take to prevent malnutrition
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Vitamin A and zinc
also breastfeed for 6months |
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Cryptococcus neoformans mold or yeast?
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yeast
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coenocytic means
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multinucleated w/o partitions
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examples of dimorphic fungi
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Blastomyces dermatitidis
Coccidioides immitis Histoplasma capsulatum Paracoccidioides brasiliensis Sporothrix schenckii BCHPS |
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Example of a fungi that may produce a capsular polysaccharide that may enhance virulence and escape host defenses
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Crytococcus Neoformans
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2 common fungal stains for cell wall
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PAS (periodic acid shift stain) which stains fungi a bright pink.
Methenamine silver stain which stains the cell wall black. |
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Primary pathogenic fungi
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Blastomyces dermatitidis
Coccidioides immitis Histoplasma capsulatum Sporothrix schenckii |
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Oppurtunistic fungi
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Aspergillus species
Candida species Pneumocystis jirovecii |
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Organisms that infect people with defective neutriphils
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Candida
Aspergillus Mucor CAM! neutrophils |
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Stain used to visualize Cryptococcus neoformans capsule
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india ink
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apotheosis
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the elevation or exaltation of a person to the rank of a god.
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Malassezia furfur agar must be supplemented with...
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olive oil
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- 3 main causative agents of cutaneous mycoses
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1) Microsporum , 2) Trichophyton, 3) Epidermorphyton
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LYMPHOCUTANEOUS SPOROTRICHOSIS is cause by?
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Sporothrix schenckii
clinical manifestation: nodule at site of entry ulcerates and form other nodules along lymphatic drainage channels |
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Fonsecaea or Cladosporium fungi cause?
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CHROMOBLASTOMYCOSIS
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Pseudallescheria boydii and Madurella grisea fungi cause
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EUMYCOTIC MYCETOMA
purulent drainage from sinus tracts |
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The characteristic finding of a mycetoma is a?
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sulfur granule
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Primary fungal pathogens portal of entry
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inhalation
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Blastomyces dermatitidis pathology
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pathology: broad base budding yeast (8-16 m) within microabscesses and granulomas
slowly blast out buds cutaneous, skin and prostate in men It is characterized by delayed separation between the daughter and parent cell |
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What type of stain reveals Blastomyces dermatitidis in prostate
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Papanicolaou stain
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Coccidioides immitis dissemenates to
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CNS
Bone Skin CBS |
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Coccidioides immitis has a predispotion for these individuals
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pregnant womens
AIDS dark skinned individuals |
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Coccidioides immitis pathology
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endospores within a spherules
seen in pyogenic and granulomatous reaction |
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What form of COCCIDIOIDOMYCOSIS can infect lab workers
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the mold form since this is the form growing at ambient temperatures.
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This organism is found in soil contaminated by bird or bat excreta, primary lung infection may be symptomatic in 5%
lung lesion heals with calcification and fibrosis |
Histoplasma capsulatum
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Histoplasma capsulatum has a predisposition for what patients?
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aids
chronic corticosteroid therapy |
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Histoplasma capsulatum pathology
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This is a very small yeast that can be phagocytosed and ingested by monocytes, histiocytes, and neutrophils. It causes a chronic granulmatous reaction with lymphocytes, monocytes, and macrophages.
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Macroconidias are characteristic of Histoplasma capsulatum. It has a trabeculated spore. There are tiny little spores around a main macroconidia
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ulcerations along the gingival are pretty unique
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Histoplasma capsulatum
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Paracoccidioides brasiliensis pathology
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mariners wheel, exists in nature as a mold
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Paracoccidiodes disseminates to
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disseminates to mucus membranes, GI tract and skin
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What is unique about chronic mucocutaneous candidiasis
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it is caused by T-cell defects or endocrine deficinencies
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predispositions for candidiasis
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neutropenia (ANC<500)
defective neutrophils (CGD) broad-spectrum antibiotics indwelling intravenous catheters |
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CANDIDIASIS culture test
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germ tube test: C. albicans yeasts form hyphal outgrowths during 2-3 h incubation in serum at 37oC
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3 disease manifestations of Aspergillus
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allergic bronchopulmonary aspergillosis: asthma, central bronchiectasis, immediate skin hypersensitivity to Aspergillus antigens, Aspergillus precipitins
aspergilloma: fungus ball in old lung cavity which may cause severe hemoptysis invasive aspergillosis: lungs, sinuses and systemic infection causing infarctions (eyes, CNS, skin, bone |
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Aspergillus pathology
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acute angle branching
likes blood vesses --- thrombosis halo sign - wedge shaped infarction |
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Zygomycosis predispostions
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poorly controlled diabetes with acidosis, trauma and burns which have removed the primary barrier of skin, neutropenic patients, and patients on chelating therapy like deferoxamine therapy which takes up iron.
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Zygomycosis presents as this in patients with poorly controlled diabetes
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Rhinocerebral infection
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How does zygomycosis present in neutropenic patients
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pneumonia
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how does zygomycosis look in culture
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you see broad, fat non-septated hyphae.
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The patients may have an eschar or a black appearing lesion in their hard palate. This is characteristic of...
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a spreading rhinocerebral infection in zygomycosis
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Zygomycosis branching
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right angles
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Cryptococcus neoformans is found in
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pigeon shit
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predispositions for Cryptococcus neoformans
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AIDS, prolonged steroid therapy, and lymphoma
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Where does Cryptococcus neoformans like to go in the brain
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It likes ganglia that are rich in dopamine
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Cryptococcus neoformans brain complication
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. It is often complicated by hydrocephalus or water in the ventricles. The polysaccharide in the organism prevents water from being reabsorbed and returning to the bloodstream.
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Why can't Pneumocystis jirovecii be treated with antifungal medication
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It does not have ergosterol in its cell wall.
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The main predisposition to PJP is
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AIDs and transplant patients
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how is PJP acquired
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it is most likely inhaled early in life. It lies dormant until the patient becomes immunocomprimised
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How would PJP appear on X-ray
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On a chest X-ray with mild disease, you would see a fine lacy appearing marking, suggesting interstitium involvement. Over time or severity of the disease, you can see a more remarkable infiltrate, sometimes called a butterfly distribution in the lungs.
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The main predisposition to PJP is
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AIDs and transplant patients
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how is PJP acquired
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it is most likely inhaled early in life. It lies dormant until the patient becomes immunocomprimised
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How would PJP appear on X-ray
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On a chest X-ray with mild disease, you would see a fine lacy appearing marking, suggesting interstitium involvement. Over time or severity of the disease, you can see a more remarkable infiltrate, sometimes called a butterfly distribution in the lungs.
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Trichuris trichiura
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only STH where adults live in colon
Rectal prolapse Dysentary Colitis football shaped eggs amipathic pore-forming proteins |
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Ascaris lumbricoides life cycle
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ingest eggs
larve go to liver, lungs, cough and swallow, adults mature in intestine |
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Why can Ascaris lumbricoides be found in urban environments as well as rural ones?
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The eggs have a ascaroside capsule
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Ascaris lumbricoides lung manifestations
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Loefflers pneumonitis which is eosinophila inflitrates
Asthma like symptoms |
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Why is Ascaris lumbricoides a major cause of surgical abdomen
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worms result in intestinal obstruction and hepatobiliary ascariasis
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Toxocara canis life cycle
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Eggs from dogs are taken up by children in a playground. Larvae penetrate small intestine and are delivered to all tissues.
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Toxocara canis clinical manifestations
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Visceral larva migrans
- larva are lost so they go all over - high IGs, eosinophilia, lung, liver, cns Ocular larva migrans - strabismus Covert toxocariasis The larva basically wander aimlessly then die |
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Necator Americanus (Hookwork) lifecycle
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larve penetrate skin
enter lungs, coughed up adults mature in small intestine |
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Necator Americanus manifestations 4
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1) Iron deficiency anemia
2) protein malnutrition 3) impaired cognition 4) extreme fatigue |
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What organism that usually infects cats and dogs, can infect humaneous causing Cutaenous Larva migrans "creeping eruption"
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Ancylostoma Braziliense
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Enterobius vermicularis life cycle
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ingest eggs
larvae hatch in SI adults migrate to colon |
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Where does Enterobius vermicularis lay its eggs
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on the perinium
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Enterobius vermicularis clinical manifestations
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pruritus ani, especially at night
if they enter the female urogenital tract may cause vulvovaginitis, anoxerixa, irritability, abdominal pain |
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Enterobius vermicularis diagnostic
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apply tape to perineal area to look for eggs
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Trichuris location
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tropics
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Ascaris location
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urban and rural
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Toxocara location
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US, Europe, peurto rican populations in NE
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Necator americanus location
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africa asia, tropics
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Strongyloides stercoralis life cycle
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larvae pentrate skin
to lungs, cough, swallow mature in SI larvae pass out feces or reinfect |
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Strongyloides stercoralis location
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tropics, subtropics, appalacia
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What type of patients are prone to Strongyloides stercoralis hyperinfection
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patients that are on steroids
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Trichenella Spiralis life cycle
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ingest undercooked meat w/ larvae
mature to adults in SI release larvae the pentrate SI encyst in muscles |
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Trichenella Spiralis clinical manifestations
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intestinal phase
muscle phase (pain) can invade heart muscle, CPK, LDH elevated |
