micro_mod8_the_dregs

Filamentous G+ rod

strictly anaerobic

Sulfur granules

Endogenous flora of the mouth and GI tract

Non-acid fast

Trauma (abscessed tooth, appendicitis, wounds, dental extraction, broken jaw)

bacteriaform filaments surrounded by areas of inflammation

Actinomycosis – hard, non-tender swelling of the face/neck or abdomen, spreads through draining sinus tracts; NOT communicable

Pelvic actinomycosis – in women with an IUD

Hard yellow granules (sulfur granules)composed of filamentous mass form in pus

Tx: penicillin G with drainage

SNAP -- Sulfa for Nocardia; Actinomyses give Pen

Filamentous G+ rod

facultative aerobe

Found in exogenous environment (soil)

Infection through inhalation

Weak acid fast staining (esp. if weak HCl is used)

Nocardiosis – immunocompromised person --> lung infection (pneumonia) --> abscesses, sinus tracts --> brain, skin, and kidneys; NOT communicable

Ziehl-Neelsen stain

Tx: trimethoprim-sulfamethoxazole

SNAP -- Sulfa for Nocardia; Actinomyses give Pen

spirochete, microaerophilic

Not seen on Gram stain, use dark field microscopy or fluorescence

Non-specific serology – positive in primary and secondary syphilis

Venereal Disease Research Laboratory (VDRL) test: cardiolipin (antigen) combined with patient serum --> flocculation if reagin (non-specific antibody) is present; used for congenital syphilis because titer is higher in the baby vs. mother

• Rapid Plasma Reagin (RPR) test: cardiolipin on charcoal + patient serum --> agglutination:
• *False positive – if you have HBV, leprosy, or infectious mononucleosis
• *False negative – prozone phenomenon

Specific serology – stay positive for life, so you can’t use it to determine response to treatment

Fluorescent treponemal antibody-absorption (FTA-ABS) test: serum is adsorbed with antigens from a nonpathogenic treponemal Reiter’s stain to remove antibodies that react with normal flora --> serum added to syphilis antigen on a slide --> fluorescent anti-human antibody detects syphilis antibodies

Microhemagglutination test (MHA-TP) test: sheep or turkey RBCs are coated with syphilis antigens; agglutinates if added to serum with syphilis antibodies

Transmission – sexual and transplacental

Infects endothelium --> endarteritis (for all stages, but most important in tertiary stage)

Congenital syphilis – Hutchinson’s or “mulberry” incisors, facial and tooth abnormalities seen by 2 years; in 3rd month of pregnancy, get skin and bone lesions with hepatosplenomegaly

Immunity is incomplete

Tx: benzathine penicillin for all stages – grows very slowly so you must treat for a long time. For neurosyphilis use aqueous penicillin (benzathine penicillin does not penetrate the CNS)

Non-pathogenic treponemes are part of the normal flora and can be cultured

Primary syphilis – hard, painless chancre at site of contact (tissue damage with migration of neutrophils, lymphocytes, and macrophages to the entry site)

heals spontaneously within 6 months and spreads systemically through the blood; contagious

Secondary syphilis – in ½ of patients: spread from blood to lymph nodes, CNS, mucousmembranes, and skin --> lymphadenopathy and generalized rash on the palms and soles, patchy alopecia

moist lesions on genitalia = condyloma lata; low fever, malaise, anorexia,headache, and maybe meningitis, hepatitis, or nephritis; contagious

Latent stage – organisms persist in spleen and lymph nodes; 1/3 of cases, can last decades:

Early: secondary symptoms can recur; contagious

Late: no symptoms; not contagious

Tertiary syphilis – ½ of people with latent syphilis; tissue destruction is caused by host response to treponemal antigens, get gummas (soft masses in bone and skin consisting of inflammatory cells and few treponemes) and hepatosplenomegaly; neurosyphilis (tabes dorsalis)

motile spirochete

microaerophilic

LYME DISEASE

can see it with dark field microscopy, Giemsa, and silver stain(but patient culture is usually negative)

Most common tick-borne disease in US – transmitted from the white-footed mouse (reservoir) to humans via the bite of Ixodes scapularis (East coast) or Ixodes pacificus(West coast); Deer are needed for the life cycle; nymphal stage transmits more often

Stage 1 – local; multiplication in the skin and dissemination to the blood; 1 – 5 weeks after bite get erythema migrans (target-like) lesion (but 25% do not get the rash) with flu-like symptoms

Stage 2 – spread to nervous system, joints, heart, and eyes, with secondary annular skin lesions, meningitis, myocarditis, MSK pain, Bell’s palsy, and eye abnormalities; aseptic. Intermittent symptoms with latency

Stage 3 – chronic infection of large joints, nervous system, or skin

Lyme arthritis – autoimmune

ELISA – IgM after 2 weeks, IgG after 30 days; confirm with Western or PCR(there are cross-reacting antibodies in the normal flora)

Tx: for stage 1 give doxycycline or amoxicillin; for late stage give ceftriaxone; doxycycline for prophylaxis

aerobic spirochete

may see in blood smear

major antigenic proteins from linear plasmids that can undergo antigenic variation

Transmitted from rodents (reservoir) to humans via the Ornithodoros tick bite

In the US: endemic relapsing fever – blood --> multiplies in kidney, liver, eye,and/or brain --> headache, fever, chills, and organ dysfunction --> antibody responses kill pathogen --> antigenic variation --> fever again…

Tx: tetracycline

spirochete

may see in blood smear

Can produce major antigenic proteins from linear plasmids that can undergo antigenic variation

Humans are the only known reservoir; transmitted by the human body louse

In Africa: epidemic relapsing fever – blood --> multiplies in kidney, liver, eye, and/or brain --> headache, fever, chills, andorgan dysfunction --? antibody responses kill pathogen --> antigenic variation --> fever again…

Tx: tetracycline

Treatment with penicillin causes flu-like symptoms due to endotoxin release uponbacteria lysis

• occurs in:
• Secondary syphilis
• Lyme disease
• Leptospirosis
• Relapsing fever

Mediated by TNF, so passive immunization with anti-TNF can prevent

Spirillum minor and Streptobacillus moniliformis

cause rat bite fever --> reddish brown rash with fever and local lymphadenopathy

stain G-negative

non-motile

lack peptidoglycan in cell wall

Obligate intracellular with a complex life cycle – spore-LIKE elementary body enters the epithelial cell and changes into reticulate body that replicates by binary fission

daughter reticulate bodies (these are seen as inclusions with Giemsa stain) eventually turn into elementary bodies and are released

Cannot be cultivated because they can’t generate their own energy

Infect epithelial cells and are rarely invasive

All share group-specific LPS antigen that can be detected with complement fixation

Exudates can be subjected to IF, ELISA, and DNA probes

most common cause of preventable blindness

most common cause of bacterial STD in US; 15 immunotypes that only infect humans

Inclusions contain glycogen and will stain with iodine

Reservoir – people with asymptomatic genitourinary tract infection

Transmission is usually sexual or through the birth canal

Trachoma (chronic conjunctivitis) – conjunctival scarring causes eyelashes to turn inward which scars the cornea and leads to vascularization (pannus) --> blindnessTypes A, B, and C

Transmission – finger/fomite-to-eye

Nongonococcal urethritis (TYPES D-K) --> disseminated disease involves epididymitis and salpingitis or pelvic inflammatory disease; infected cells are restricted to nonciliated epithelial cells on mucous membranes of the urethra, endocervix, endometrium, fallopian tubes, and rectum

Extensive PID may cause infertility or ectopic pregnancy

Tx: azithromycin

Neonatal conjunctivitis (onset: 7 – 12 days) and pneumonia (onset: 2 – 12 weeks), Tx: erythromycin

Lymphogranuloma venereum (LGV, TYPES L1-3) – highly invasive; primary genital lesion --> systemic spread and replication in mononuclear phagocytes in the lymphatics (swollen draining lymph nodes = buboes that can rupture and lead to abscesses). Most common in Africa, Asia, and South America. Tx: tetracycline, doxycycline

Reiter’s syndrome – associated with genitourinary and gastrointestinal infections; urethritis, conjunctivitis, mucocutaneous lesions, and reactive polyarthritis (damages cartilage without infecting synovial fluid)

Can’t see, can’t pee, can’t bend my knee

Linked with the HLA-B27 haplotype (maybe autoimmune response/complexes formed?)

10 – 30% are co-infected with N. gonorrheae, so always give azithromycin with thetetracycline

Produces a cell-mediated response and antibodies but no immunity forms

Serology is useless because infection rate is high

• Neisseria gonorrheae
• Ureaplasma urealyticum
• Salmonella spp.
• Shigella spp.
• Yersinia spp.
• Campylobacter spp.
• Chlamydia trachomatis

Primary reservoir is birds (turkeys and parrots) – spread by inhalation of dried excretions

INTRACELLULAR GROWTH

Parrot fever (ornithosis) – infected alveolar macrophages spread infection to lungs (pneumonia with high fever) --> bloodstream --> spleen, heart, liver

Rarely communicable

Inclusions do not contain glycogen

Can use serology – 1 immunotype

Tx: tetracycline, doxycycline

Atypical pneumonia – URT, LRT

sinusitis spread from person to person

Inclusions do not contain glycogen

Can use serology – 1 immunotype

Associated with coronary artery disease

Tx: tetracycline, doxycycline

Gram-negative (poor-staining) coccobacillus

outer membrane and thin peptidoglycan layer

Obligate intracellular parasite that multiplies intracellularly by binary fission

Can synthesize some of the ATP needed for metabolism (not an energy parasite)

Cause zoonotic disease transmitted by arthropod vectors and do not survive in the outside environment

Infect vessel wall endothelium --> vasculitis --> hemorrhage and edema

For R. rickettsii, R. prowazekii, and R. tsutsugamushi – antigen cross-reacts with the OX strain of Proteus vulgaris --> basis of agglutination in the Weil-Felix test using patient serumantibodies

ROCKY MOUNTAIN SPOTTED TICK FEVER

Spread from dogs and rodents (reservoirs) to humans

Dermacentor tick bite; US East coast

Skin --> blood --> attach to endothelial cells of small blood vessels and enter by pathogen directed endocytosis

Phagosome lysis via phospholipase A and growth in cytosol until the cell bursts --> hemorrhagic spots associated with a characteristic rash

Rocky Mountain Spotted Fever – acute fever, headache, myalgia, prostration; macules appear first on hands and feet and progress to petechiae. Severe DIC and coma

No person-to-person transmission

Diagnosis by IFA, ELISA, and direct detection of antigens in skin biopsies

Tx: need something that gets inside the host cell – doxycyline, tetracycline, or chloramphenicol

Sulfa drugs exacerbate infection

Epidemic typhus: 1–3 weeks after bite: sudden onset of chills, fever, headache with a maculopapular rash (that spares face, palms, and soles) coming a week later --> severe meningoencephalitis with rash --> delirium and coma (if nottreated)

Spread by human body louse (Pediculus); only infects humans

Associated with war and poverty

Tx: tetracycline, chloramphenicol

Recrudescent typhus – reactivation following latent infection with epidemic typhus; less severe than epidemic form. In the US, see it in people from WW2; called “Brill-Zinsser disease”

Scrub typhus – transmitted by mites or chiggers from rodents

Reservoir is mice, transmitted by mites

Causes rickettsial pox

Reservoir is rodents, spread by fleas

Causes endemic (murine) typhus

May see it in California or Texas

Transmitted from cattle, sheep, or goats to humans by inhalation of dried excretions

INTRACELLULAR GROWTH

Spore-like structure makes it resistant to the environment and phagolysosome

Q fever – fever, severe headache, chills, myalgia; may cause pneumonia with granuloma formation in the lungs, liver (--> hepatitis), bone marrow, and spleen; no rash!

Phase I: isolated, virulent, has surface antigen

Phase II: after repeated passage, nonvirulent, surface antigen is lost

Chronic Q fever – associated with higher phase I titers, may involve heart valves as a subacute bacterial endocarditis that is blood culture-negative

Very low ID50 – only need about 1 for infection

INTRACELLULAR GROWTH

Forms morulae in cytoplasm

Endemic in dogs, transmitted by the Lone Star tick (Amblyomma and Dermacentor)

Human monocytic ehrlichiosis (HME) – infection of monocytes and macrophages --> fever, headache, myalgia, thrombocytopenia, leukopenia, and increased liver enzymes

Tx: doxycycline

LONE STAR TICK

The ehrlichioses are clinically indistinguishable

Transmitted by Ixodes ticks

Infection of granulocytes --> fever, headache, myalgia, thrombocytopenia, leukopenia, increased liver enzymes(ehrlichiosis)

Tx: doxycycline

The ehrlichioses are clinically indistinguishable

renamed Anaplasma phagocytophilum

CUTANEOUS MYCOSES

DERMATOPHYTOSES

hypopigmented skin patches inwarm humid areas of the skin (infects outer layer of dead cells)

May get outbreaks in the NICU

Transmitted through direct contact

Tx: topical miconazole; selenium sulfide on skin

CUTANEOUS MYCOSES

DERMATOPHYTOSES

infects skin, hair, and nails; characteristic targetlesion; get it from infected cats, dogs, and other people

Causes tinea ______, or ringworm

A zoonotic fungal pathogen

Scrapings show macroconidia on short conidiophores and branched,septate hyphae; may also form microconidium – non-dimorphic mold

Highly infectious/contagious

Tx: topical miconazole, tolnaftate or undecylenic acid; oral griseofulvin

CUTANEOUS MYCOSES

DERMATOPHYTOSES

Trichophyton tonsurans is the most common cause of outbreaks of tinea capitis in children; seasonal (September)

Superficial fungal infection of skin = dermatophytosis

Many major pathogens are dimorphic

SUBCUTANEOUS MYCOSES

Spirotrichosis, aka Roseberg’s disease – formation of local abscess orulcer with nodules in regional lymphatics (subcutaneous)

Introduced into skin by thorns and other puncture wounds

Mold – has a rosette/daisy pattern of oval conidia (chlamydiophore)

Yeast – cigar-shaped with buds

Dimorphic

HIV & GARDENERS (THORNS)

Tx: itraconazole,heat, iodine

MOLD

• YEAST (CIGAR)

SYSTEMIC MYCOSES

endemic in Ohio and Mississippi River valleys

Dimorphic – mold has tuberculate macroconidia and microconidia (looks like sea mines); yeast issmall and ellipsoid

Extremely slow grower

Can get in from bat caves (due to high levels of nitrogen in guano) and starling droppings, inhaled

Phagocytosed, but can exist within or kill macrophages (produces bicarbonate and ammoniathat raise the pH of phagolysosome)

After 2 weeks causes acute respiratory illness – fever, chills, night sweats, fatigue, headache, cough, myalgia, andweight loss

Causes disseminated histoplasmosis in patients with compromised CMI – ulcerative lesions of tongue and gingiva,severe pulmonary infection

RIA detects Histoplasma antigens or RNA (DNA probe); complement fixationand immunodiffusion

Tx: amphotericin B, itraconazole is used for preventing disease in AIDS patients; fluconazole for meningitis

• MOLD

• YEAST (SMALL, ELLIPSOID)

SYSTEMIC MYCOSES

Dimorphic – mold has hyphae with pear-shaped microconidia; yeast is round with adoubly refractive wall and a single broad-based bud

Causes blastomycosis – fever, productive cough, pleuritic chest pain, and weight loss,erythematous lesion and lung crackles; CXR shows nodular lesions

Soil is natural reservoir – inhalation of aerosolized microconidia

Endemic in eastern north America (Ohio, Mississippi, and St. Lawrence ribers)

Affects AIDS patients but not as much as the others (disseminated disease – ulceratedgranulomas of skin, bone, or other sites)

Tx: itraconazole, amphotericin B for severe disease

• YEAST (BROAD-BASED BUD)

• MOLD (w MICROCONIDIA @ 20^C)

SYSTEMIC MYCOSES

Endemic in Southwestern US and Latin America – lots in Phoenix and South Texas

Hyphae w/alternating arthrospores (soil) and spherules filled withendospores (diagnostic because it isn’t a classic yeast, in tissues)

Spherule – kind of a parasitic cycle

Inhaled

Causes coccidioidomycosis – influenza-like illness with fever, nightsweats, joint pain, dry cough, headache, and fatigue - patients maydevelop infiltrates or arthralgias;

erythema nodosum (EN) - red, tendernodules, also called "desert bumps," may occur on extensor surfaces; it isa delayed hypersensitivity reaction to fungal agents and an indicator of good prognosis; NOT specific for Coccidioides (histoplasmosis, tuberculosis, and leprosy can do the same thing)

Filipinos, African Americans, and pregnant women in 3rd trimester -higher incidence of disseminated disease

Defect in CMI predisposes

Complement-fixing antibodies are very increased in disseminated disease

Tx: amphotericin B for disseminateddisease

• SPHERULE

• ARTHROSPORES (INHALED)

SYSTEMIC MYCOSES

endemic in the soil of rural Latin America

“captain’swheel” appearance of yeast in tissue (thick wall with multiple buds)

Dimorphic

Transmission through airborne conidia

Causes paracoccidioidomycosis – ulcerations in the oral cavity and at bothangles of the lips; cough and purulent sputum; CXR shows bilateral micronodularinfiltration, some fibrosis, and a cavity in the upper right lung

Tx: itraconazole

• YEAST

OPPORTUNISTIC MYCOSES

Crushed ping-pong ball morphology

CXR: diffuse interstitial pneumonia and bilateral infiltrates with a ground glass appearance

Classified as a protozoan medically and a fungus genetically but has cholesterol (not ergosterol) in the cell membrane

Major surface glycoprotein (encoded on multiple genes) exhibits antigenic variation

Cysts are visualized with methenamine-silver, Giemsa, or fluorescent-abstaining

Causes plasma cell pneumonia – sudden onset of fever, non-productivecough, progressive dyspnea, tachypnea, and fatigue

Infection of alveoli leads to an inflammatory response with plasma cells and afrothy exudate that blocks oxygen exchange

70% of the population has been infected (mostly asymptomatic)

Found in domestic animals (horses and sheep) and rodents, but they are not areservoir

Mortality is 100% if untreated

Tx: trimethoprim and sulfamethoxazole

Px: trimethoprim-sulfamethoxazole or aerosolized pentamidine should be usedas a chemoprophylaxis in patients whose CD4 counts are below 200

OPPORTUNISTIC MYCOSES

Mucormycosis (caused by Rhizopus, Mucor, and Absidia spp.) MOLD

Fastest growing fungus – emergency surgery needed

See it in people with diabetic ketoacidosis, burns, or leukemia

Yeast: non-septate hyphae with right-angle branges and ribbon-likeappearance; mold: spores within a sporangium

Saprophytic, non-dimorphic mold, transmission is through inhalation

Invades and leaves the lungs to proliferate in the walls of blood vessels

infarction and necrosis

Chills, fever, pleuritic chest pain, bloody sputum, infiltrates on CXR; also likesthe paranasal sinuses: may get a necrotic lesion under the eye with periorbitalswelling and ptosis

Tx: amphotericin B and removal of necrotic tissue

• MOLD (CONTAINED)

• YEAST (RIGHT-ANGLE BRANCHING)

OPPORTUNISTIC MYCOSES

Aspergillus fumigatus

Find it in any decomposing plant matter; very thermophilic

Not dimorphic – only exists as a mold

Outside the body: spores form radiating columns; inside the body: septate hyphae form V- shaped branches

Risk factor – neutropenia, bone marrow transplant, cancer, and things that cause lungcavities (aerobic)

AIDS patients – don’t expect it early on, but it may happen once their lungs are damaged

Often associated with secondary colonization

Causes a variety of different things: acute invasive pulmonary aspergillosis (dry cough,dyspnea, chest pain --> fever, bloody cough), aspergilloma, acute bronchopulmonaryaspergillosis (high eosinophils)

Colonizes and invades lungs – hematogenous dissemination to organs may occur (abscessesin brain, kidney, heart, bone, and GI)

More likely to get an aspergilloma if you had a TB granuloma or sarcoidosis

Tx: amphotericin B

• MOLD (RADIATING)

• YEAST (V BRANCHES)

OPPORTUNISTIC MYCOSES

most common life-threatening fungal disease in AIDS patients

Grows in soil that contains bird (esp. pigeon) droppings – gets to human throughinhalation

Oval, budding yeast surrounded by a wide polysaccharide capsule (not dimorphic)

India ink is used to see the capsule

Forms a narrow-based bud

Colonies will be very mucoid

Cryptococcal antigen test (“crag”) – capsular antigen is detected through latexagglutination

Highly elevated “opening pressure” when you do spinal tap

It is neurotropic – brain has lots of dopamine compounds (melanin precursors), and Cryptococcus has the ability to make melanin (which functions as an electron sink)

Causes cryptococcal meningitis – fever, headache, nausea, vomiting, nuchal rigidity, and disorientation

Subcutaneous nodules may also appear in disseminated disease

Tx: combined treatment with amphotericin B and flucytosine; use fluconazole for disease suppression long-term

• YEAST (NARROW-BASED BUD)

• INDIA INK

OPPORTUNISTIC MYCOSES

Oral thrush and diaper rash (red, weeping)

Dimorphic – mold and yeast

Germ tubes form in serum at 37 degrees celsius (serves to distinguish C. albicans frommost other Candida species)

60% oral carriage, most infections are endogenous

Infections with Candida are more frequent than those of all the other fungi combined

Yeast is the form found in normal flora – hyphae = invasive phaseYeast cell = colonizersHyphae = invaders

Budding yeasts are G+ and can be seen using calcofuor

Forms chlamydospores at 37C but other spp. do not

AIDS can predispose to systemic infection (defect in T cell immunity)

Cadida glabrata may occur in organ transplants

Skin tests with Candida antigens are uniformly positive in immunocompetent adults and are used as an indicator that theperson can mount a cellular response

Tx: topical antifungals (clotrimazole or nystatin); fluconazole for oropharyngeal or esophageal thrush

• YEAST/MOLD (SABOURAUD 25^C)

• YEAST (PSEUDOHYPHAE, SEEM G+)