Listeria monocytogenes 

(morphology and physiology)

• Gram+ rod
• non-spore-forming
• catalase +
• facultative anaerobe
• live in refrigerator (4C), low pH, high salt
• Motile
• weak beta-hemolysis 
• esculin hodrolysis +

Neisseria meningitidis

(morphology/physiology)

• Gram-, diplococci
• catalase +
• oxidase +
• aerobic
• oxidizes maltose and glucose (acid as byproduct)
• fastidious growth requirement, can grow on chocolate agar at 37C)
• Nonmotile

Mycobacterium leprae 

(morphology/physiology)

• Gram+ (weakly), bacillus
• lipid-rich cell wall makes it acid-fast
• colonies are non-pigmented or tan
• Acid-fast
• nonmotile 
• takes a long time to grow
• in armadillos
• impossible to grow on artificial medium

Naegleria fowleri 

(morphology)

• amoeba (a parasite)

Acanthamoeba castellani

(morphology)

• amoeba (parasite)

Toxoplasma gondii

(morphology)

• spoozoa (parasite)

Trypanosoma brucei gambiense 

(morphology)

• Hemoflagellate
• Trypomastigote (stage with free flagellum and an undulating membrane for locomotion)
• Epimastigote (stage with free flagellum and partial undulating membrane
• VSPs (variant surface proteins) for antigenic diversity 

Trypansonoma brucei rhodesiense 

(morphology)

• Hemoflagellate
• Trypomastigote (free flagellum, undulating membrane for locomotion)
• Epimastigote (free flagellum, partial undulating membrane)

Trypanosoma cruzi

(morphology)

• Hemoflagellate
• Trupomastigote
• Amastigote (no flagellum, no undulating membrane; found in tissues so is intracellular; is an oval)

Listeria monocytogenes

(epidemiology)

• 1/2 a serotype, 1/2 b serotype, 4b serotype
• 4b serotype caues most food-bourne outbreaks
• lives in feces of mammals, bids, fish, insects

Neisseria meningitidis

(epidemiology)

• Humans are only host
• spread by respiratory droplets
• worldwide, most common in children >5, in immunocompromised (complement deficiencies), and ppl living in close quarters 
• meningitis and meningococcemia serotypes: B, C, Y (seen in US)
• neuromonio serotypes: Y and W135
• in underdeveloped countries see serotypes: A, W135
• meningococcal pneumonia serotype: Y, W135

Mycobacterium leprae

(epidemiology)

• shed in mucous nasal secretions, in open sores
• small kids get it when around other infected kids for a long time
• incubation period = 2-10 years (up to 20)
• Tuberculoid leprosy: more common in US than lepromatous lepracy, lepromin+ (T cells operate hypersensitivity rxn)
• Lepromatous lepracy: endemic to armadillos in TX and LA, common in Asia, lepromin-, infect schwann cells, antibody/humoral response

Naegiera fowleri

(epidemiology)

• Same as for Acanthamoeba catellanii
• Free-living amoeba in soil and contaminated water 
• get after pt swims in warm-water (pond, river)
• get from contaminated contact lenses

Acanthamoeba castellanii 

(epidemiology

• Same as for Naegieria fowleri
• free-living amoeba in soil, contaminated water
• get after swimming in warm water (rivers. ponds)
• get from contaminated contact lenses

Toxoplama gondii

(epidemiology)

• birds, other animals
• mainly cats, other felines
• humans = intermediate hosts where only sexual reproduction occurs

Trypanosoma brucei gambiense

(epidemiology)

• West and central africa
• causes African trypanosomiasis (sleeping sickness)
• carried by Tsetse fly 

Trypanosoma brucei rhodesiense

(epidemiology)

• East africa
• causes African trypanosomiasis (sleeping sickness like trypanosoma brucei gambiense)
• carried by sheep and cattle 

Trypanosoma cruzi

(epidemiology)

• American trypanosomiasis (Chagas' disease)
• carried by Reduviids (kissing bugs)

Listeria monocytogenesme

(pathogenesis)

• enters via GI (stress response genes protect it bacteria from stomach acids)-->
• Ami, Fbp, flagellin adhesion proteins &
• Internalin A binds receptor E cadherin--> phagocytosis-->
• low pH in phagosome-->activate lysteriolysin O and Phospholipase C-->bacteria escapes to cytosol
• Act A rearranges host cell actin-->create filopods-->move now replicated bacteria to membrane of protrustions-->filopods eaten by macros-->spread
• see siderophores that steal Fe from transferrin
• prFA: protein regulatory factor; require cell-mediated immunity

Neisseria meningitidis

(pathogenesis)

• polysaccharide capsule = major virulence factor
• Bacterium pili extend through outer capsule--> adhesion to non-ciliated epithelial cells and protection from neutrophils and gene transfer (form pilins for gene transfer)
• PilC protein is on the C' of pilins & contributes to antigenic diversity 
• PorB (porin) inhibits phagosome fusion and inhibits degranulation of neutrophils; helps bacteria, enter host cells, and confers resistance to complement
• Bind serum transferrin to get Fe (does not make siderophores)
• Cell wall has lipooligosaccharides (LOS); lacks the O-portion; Lipid A portion confers endotoxicity; blebs outer membrane (vascular damage)
• Ig A1 protease; Opa(cell-cell signal); Rmp(stimulate antibodies) 

Mycobacterium leprae

(pathogenesis)

• Lipid-rich cell wall-->gives resistance to detergence, antibiotics, tendency to form granulomata
• Lipoarabinomannan (LAM) is similar to O-antigenic of LPS; acts as endotoxin
• Neurological deficits caused by nerve thickening-->anethesia, neuritis, parasthesia, trophic ucers, bone resorption, shortening of digits 
• Pigmented mycobacterium produce           O-diphenoloxidase

Naegleria fowleri

(pathogenesis)

• enter via nasal mucosa-->olfactory receptors-->through cribriform plate of ethmoid bone--> into basilar portions of the cerebrum--> cerebellum
• forms nests, which cause hemorrhaging and other damage 
• GETS INTO CNS

Acanthamoeba castellanii

(pathogenesis)

• enter via nasal mucosa
• traumatic skin puncture-->enters 
• or through eye by contaminated soil/dust
• or through previous injury (keratitis)
• invades CNS and will form a granulomata 
• GETS INTO CNS

Toxoplasma gondii

(pathogenesis)

• only reproduce sexually in cats; asexual in humans
• sporozoites from oocysts or bradyzoites from tissue cysts ingested by cat-->mucosal cells in cat--> gametocytes (sexual)-->sexual fusion of schizonts into oocysts -->into gut lumen --pass via feces--> human ingestion (or ingested by cat again and above cycle occurs again)-->asexual cycle--> oocyst opens in duodenum-->sporozoites released, infect macrophages and form trophozoites --> break out and infect lymph nodes-->become tachyzoites (acute phase) that penetrate nerve cells OR bradyzoites that form cysts (chronic stage) 

Trypanosoma brucei gambiense

(pathogenecity)

• trypomastigote has fine flagellum and undulating membrane 
• trypomastigotes injected when tsetse bites (parasite held in salivary glands)-->move into blood, lymph and--> replicate by binary or longitudinal fission in blood, lymph, spinal fluid --> still called trypomastigotes here (still infective for tsetse fly)
• tsetse fly injest trypomastigotes when bite human-->parasite to salivary glands of tsetse-->replicates as epimastigote-->fly becomes infectious to humans in 4-6weeks

Trypanosoma brucei rhodesiense

(pathogenecity) 

• similar to gabiesense
• exceptions: vectors are sheep and cattle, not tsetse flies --> more difficult to control 
• shorter incubation period
• develops in greater numbers in blood
• lymphadenopathy uncommon 

Trypanosoma cruzi 

(pathogenecity)

• Unique: has extra stage in life cycle, the amastigote. has flagellum or undulating membrane that is oval (not crescent shape)
• Kissing bug bites and defecates the trypomastigote into human-->to cardiac muscle, liver, brain--> penetrate host cells-->become amastigotes--> replicate by binary fission intracellularly -->destroy host cells-->amastigotes infect more cells or infect Reduviid (kissing bug) as trypomastigotes
• bug ingests trypomastigotes and becomes epimastigotes (becomes infectious trypomastigote in salivary gland) when bite humans-->parasite moves to midgut-->replicates by longitudinal binary fission--> moves to hindgut-->becomes a metacyclic trypomastigote-->bug defecates into bit wounds-->perpetuates cycle 

Listeria monocytogenesme

(Immunity)

• immunity is cell-mediated, hence increased prevalence of disease in immunocompromised

Listeria monocytogenesme

(natural course/clinical presentation)

• Early onset (granulomatosis infantiseptica): in utero infection causes infant sepsis, pustular lesions and granulomata in multiple organs
• Granulomatatosis infantiseptica 
• Late onset: causes meningitis between brith and third week (4b serotype)
• Adults Meningitis listeria meningoencephalitis: common in immunocompromised. febrile gastroenteritis, fever, headache, myalgia, abdominal pain, diarrhea. Self-limiting. 
• Adult treatment: treat with ampicillin or penicillin + gentamycin 

Neisseria meningitidis

(natural course/clinical presentation)

• Meningitis: abrupt headaches, fever, meningeal signs, sometimes vomiting
• Meningococcemia: thrombosis of small vessels -->petechiae, multiorgan involvement. Petechiae can join to form hemorrhagic lesions
• Waterhouse-Friderichsen Syndrome=DIC and bilateral destruction of the adrenal glands
• Pneumonia: cough, chills, chest pain, rales, fever
• Treatment: penicillin or vancomycin + 3rd generation cephalosporin, or ampicillin +/- gentamycin; if neurolgic sequelae, posible hearing loss and arthritis 

Mycobacterium leprae

(natural course/clinical presentation)

• Lepromatous (multibacilary) leprosy: immune response through Ab serotype. Ineffective against cell wall. Large numbers of organisms in skin, macrophages, schwann cells. skin infiltrated with Suppressor T cells. Lipromin-
• Tuberculoid (pauciba cillary) leprosy = strong cellular immune rxn: many lymphocytes in tissues with few bacteria, macular skin lesions (granulomata) and asymmetric severe nerve involvement, lipromin+
• all leprosy cases: macular/nodular anesthetic lesions, may be pale/erythematous. involve skin, superficial nerves, nose, eyes, larynx, pharynx, testicles 
• attacks cooler areas of the body; find in armadillos 

Naegleria fowleri

(natural course/clinical presentation)

• primary amoebic meningocephalitis (PAM): incubation 1-14 days, quick death after coma within 1 week. 
• Presents with fever, frontal headaches, nausea, fatigue, rhinitis, loss sense of smell, kernig sign, vomiting, disorientation.
• only see trophozoites in tissue during infection (no cysts)  
• Treatment: unresponsive but try amphotericin B, miconazole, and rifampin

Acanthamoeba castellanii

(natural course, clinical presentation)

• Granulomatous amoebic encephalitis (GAE): incubate weeks to months. slower onset than PAM
• get a disseminated subcutaneous nodular infection of the skin; occur in immunocompromised 
• See trophozoites and cysts in infected tissue
• Treatment: amoebic meningitis is unresponsive to treatment; try pentamidine, ketoconazole, flucytosine
• keratitis and cutanous infection treated with tropical miconazole, chlorhexidine, gluconateor, proamidine, isoethionate

Toxoplasma gondii

(natural course/clinical presentation)

• Prenatal Toxoplasmosis: mother infected for first time during pregnancy; effect is worse earlier in course of pregnancy. Congenital infection -->stillbirth (see horioretinitis, intracerebral calcifications, hydrocephalus, microcephaly, psychomotor disturbances and blindness)
• Postnatal toxoplasmosis: less severe unless in immunocompromised patient (see retinitis, chorioretinitis, encephalitis and pneumonitis. In healthy patients, get mono-like symptoms with ruptured cysts and release of bradyzoites (hypersensitivity reaction) and cell death in that area.)

Trypanosoma brucei gambiense

(natural course/clinical representation)

• No animal reservoir! VSPs for antigenic diversity 
• Gambian Sleeping Sickness: incubation in days to weeks. Chronic disease; usually fatal after years of CNS involvement. Ulcer at site of bite can indicate infection. 
• Also see: fever, myalgia, arthralgia, lymphadema (especially in posterior cervical lymph nodes = Winterbottom sign).
• Acute phase: hyperactivity
• Progresses to lethargy, tremors, meningoencephalitis, mental retardation, convulsions, hemiplegia, incontinence, death
• Treatment: suramin and pentanamide for acute phase (don't cross BBB so later phases give melarsoprol); can give difluoromethylornithine as cytostatic in acute and late stages 

Trypanosoma brucei rhodesiense

(natural course/clinical presentation)

• incubation faster than gambiense; develop fatal disease in 9-12 mo
• Symptoms: shorter incubation period and acute symptoms similar to gambisense but no lymphadenopathy
• Disease moves to CNS more quickly than gambisense 
• Kidney damage and myocarditis contribute to mortality. 
• Larger quantities of organisms in blood and CSF
• Treatment: same as for gambisense; suramin and pentanamide for acute phase (don't cross BBB so later phases give melarsoprol); can give difluoromethylornithine as cytostatic in acute and late stages 

Trypanosoma cruzi

(natural course/clinical presentation)

• Chagas' Disease: asymptomatic, acute (fever, chills, myalgia, fatigue) or chronic (proliferate to liver, heart, CNS)
• Early sign is an erythematous indurated Chagoma at bite-->then get rash and edema around mouth and eyes (Romana's sign)
• Chronic disease often show hepatosplenomegaly, myocarditis, enlargement of esophagus and colon due to nerve destruction, megacardia with electrocardiographic charge, granulomata in brain and meningoencephalitis; severe in kids < 5yo with no CNS
• Treatment: nifurtimox against acute phase (not effective for amastigotes)

• 2 forms of the disease:

1. African Trypanosomiasis (Sleeping Sickness); this is from T. brucei gambiense and T. brucei rhodesiense. Transmitted by Tsetse fly
2. American Trypanosomiasis (Chagas' disease): produced by T. cruzi. Transmitted by kissing bugs

Listeria Monocytogenes

(Diagnosis)

• CAMP test: increased hemolysis when grown next to beta-hemolytic staph aureus 
• No organisms in CSF
• Tumbling motility at 22-28C
• On 5% Sheep Blood Agar, show clear zone of hemolysis (hemolysin)
• Grow at colder temperatures "cold-enriched"
• Gram stain not helpful

Neisseria meningitidis

(diagnosis)

• Gram stain with CSF to detect meningitis (are gram-)
• Few organisms in blood (no real septicemia)

Mycobacterium leprae

(diagnosis)

• Biopsy from earlobe and stain with Ziehl-Neelsen Technique
• for Lepromatous, microscopy sufficient for diagnosis
• Negative lepromin tuberculoid: skin testing
• Positive lepromin M. leprae will not grow in culture
• Do acid fast
• Unique O-diphenoloxidase
• Impossible to grow in artificial medium 

Naegleria fowleri

(diagnosis)

• Similar to Acanthamoeba castellanii
• Collect CSF and nasal discharge
• CSF=purulent, some motile amoeboid trophozoites
• culture on agar plates seeded with G-enteric bacteria for nutrition source
• Must be grown on agar with gram- food source

Acanthamoeba castellanii

(diagnosis)

• similar to naegleria fowleri
• collect CSF, corneal scrapings
• Sterile tissues may contain amoebic cysts or trophozoites = diagnostic!
• culture on plate with gram- bacteria for food 

Toxoplasma gondii

(diagnosis)

• serologic screening for IgG and IgM
• look for T. gondii serologic profile (TSP)
• No detection of T. gondii specific for IgG, so if have this type then test will be negative unless patient is immunocompromised; if this is the case, use PCR
• Congenital infection: diagnose through ultrasound and amniocentesis then PCR

Trypanosoma Brucei gambiense

(diagnosis)

• seen microscopically in blood, lymph, CSF
• fix and stain samples immediately before organism degenerates
• Then do immunofluorescence, agglutination, precipitin, ELISA

Trypanosoma brucei rhodesiense

(diagnosis)

• Seen in CSF and blood
• Limited serological testing 

Trypanosoma cruzi 

(diagnosis)

• Chagas': seen in blood, lymph, or CNS early in acute phase
• Biopsy of lymph nodes, liver, spleen, or marrow may show amastigotes (only one of our bugs with amastigote stage)
• No serological tests
• Xenodiagnostics can be used 

• listeria monocytogenes (gram+): granulomatosis infantiseptica, adult meningitis, early and late onset; forms siderophores; CAMP test
• neisseria meningitidis (gram-):meningitis and meningococcocemia; binds host transferrin; has LOS
• Mycobacterium leprae (don't gram stain b/c of lipid wall):Tuberculoid leprosy and Lepromatons leprosy; in armadillos, can't grow on artificial medium; has o-diphenoloxidans

• Acarthamoeba:granulomatous amoeba encephalitis, eyes and skin infection; contact lenses; trophozoites and cysts found; need gram-
• Naegleria fowler: amoebia meningoencephalitis; trophozoites found; need gram-
• Toxoplasma gondii: prenatal and postnatal toxoplasmosis; humans as intermediate host with sexual reproduction here; feline host
• T. brucei gambiense:Gambian Sleeping sickness; Winterbottom sign in cervical lymph node;no animal reservoire; west, central africa
• T. brucei rhodesiense: African Trympanosomiasis; faster onset, reservoir host in cattle, sheep; lymphadenopathy uncommon; east africa
• T. cruzi: American Trympanosomiasis (Chagas' disease); kissing bugs; South and central america; chagma, roman sign; megacardio; amastigotes