Morphology of this viral illness is described as follows: - multinucleated syncitia with large, pink-to-purple intranuclear inclusions (Cowdry type A bodies) - several disease entities: gingivostomatitis, genital infection, temporal lobe encephalitis, epithelial keratitis, stromal keratitis, disseminated disease (esophagitis, hepatitis, Kaposi varicelliform eruption, bronchopneumonia, eczema herpeticum, etc.)

Herpes simplex virus (HSV) HSV is the can be an infectious agent of: - gingivostomatitis (HSV-1) - genital herpes (HSV-2) - temporal lobe encephalitis - herpes epithelial keratitis & herpes stromal keratitis - disseminated herpes disease (esophagitis, hepatitis, Kaposi varicelliform eruption, bronchopneumonia, eczema herpeticum, etc.)

Pathology of Infectious Diseases Flashcards by Vincent Ribaya

General pattern of infectious response with the following findings:

increased vascular permeability
PMN infiltrates
pus
release of chemoattractants

Suppurative or purulent

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General pattern of infectious response with lymphoplasmacytic infiltrates - lymphocytic (if viral) or plasmacytic (if in a case of syphilis)

Mononuclear

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General pattern of infectious response with caseating or non-caseating granuloma formation

Granulomatous

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General pattern of infectious response with the following findings:

inclusion bodies
multinucleated giant cells
host cell proliferation (such as in the case of HPV infection)
usual association with neoplasia

Cytopathic or cytoproliferative

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General pattern of infectious response with the following findings:

severe gangrenous tissue necrosis
ulcers
rapid progression
toxin- or lysis-mediated destruction
lack of inflammatory cell infiltrate

Tissue necrosis

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General pattern of infectious response with the following findings:

repetitive injury
fibrosis
loss of normal parenchyma

Chronic inflammation and scarring

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General pattern of infectious response associated with the following:

extra cellular Gram-positive cocci
Gram-negative rods (pyogenic organisms)

Suppurative or purulent

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General pattern of infectious response associated with the following:

general chronic infections
acute viral infectious
acute intracellular bacterial infections
parasitic infections

Mononuclear

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General pattern of infectious response associated with the following:

Mycobacterium tuberculosis
fungal infections
schistosome eggs

Granulomatous

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General pattern of infectious response associated with generally all viral infections

Cytopathic or cytoproliferative

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General pattern of infectious response associated with the following:

clostridia
diphtheria
Entamoeba histolytica infections of the colon or liver
HBV infection of the liver
herpesvirus infection of the brain

Tissue necrosis

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General pattern of infectious response associated with the following:

HBV infection
schistosome infection

Chronic inflammation and scarring

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RNA or DNA virus?

Measles virus (MeV)

RNA

Common RNA viruses include: Measles virus,
Mumps virus

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RNA or DNA virus?

Mumps virus (MuV)

RNA

Common RNA viruses include: Measles virus,
Mumps virus

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RNA or DNA virus?

Herpes simplex virus (HSV)

DNA

Common DNA viruses include: HSV, VZV, CMV, EBV

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RNA or DNA virus?

Varicella zoster virus (VZV)

DNA

Common DNA viruses include: HSV, VZV, CMV, EBV

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RNA or DNA virus?

Cytomegalovirus (CMV)

DNA

Common DNA viruses include: HSV, VZV, CMV, EBV

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RNA or DNA virus?

Epstein-Barr virus (EBV)

DNA

Common DNA viruses include: HSV, VZV, CMV, EBV

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Morphology of this viral illness is described as follows:

Warthin-Finkeldey cells
Koplik spots (prodrome)
blotchy, reddish-brown rash of the face, trunk, and proximal extremities

Measles

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In measles, the multinucleated giant cell with eosinophilic intranuclear AND cytoplasmic inclusions

Warthin-Finkeldey cells

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In measles, described as necrotic lesions with PMN infiltrates and neovascularization near the opening of the Stensen ducts

Koplik spots (seen at the prodrome phase of measles)

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Morphology of this viral illness is described as follows:

mononuclear infiltrates predominantly in parotid gland, testes, and brain
parotitis: bilateral (70%) with necrotic debris and duct damage
orchitis: swelling against tunica albuginea predisposing to infarction, atrophy, scar formation, and sterility
pancreatitis: fat necrosis
encephalitis: perivascular infiltrates (mononuclear cuffing) and perivenous demyelination

Mumps

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Morphology of this viral illness is described as follows:

multinucleated syncitia with large, pink-to-purple intranuclear inclusions (Cowdry type A bodies)
several disease entities: gingivostomatitis, genital infection, temporal lobe encephalitis, epithelial keratitis, stromal keratitis, disseminated disease (esophagitis, hepatitis, Kaposi varicelliform eruption, bronchopneumonia, eczema herpeticum, etc.)

Herpes simplex virus (HSV)

HSV is the can be an infectious agent of:

gingivostomatitis (HSV-1)
genital herpes (HSV-2)
temporal lobe encephalitis
herpes epithelial keratitis & herpes stromal keratitis
disseminated herpes disease (esophagitis, hepatitis, Kaposi varicelliform eruption, bronchopneumonia, eczema herpeticum, etc.)

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These are the large, pink-to-purple intranuclear inclusion bodies found in the multinucleated syncition in a herpes simplex virus (HSV) infection

Cowdry type A bodies

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Morphology of this viral illness is described as follows: - centrifugal rash - intraepithelial vesicles, described as "dewdrops on a rose petal" - inclusion bodies within epithelial cells of the vesicle base - reactivation leads to shingles (herpes zoster)

Varicella zoster virus (VZV) or chickenpox

Classic pattern or distribution of the chickenpox or VZV rash

Centrifugal

Reactivation of this VZV leads to a viral illness described with the following morphology: - dermatomal distribution of vesicular rash - dorsal root ganglion cell necrosis, painful radiculoneuritis, with mononuclear cell infiltrates - herpetic inclusion bodies within the dorsal root ganglion cell

Shingles or herpes zoster

Syndrome associated with VZV, like shingles, described to have herpetic inclusion bodies and mononuclear cell infiltrates, but additionally described to be with facial paralysis and hearing loss

Ramsay Hunt syndrome

Morphology of this viral illness is described as follows: - large cells with atypia and intranuclear basophilic inclusions surrounded by a clear "halo" (owl's eye inclusions) - responsible for heterophile-negative or Monospot-negative mononucleosis - associated with congenital infections (blueberry muffin baby)

Cytomegalovirus (CMV)

Most oral herpes or herpes gingivostomatitis cases are caused by this particular HSV type

HSV-1 (herpes simplex virus type 1)

Most genital herpes cases are caused by this particular HSV type

HSV-2 (herpes simplex virus type 2)

Morphology of this viral illness is described as follows: - "transforming virus", responsible for mononucleosis, nasopharyngeal carcinoma, and lymphomas (especially Burkitt lymphoma) - atypical lymphocytes in peripheral blood and tissue (Downey cells) - expanded paracortical areas by over-activated T cells, causing lympadenopathy (paracortical hyperplasia) - responsible for hereophile-positive or Monospot-positive mononucleosis - splenic rupture due to rapid splenomegaly producing increased tension over a fragile splenic capsule or the capsula fibrosa splenica

Epstein-Barr virus (EBV) infection

CMV infection's unique inclusion bodies described as intranuclear basociphilic inclusions surrounded by a clear "halo"

Owl's eye inclusions

Atypical lymphocytes found in the peripheral blood and tissue of an Epstein-Barr virus infection

Downey cells

Expression of heterophile (Monospot) antibodies in EBV infection

Positive

Expression of heterophile (Monospot antibodies in CMV infection

Negative

Gram-positive bacteria involved in pyogenic, suppurative infections with extensive tissue destruction, most commonly in the form of the following: - skin and soft tissue infections: folliculitis, furuncles, carbuncles, cellulitis, hidradenitis suppurativa, mastitis, SSI, paronychia, and felons - pneumonia: post-viral pneumonia and necrotizing pneumonia - scaled skin syndrome (SSS) or Ritter disease

Staphylococcus aureus

Pneumonia caused by Staphylococcus aureus described to involve a greater degree of tissue destruction, further complicated by empyema, abscess, or a pneumatocoele

Staphylococcal necrotizing pneumonia

Syndrome where Staphylococcus aureas exfoliatin cleaves desmoglein in the desmosomes, separating the epidermis at the stratum granulosum

Scalded skin syndrome (SSS) or Ritter disease

Staphylococcus aureas exotoxin responsible for cleaving desmoglein in the desmosomes in SSS or Ritter disease, separating the epidermis at the stratum granulosum

Exfoliatin

Desmosome cadherin cleaved by the Staphylococcus aureus exotoxin exfoliatin in Ritter disease or SSS

Desmoglein

Area of skin separated in Ritter disease or SSS

Stratum granulosum in the epidermis

Spectrum of illness where drug reactions (or rarely, infection with Mycoplasma pneumoniae, Dengue virus, or cytomegalovirus) creates a CD8+ T cell-mediated destruction of keratinocytes, separating the skin at the dermo-epidermal junction (DEJ)

Toxic epidermal necrolysis (TEN) or Lyell disease or Stevens-Johnson syndrome (SJS)

Usual pathogenesis of skin separation in toxic epidermal necrolysis (TEN) or SJS destroying keratinocytes, ultimately separating the dermo-epidermal junction

CD8+ T-cell mediated reaction initiated by drug reaction ``` TEN/SJS is commonly caused by the following: (mnemonic PCP LAPSE) - phenytoin - carbamazepine - phenobarbital - lamotrigine - allopurinol - penicillin - sulfa drugs - erythromycin ``` < 20% is caused by M. pneumoniae, DENV, CMV infections; HIV/AIDS and SLE known to increase the risk

Area of skin separated in Lyell disease or TEN

Dermo-epidermal junction (DEJ)

The more severe form of the TEN/SJS spectrum

Toxic epidermal necrolysis (TEN) or Lyell syndrome

The less severe form of the TEN/SJS spectrum

Stevens-Johnson syndrome (SJS)

8 common TEN/SJS-causing drugs

Mnemonic: PCP LAPSE - phenytoin - carbamazepine - phenobarbital - lamotrigine - allopurinol - penicillin - sulfa drugs - erythromycin

2 disease states known to increase the risk of TEN/SJS

HIV/AIDS & SLE

Gram-positive bacteria involved in pyogenic, suppurative infections with mild tissue destruction, classically associated with the following: - erysipelas - pharyngitis - scarlet fever

Streptococcus pyogenes (group A streptococcus)

Group A streptococcal (Streptococcus pyogenes) diffuse, edematous, neutrophilic, PAINFUL inflammatory reaction of the dermis and epidermis, usually extending into the subcutaneous tissue; with well-demarcating serpiginous borders

Erysipelas

Group A streptococcal (Streptococcus pyogenes) edematous inflammation of the pharynx, presenting with the following: - epiglottic swelling - punctate tonsillar crypt abscesses - cervical lymphadenopathy

Streptococcal pharyngitis or GAS pharyngitis or "strep throat"

Group A streptococcal (Streptococcus pyogenes) post-pharyngitic pyogenic illness presenting with fever, strawberry tongue, centrifugal sandpaper rash, Pastia's lines, and desquamation

Scarlet fever

Toxin seen in lysogenized strains of GAS responsible for scarlet fever

Erythrogenic toxin

Susceptibility test for scarlet fever

Dick test

Gram-positive bacteria involved in suppurative infections, classically associated with the following: - pseudomembranes - airway obstruction - marked vascular congestion - interstitial edema - myocarditis due to fatty change with isolated myofiber necrosis - polyneuritis due to degeneration of myelin sheaths and axis cylinders

Corynebacterium diphtheriae

Corynebacterium diphtheriae toxin (diptheria toxin) can cause necrosis of the epithelium, followed by an outpouring of dense, fibrinosuppurative exudate, forming this thick layer of debris resembling a membrane

Pseudomembrane

Gram-positive bacteria involved in suppurative infections classically associated with the following: - the typical cause of bacterial meningitis - creation of focal abscesses that are grayish-to-yellow in color and nodular in shape, representing necrotic amorphous basophilic tissue debris - intrcellular Gram-positive bacilli in CSF - etiologic agent of granulomatosis infantiseptica

Listeria monocytogenes

Gram-positive bacteria involved suppurative infections of BOTH neutrophilic and macrophagic infiltrates, associated with the following: - tissue necrosis and exudative inflammation - mediastinal hemorrhagic lesions (vasculitis, enlarged hilar and peribronchial lymph nodes) - large, boxcar-shaped extracellular bacteria in chains - spread cutaneously, inhalationally, or via ingestion

Bacillus anthracis

Gram-positive bacteria involved suppurative infections, particularly with central liquefaction that does NOT form granulomas, further described as: - slender, beaded, Gram-positive bacteria with branching filaments - seen best in a modified acid-fast stain called Fite-Faraco stain

Nocardia asteroides

This modified acid-fast stain is used to better visualize acid-fast staining bacilli and bacteria with branching filaments such as Nocardia asteroides

Fite-Faraco modified acid-fast stain

Gram-negative bacteria involved in suppurative infections, associated with the following: - hemorrhagic lesions eventually leading up to DIC - Gram-negative intracellular diplococci - etiologic agent in meningococcemia

Neisseria spp. (N. gonorrhoeae and N. meningitides)

Gram-negative bacteria involved in suppurative infections, associated with the following: - laryngotracheobronchitis (pertussis or whooping cough) - bronchial mucosal erosion and hyperemia - copious mucopurulent exudate - haze of bacilli entangles with bronchial epithelial cilia

Bordatella pertussis

The laryngotracheobronchitis known as whooping cough

Pertussis (agent: Bordatella pertussis, a Gram-negative bacillus)

The layngotracheobronchitis known as barking cough

Croup (agent: Parainfluenza virus - 75%) (Other viral agents: - Influenza virus types A and B - Measles virus - Adenovirus - Respiratory syncytial virus (RSV) Other bacterial agents: - Corynebacterium diphtheriae in laryngeal diphtheria - Post-viral secondary bacterial growth of Staphylococcus aureus, Streptococcus pneumoniae, Hemophilus influenzae, and Moraxella catarrhalis in bacterial tracheitis, laryngotracheobronchitis, and laryngotracheobronchopneumonitis Spasmodic croup: same etiology and pathophysiology, but lacking the usual signs of fever, inflammation, etc.)

Gram-negative bacteria involved in suppurative infections, associated with the following: - etiology of necrotizing pneumonia with fleur-de-lis pattern of necrosis: necrotic centers with red, hemorrhagic peripheries - etiology of ecthyma gangrenosum - etiology of Gram-negative bacterial vasculitis: masses of pseudomonads forming a pervascular blue haze

Pseudomonas aeruginosa

Pseudomonal pneumonia with fleur-de-lis pattern of necrosis, described as necrotic centers with hemorrhagic peripheries

Pseudomonal necrotizing pneumonia

Pattern of necrosis seen in the necrotizing pneumonia caused by Pseudomonas aeruginosa, described as necrotic centers with hemorrhagic/red peripheries

Fleur-de-lis pattern

Pseudomonal (Pseudomonas aeruginosa) infection of the skin, causing well-demarcated necrotic and hemorrhagic oval lesions

Ecthyma gangrenosum

Gram-negative bacteria involved in massive proliferating infections with the following histologic features: - early appearance of protein and polysaccharide-rich effusions - few cells - tissue AND vascular necrosis - PMN infiltrate at the sites of healing (healing margins)

Yersinia pestis

Yersinia pestis infection associated with lymph node enlargement or buboes

Bubonic plague

Yersinia pestis infection associated with severe, confluent, necrotizing AND hemorrhagic bronchopneumonia

Pneumonic plague

Yersinia pestis infection associated with mononucluear phagocytes, developing foci of necrosis, leading to a more diffuse disease presentation

Septicemic plague

Gram-negative, usually genital, infection involved in the following: - painful genital ulcers with shaggy, irregular, non-indurated borders (chancroid) - yellowish-gray exudate - layered: superficial zone of neutrophilic debris and fibrin, underlying zone of granulation tissue of necrotis and thrombosed vessels, and a dense lymphoplasmacytic infiltrate with Gram-negative coccobacilli beneath the granulation tissue - lymph node buboes eventually eroding into sinuses

Haemophilus ducreyi (chancroid or soft chancre)

Gram-negative, usually genital, infection involved in the following: - beefy-red genital ulcer with indurated borders (due to marked epithelial hyperplasia at the borders or pseudoepitheliomatous hyperplasia) - associated with scarring and strictures - seen as minute, encapsulated coccobacilli in macrophages on Giemsa/Warthin-Starry stain (Donovan bodies)

Klebsiella granulomatis

The soft, painful, irregular/shaggy-bordered genital ulcer of Haemophilus ducreyi infections

Chancroid or soft chancre

Appearance of Klebsiella granulomatis on Giemsa or Warthin-Starry stain as encapsulated coccobacilli in macrophages

Donovan bodies

Specific stain used to visualize Klebsiella granulomatis as "Donovan bodies" encapsulated in macrophages

Giemsa stain or Warthin-Starry stain

Acid-fast staining bacteria involved in tuberculosis, characterized with the following: - granuloma-forming, surrounded by epithelioid (activated macrophages) and multinucleated giant cells (Langhans type cells) - caseation necrosis - relies on an intact cell-mediated immunity: chronic, granulomatous

Mycobacterium tuberculosis

In the setting of tuberculosis, this cytokine is released by antigen-presenting cells (APCs) to mediate T cell differentiation into helper T cells type 1 (TH1 cells)

Interleukin-12 (IL-12)

In the setting of tuberculosis, this cytokine is released by helper T cells type 1 (TH1 cells) to mediate the activation of macrophages, enabling them to be bacteriocidal against Mycobacterium tuberculosis and further serve purpose as an epithelioid cell in granuloma formation

Interferon-gamma (IFN-g)

In the setting of tuberculosis, IL-12 is released by these types of cells to mediate T cell differentiation into helper T cells type 1 (TH1 cells)

Antigen-presenting cells (APCs)

In the setting of tuberculosis, IFN-gamma is released by these cells to mediate the activation of macrophages, enabling them to be bacteriocidal against Mycobacterium tuberculosis and further serve purpose as an epithelioid cell in granuloma formation

Helper T cells type 1 (TH1 cells)

Product of granulomatous response in tuberculosis, made up of epithelioid cells (activated macrophages) and multinucleated giant cells (Langhans type cells)

Granuloma

These are the activated macrophages that make up the granuloma in tuberculosis

Epithelioid cells

These are the multinucleated giant cells are involved in the granuloma formation in tuberculosis

Langhans type cells

Primary tuberculosis infection in children, characterized as: - non-contagious - gray-white inflammation with consolidation - middle-to-lower lung lobes - Ghon complex = subpleural granuloma (Ghon focus) + associated pulmonary hilar lymph node - healing by fibrosis

Primary complex tuberculosis

Granuloma of primary complex TB

Ghon focus

Granuloma of primary complex TB with its associated pulmonary hilar lymph node

Ghon complex

The granuloma of primary complex TB with its associated pulmonary hilar lymph node detected radiologically as a calcification

Ranke complex (calcified presentation of a Ghon complex on radiograph)

Usual location of primary complex TB on the lungs

Middle-to-lower lung lobes

Pulmonary TB or reactivation TB's granuloma, described as a sharply circumscribed, firm, grayish-white-to-yellow area with variable amounts of central caseation and peripheral fibrosis

Simon focus

The usual location of primary and reactivation pulmonary TB

Lung apices

Pulmonary TB poorly isolated, and merely walled-off by fibrous tissue which may erode into the surrounding blood vessels and the pleural cavity; caused by a lowered/inhibited cell-mediated inflammatory response

Progressive primary tuberculosis

Pulmonary TB in the setting of decreased cell-mediated inflammatory response, resulting to poor isolation of the infectious agent and a scattered distribution of multiple, small, visible, 2mm foci of yellow-white consolidation

Miliary tuberculosis

Extrapulmonary tuberculosis of the spine

Pott's disease

The paraspinal "granulomas" of Pott's disease

Cold abscess

Most frequent presentation of extrapulmonary tuberculosis, usually involving cervical lymph nodes (scrofula)

Tuberculosis lymphadenitis (or "TB lymph")

Cervical lymphadenopathies caused by the most frequent extrapulmonary tuberculosis (or TB lymphadenitis)

Scrofula

Extrapulmonary tuberculosis presenting as mucosal lymphoid aggregates of the small and large intestine

Intestinal tuberculosis

Most common site of intestinal tuberculosis

Ileum

Acid-fast staining bacteria involved in immunocompromised hosts, such as an AIDS patient with CD4 count of <50 or post-transplant surgery patients, with the following morphology: - disseminated disease - macrophages filled with acid-fast bacilli (rarely with granuloma formation due to the lack of an intact cell-mediated immune immune system)

Mycobacterium avium intracellulare (MAC)

Acid-fast staining bacteria involved in Hansen disease, affecting the skin and peripheral nerves, with varying manifestations dictated by the host's cell-mediated immunity

Mycobacterium leprae (Hansen disease is leprosy)

Acid-fast bacilli infection that is characterizes as a disease of the skin and peripheral nerves, with 2 classic manifestations determined by the host's cell-mediated immunity

Hansen disease or leprosy

Paucibacillary manifestation of leprosy with granulomatous appearance, indicating an intact cell-mediated immunity and TH1 response

Tuberculoid leprosy | TopNotch 2017

Multibacillary manifestation of leprosy with non-granulomatous morphology of lipid-laden macrophages (Lepra cells) with intracellular globi (acid-fast bacilli), indicating a depressed cell-mediated immunity and a TH2 response greater than the TH1 response

Lepromatous leprosy

The intermediate manifestation of leprosy

Borderline leprosy

Manifestation of leprosy that presents without antibodies but is Lepromin skin test-positive

Tuberculoid leprosy

Manifestation of leprosy that presents with non-protective antibodies that may cause glomerulonephritis and vasculitis via a type III hypersensitivity response but is Lepromin skin test-negative

Lepromatous leprosy

Lipid-laden macrophages described as "red snappers" with intracellular acid-fast bacilli in the morphology of lepromatous leprosy

Lepra cells

Multiple intracellular bacilli (multibacillary appearance) found in the Lepra cells of lepromatous leprosy

Globi

Manifestation of leprosy best described with granulomatous lesions of hyperpigmented plaques, thickened superficial nerves, and significant anesthesia that may lead to contractures, paralysis, and autoamputation

Tuberculous leprosy

Manifestation of leprosy best described with histologic findings of Lepra cells and globi, associatade with ulnar and peroneal nerve involvement and sterility due to the destruction of seminiferous tubules

Lepromatous leprosy

Bacterial agent responsible for a four-stage infection (with a congenital form) primarily associated with a non-painful genital ulcer or chancre

Treponema pallidum or syphilis

Stage in treponemal infection (syphilis) associated with the formation of an elevated papular genital ulcer/chancre described as solitary, indurated, and painless, with visible treponemes from the chancre surface using silver stain immunofluorescence; further described with intense plasma cell infiltrates and proliferative endarteritis

Primary syphilis (stage 1)

Stage in treponemal infection (syphilis) associated with the formation of painless flat-topped papules at mucocutaneous areas 2-10 weeks after chancre appearance (condyloma lata), further described with the following symptoms: - maculopapular rash, palmar rash - fever - headache - malaise - anorexia - lymphadenopathy - plasma cell infiltrate - obliterative endarteritis - less intense/mild inflammation

Secondary syphilis (stage 2)

Stage in treponemal infection (syphilis) associated with no symptoms

Latent stage of syphilis (stage 3)

Stage in treponemal infection (syphilis) associated with formation of gummas, or grey and rubbery lesions with coagulated, necrotic material of plump, palisading macrophages an fibroblasts surrounded by mononuclear leukocytes and plasma cells; also with endarteritis causing aortitis

Tertiary syphilis (stage 4)

Manifestation of congenital treponemal infection, if not causing late abortion or stillbirth, characterized with the following: - bullous eruptions (rash) and epidermal sloughing - osteochondritis and periostitis - saber shins and saddle nose - diffuse hepatic fibrosis with lymphoplasmacytic infiltrate - pale, airless lungs (pneumonia alba) due to lung fibrosis and interstitial pnuemonia

Infantile congenital syphilis

Manifestation of congenital treponemal infection, if not causing late abortion or stillbirth, characterized with the following (triad of late manifestation syphilis): - interstitial keratitis - Hutchinson teeth - cranial nerve VIII deafness

Childhood (or late manifestation) congenital syphilis

Elevated, painless papule with indurated boredes and a clean based shallow ulcer characteristic of primary syphilis

Chancre

Flat-topped plainless superficial lesions at mucocutaneous sites characteristic of secondary syphilis

Condyloma lata

Period of time after chancre appearance in which the condyloma lata of secondary syphilis is expected to appear

2-10 weeks (after chancre)

Grey, rubbery lesions of tertiary syphilis, described to have coagulated, necrotic material of plump, palisading macophages and fibroblasts, surrounded by mononuclear leukocytes and plasma cells

Gummas

Pale, airless lungs of tertiary syphilis caused by lung fibrosis and interstitial pneumonia

Pneumonia alba

Neurologic involvement of tertiary syphilis, which may be asymptomatic but also associated with CSF abnormalities, meningovascular involvement, tabes dorsalis, and general paresis

Neurosyphilis

End-stage liver deformity seen in tertiary syphilis

Hepar lobatum

Excessive new bone growth along the tibia seen in infantile congenital syphilis

Saber shin

Gradual destruction of the vomer seen in infantile congenital syphilis

Saddle nose

Screwdriver-shaped or peg-shaped teeth usually with enamel notching seen in late manifestation or childhood congenital syphilis

Hutchinson teeth

Particular deafness seen in late manifestation or childhood congenital syphilis

CN VIII or eighth nerve deafness

Similar to the presentation of pyogenic organisms, this is the usual morphological formation of anaerobic infections, which are usually polymicrobial

Abscess formation

Anaerobic oral commensal associated with Lemierre syndrome (infection of the lateral pharyngeal space + septic jugular vein thrombosis)

Fusobacterium necrophorum

Infection of the lateral pharyngeal space acccompanied with septic jugular vein thrombosis, usually caused by the oral commensal Fusobacterium necrophorum

Lemierre syndrome

Etiologic agent responsible for the 3-stage disease known as Lyme disease

Borrelia recurrentis

Stage 1 manifestation of Borrelia recurrentis infection involving edema and lymphoplasmacytic infiltrate after receiving a erythematous papule secondary to a tick bite

Erythema chronicum migrans

Destructive stage 3 manifestation of Borrelia recurrentis infection involving villous hypertrophy, lining-cell hyperplasia, and abundant lymphocytes and plasma cells with onion-skin-like lesions in the form of chronic arthritis

Lyme arthritis

Manifestation of Borrelia recurrentis infection, beginning in stage 2 of the disease, involving marked lymphoplasmacytic infiltrate into the CNS, causing meningoencephalitis and eventual cranial neuritis

Lyme meningitis

3-stage disease caused by Borrelia recurrentis, spread via tick bite

Lyme disease

Responsible for 2 clostridial skin diseases, namely clostridial cellulitis and clostridial gas gangrene

Clostridium perfringes

Clostridium perfringes infection characterized by the following: - foul odor - discolored exudate - wide tissue necrosis disproportionate to the number of neutrophils and bacteria present

Clostridial cellulitis

Clostridium perfringes infection characterized by the following: - marked edema with enzymatic myonecrosis - extensive fluid exudate with gas bubbles - extensive hemolysis and marked vascular injury and thrombosis - dusk-colored, wedge-shaped infarcts in the small bowel

Clostridial gas gangrene

Toxin released by Clostridium perfringes, involved in clostridial cellulitis and clostridial gas gangrene

alpha-toxin (lecithinase)

Clostridial infection responsible of spastic paralysis

Clostridium tetani (or tetanus)

Toxin responsible for spastic paralysis in tetanus

Tetanospasmin

Clostridial infection responsible for flaccid paralysis

Clostridium botulinum (or botulism)

Toxin responsible for flaccid paralysis in botulism

Botulinum toxin

Clostridial infection responsible for pseudomembranous colitis and mucopurulent exudate reminiscent of a volcano

Clostridium difficile

Clostridium difficile toxin responsible for pseudomembranous colitis

A-B endotoxin (with A as the chemokine and B as the cytotoxin)

Infectious agent known as the most common sexually transmitted bacterial disease in the world, causing purulent urethritis

Chlamydia trachomatis

Manifestation of chlamydial infection involving L-strains of the Chlamydia trachomatis, characterized with stellate abscesses - a granulomatous inflammatory reaction of irregular necrotic foci and PMN infiltrate with chlamydial inclusions in cells, predisposing to chronic inflammation and fibrosis

Lymphogranuloma venereum (LGV)

Variety of infections causing small-vessel lesions, focal areas of hemorrhage/inflammation, and focal microglial proliferations, usually caused by members of the Rickettsia genus

Typhus fever

Focal microglial proliferations with mixed T lymphocytic and macrophagic infiltrate seen in infections usually caused by members of the Rickettsia genus

Typhus nodule

Rickettsial disease: - Agent: Ricekttsia prowazekii - Vector: body LOUSE

Epidemic typhus

Rickettsial disease: - Agent: Ricekttsia typhi - Vector: rat FLEA

Endemic typhus

Rickettsial disease: - Agent: Ricekttsia ricketsii - Vector: dog TICK

Rocky Mountain spotted fever

Rickettsial disease: - Agent: Ricekttsia akari - Vector: MITES

Rickettsial pox

Rickettsial disease: - Agent: Orienta tsutsugamushi - Vector: CHIGGERS ("berry bugs")

Scrub typhus

Rickettsial disease: - Agent: Coxiella burnetti - Vector: none

Q fever

Rickettsial disease: - Agent: Ehrlichia chaffeensis - Vector: TICK

Ehrlichiosis (predominantly a monocytic infection)

Rickettsial disease: - Agent: Anaplasma phagocytophilum - Vector: TICK

Anaplasmosis (predominantly a neutrophilic infection)

Common yeast infection characterized with pseudohyphae and hyphae, responsible for the following: - oral thrush - dirty-looking pseudomembrane composed of matted organisms and inflammatory debris with underlying mucosal hyperemia and infection - mucosal infections (esophagitis, vulvovaginitis with thick curd-like discharge, oral thrush) - cutaneous infections (onychomycosis, paronychia, folliculitis, intertrigo, balanitis, diaper rash) - invasive infections (liver abscess, endophthalmitis, meningoencephalitis, tricuspid valve involvement, the most common form of fungal endocarditis)

Candida albicans

Yeast infection associated with a prominent, thick, gelatinous, polysaccharide capsule with the following characteristics: - PAS-positive - mucicarmine-positive - predominantly CNS in involvement - contains melanin (antioxidant) - granulomatous pattern in the immunocompetent host but creates soap-bubble lesions (expanding yeast growth in the meninges and perivascular Virchow-Robin spaces) in the immunodepressed host

Cryptococcus neoformans

CNS lesions caused by cryptococcal yeast spread into the meninges and perivascular Virchow-Robin spaces in an immunodepressed host

Soap-bubble lesions

Mold infection with angioinvasion and CNS involvement in its rhinocerebral forms, characterized by the following: - septate hyphae with acute branching (40 degrees) - fungus ball masses - proliferating masses of hyphae lying free within cavitations - invasive, necrotizing pneumonia with sharply delineated, rounded gray foci and hemorrhagic borders (target lesions) - primarily affecting lungs and nasal sinuses

Aspergillus fumigatus (disease: aspergillosis)

Mold infection with angioinvasion and CNS involvement in its rhinocerebral forms, characterized by the following: - non-septate hyphae branching at right angles - rhinocerebral forms usually seen in diabetic patients - pulmonary involvement includes hemorrhagic pneumonia and vascular thrombosis with distal infarcts - primarily affecting lungs, nasal sinuses, and GIT

Mucor spp. (disease: mucomycosis)

Fungal ball mass made of hyphae lying free within cavitations, as seen in aspergillosis

Aspergilloma

Pulmonary lesions described as invasive, necrotizing with sharply delineated, rounded gray foci and hemorrhagic borders, as seen in aspergillosis

Target lesions

Parasitic disease: - 2 sites of replication: hepatocytes (exoerythocytic stage) and RBC (erythocytic stage) - Mechanism: phagocytosis of infected RBC; blood vessels plugged by infected RBCs (sequestration) leading to ischemic damage; release of toxic pigment in the kidneys - Diagnosis: Giemsa-stained peripheral blood smear, visualizing hemozoin-positive asexual-stage parasite - Several organ involvement: splenomegaly with brittle fibrotic spleen and pigmentation; hepatomegaly and pigmentation; pigmented phagocytes in the BM, LN, lungs, and subcutaneous tissue; pulmonary edemal non-specific hypoxic lesions in the CVS with shock and DIC; kidneys congested and enlarged with pigmented glomeruli and Hgb casts in the tubules; perivascular ring hemorrhages in the brain

Malaria (agent: Plasmodium spp.) (Member species: - Plasmodium falciparum - malignant tertian - Plasmodium vivax - most frequent benign tertian - Plasmodium ovale - less frequent benign tertian - Plasmodium malariae - benign quartan - Plasmodium knowlesi - severe quotidian)

Drug of choice for radical cure of benign tertian malaria

Chloroquine (except in places where there is growing chloroquine-resistance, such as Malaysia) (use quinine for pregnant patients)

Perivascular ring hermorrahges in the cerebrum, seen in cerebral malaria - the most common cause of death in children with malaria

Durck granulomas (or malarial granulomas)

Microscopic dots of Plasmodium vivax

Schuffner's dots

Microscopic dots of Plasmodium ovale

Schuffner's dots

Microscopic dots of Plasmodium malariae

Ziemann's stipplings

Microscopic dots of Plasmodium falciparum

Mauer's dots or Mauer's clefts

Microscopic dots of Plasmodium knowlesi

Stinton & Mulligan's stipplings

Parasitic disease: - Site of replication: RBC - Mechanism: parasitemia (severe in asplenic patients), causing fever and hemolytic anemia - Diagnosis: Giemsa-stained peripheral blood smear, visualizing hemozoin-negative parasite (trophozoites) in the Maltese cross pattern - Several organ involvement: jaundice and hepatic necrosis; acute tubular necrosis; acute respiratory distress syndrome; erythrophagocytosis and visceral hemorrhages

Babesiosis (agent: Babesia spp. aka Nuttalia spp.) (Member species: - Babesia microti - Babesia divergens)

Pattern of intraerythrocytic ring-shaped trophozoites in tetrads, seen in Giemsa-stained PBS of babesiosis

Maltese cross pattern

Particular manifestation of leishmaniasis involving the following: - entire skin covered by nodular lesions - foamy macrophages filled with leishmania - starts from single nodule to generalized spread of nodules

Diffuse cutaneous leishmaniasis (Species involved: - Leishmania major - Old World - Leishmania topica - Old World - Leishmania mexicana - New World - Leishmania braziliensis - New World)

Particular manifestation of leishmaniasis involving the following: - granulomatous presentation with many giant cells few leishmania - skin ulcers with heaped-up exposed skin borders - starts from papule, becoming indurated, and then ulcerated followed by healing

Cutaneous leishmaniasis (Species involved: - Leishmania major - Old World - Leishmania topica - Old World - Leishmania mexicana - New World - Leishmania braziliensis - New World)

Particular manifestation of leishmaniasis involving the following: - mixed mononuclear and macrophagic infiltrate filled with leishmania - moist, disfiguring ulcerating/non-ulcerating lesions in nasopharynx - begins granulomatous with few leishmania then eventually leads to scarring - granulomas may reactivate

Mucocutaneous leishmaniasis (Species involved: - Leishmania braziliensis - New World)

Particular manifestation of leishmaniasis involving the following: - Fever, weight loss, pancytopenia - Enlarged macrophages filled with leishmania, multiple organ involvement (liver, spleen, BM, lungs, GIT, kidneys, pancreas, testes) - Spleen: splenomegaly with plasma cell infiltrate, leading to disruption of normal architecture - Liver: hepatomegaly leading to fibrosis - Skin: hyperpigmentation, usually seen in those South Asian ancestry, due to the kala-azar pigment - Kidneys: immune cell-mediated mesangioproliferative glomerulonephritis and amyloid deposition (in advanced stages) - further complicated by secondary bacterial infections due to cytopenias and hemorrhages

Visceral leishmaniasis (Species involved: - Leishmania donovani - Old World - Leishmania infantum - Old World - Leishmania chagasi - New World)

Parasitic infection associated with: - chancre post-tsetse fly bite - large numbers of parasites surrounded by mononuclear infiltrate - hemolymphatic form: splenomegaly & lymphadenopathy - cerebral form: leptomeningitis (accumulation of the parasite in perivascular Virchow-Robin spaces) leading to demyelinating panencephalitis - concentration of parasites in capillary loops (choroid plexus, glomeruli, etc.) - plasma cells with cytoplasmic globules containing Ig (Mott cells)

African sleeping sickness or African trypanosomiasis (Involved species: - Trypanosoma brucei gambiense - West African variant - Trypanosoma brucei rhodesiense - East African variant)

Tsetse fly bite lesion, involved in African sleeping sickness

Trypanosomal chancre

Plasma cells with cytoplasmic globules of immunoglobulins, seen in African trypanosomiasis

Mott cells

Parasitic infection associated with: - Reduviid bug or kissing bug or triatomine bug bites - acute myocarditis: myocardial fiber swelling and intracellular pseudocysts; focal myocardial necrosis and acute interstitial inflammatory infiltrate; 4-chamber cardiac dilation - chronic myocarditis: dilated heart; scattered foci of myocardial necrosis; mononuclear interstitial infiltrate and fibrosis; megacolon and megaesophagus (but absence of organisms in ganglia of Auerbach plexus); mural thrombi that may lead to pulmonary embolism

Chagas disease or American trypanosomiasis (Involved species: - Trypanosoma cruzi)

Parasitic infection associated with: - larval penetration of teh skin, lungs, then GIT - autoinfection: larvae hatch in GIT and invade colonic mucosa and lungs - duodenitis due to rhabditiform larvae in duodenal crypts (mild infection) - invasion of filariform larvae into colonic submucosa, lymphatics, and BV (hyperinfection)

Strongyloides stercoralis

Parasitic cestode infection associated with: - pathologic lesion: cysticerci (neurocystercercosis) - brain, muscle, skin, heart involvement - ovoid, white-to-opalescent, grape-sized lesions - cyst rupture: inflammation, focal scarring and fibrosis

Taenia solium

Pathologic lesion of Taenia solium, containing invaginated scolex bathed in clear cyst fluid

Cystircercus (pl. cysticerci)

Parasitic cestode infection associated with: - pathologic lesion: hydatid cysts (hydatid disease) - mostly liver (followed by lung, bones, brain) - mononuclear and eosinophilic infiltrates on larvae and surrounding cysts (with fibrosis) - cyst rupture: anaphylaxis

Echinococcus granulosus

Pathologic lesion of Echinococcus granulosus - clear-fluid cysts with inner germinative layer and an outer non-germinative layer of delicate laminations

Hydatid cyst

Sediment released by rupture of the hydatid cysts, creating an anaphylactic reaction in Echinogranulosus infection (hydatid disease)

Hydatid sand

Parasitic infection associated with: - coiled larvae encysted infection of the striated muscles of richest blood supply (diaphragm, EOMs, laryngeal, deltoid, gastrocnemius, intercostals) - myocarditis: patchy interstitial pattern with eosinophils and scattered giant cells - myositis: coiled larvae in membrane-bound vacuoles within the myocytes

Trichinella spiralis (disease: trichinosis)

Myocytes in trichinosis, housing the coiled larvae of Trichinella spiralis, seen encysted in membrane-bound vacuoles

Nurse cells

Pigment in visceral leishmaniasis responsible for black skin pigmentation

Kala-azar | Usually seen in those with South Asian ancestry

Larval form of Strongyloides stercoralis in hyperinfection, as it invades the colon, lymphatics, and blood vessels; associated with mononuclear infiltrate

Filariform larvae

Larval form of Strongyloides stercoralis in duodenitis, as it multiplies in the duodenal crypts; associated with eosinophilic infiltrate

Rhabditiform larvae

Parasitic infection associated with: - "dioecious" worms - GIT, liver involvement (early) - GIT, liver, kidney, lungs (late) - hemorrhagic cystitis - infective stage eliciting minimal skin reactions (cercariae) - inflammatory stage eliciting the disease state via granulomatous inflammation and fibrosis (egg)

Schistosomiasis (Involved species: - Schistosoma japonicum - GIT schistosomiasis - Schistosoma mansoni - GIT schistosomiasis - Schistosoma haematobium - hemorrhagic cystitis)

Infective stage of Schistosoma spp., usually only eliciting minimal skin reactions

Cercaria (pl. cercariae)

Inflammatory stage of Schistosoma spp., eliciting the disease state via granulomatous inflammation and fibrosis to the bowels (S. japonicum and S. mansoni) or the bladder (S. haematobium)

Schistosome egg

Parasitic filarial infection associated with: - persistent lymphedema (extremitis, scrotum, penis, vulva) - hydroceles (testes) leading to the thickening of the tunica vaginalis - elephantiasis: subcutaneous fibrosis with epithelial hyperkeratosis - dilated dermal lymphatics, widespread lymphocytic infiltrates, focal cholesterol deposits - eosinophilia in the lung - lymphatic finding: adult worms surrounded by minimal/no inflammation, intense eosinophilia with hemorrhage and fibrin (such as in the case of recurrent filarial funiculoepididimytis), and granuloma - lung finding: dead worms surrounded by hyaline, eosinophilia, embedded in small epithelioid granuloma

Filariasis (Involved species: - Wolbachia bancrofti - Brugia malayi)

Lymphedema of the lower extremities with subcutaneous fibrosis with epithelial hyperkeratosis as seen in filarial infection

Elephantiasis

Small epithelial granulomas in the lung, containing dead worms surrounded by hyaline and eosinophilia in filarial infection, caused by Th2 responses and other cytokines

Meyers-Kouvenaar bodies

Parasitic filarial infection associated with: - leading cause of preventable blindness in the sub-Sahara (river blindness) - lizard/leopard/elephant skin - punctate keratitis with eosinophilic reaction to degenerating microfilariae, causing a limbus or sclerosing keratitis - subcutanous nodule - fibrous capsule surrounding adult worms and inflammatory infiltrates

Onchocerca volvulus (disease: onchocercosis)

Blindness due to the parasitic filarial nematode Onchocerca volvulus

River blindness

Epidermal atrophy and elastic fiber breakdown alternating with hyperkeratosis, hyperpigmentation with pigment incontinence, and dermal atrophy/fibrosis as seen in onchocercosis

Lizard skin or leopard skin or elephant skin

Fibrous capsule surrounding adult worms and inflammatory infiltrates, presenting as a subcutaneous nodule, seen in onchocercosis

Onchocercoma

Accentuation of onchocercosis keratitis with the use of antifilarial treatment

Mazzotti reaction

Onchocercosis of this region of the eye will lead to iridocyclitis and glaucoma

Anterior chamber

Onchocercosis of these regions of the eye will lead to atrophy and river blindness

Choroid and retina

Pathology of Infectious Diseases Flashcards

(210 cards)