Micro Final Review

Microbes which can be repeatedly cultured from a given site over time

Microbes which may initially inhabit a site after exposure, but do not persist

Establishment of a microbial population in the animal host

Colonization of an animal host by a pathogen (disease implied)

Microbe capable of producing disease in a healthy human or animal host

Microbe capable of producing disease only in a host whose defenses have been compromised

Individual colonized with a pathogen, but free of disease, who is capable of acting as a source of infection for others

predominantly anaerobic

• Viridans streptococci
• (Staphylococcus aureus)

• Streptococcus mutans
• Actinomyces viscosus

• Porphyromonas gingivalis
• Prevotella melaninogenicus
• Fusobacteria
• Treponema denticola

Porphyromonas gingivalisPrevotella melaninogenicusFusobacteria

Streptococcus milleri group

Actinomyces israeli

• Induction of systemic inflammatory and immune responses
• Asymptomatic bacteremia
• Endotoxemia
• Direct role of periodontal pathogens (Oral bacteria present in atherotic plaques)

anaerobic

• Protection from pathogens
• Stimulation of gut maturation (e.g. angiogenesis)
• Stimulation of innate and adaptive immune systems

• symptoms: fishy odor (KOH test), white discharge, elevated vaginal pH
• bacterial vaginosis is the most common vaginal infection

• dominant bacteria:
• anaerobic vaginal microbiota (Prevotella, Porphyromonas, Bacteroides, Mobiluncus, many others)
• Gardnarella vaginalis
• Atobobium vaginae

absence of H2O2 –producing Lactobacillus species (L. crispatus and others)

• Nugent criteria (“gold standard”): scoring of Gram stain based on:
• 1. Absence of large Gram-positive rods (Lactobacilli)
• 2. Presence of small Gram variable coccobacilli (Gardnerella vaginalis) and Gram-negative rods (Bacteroides)
• 3. Presence of small Gram-variable curved rods (Mobiluncus)

• Amsel criteria: any 3 of the following
• 1. observation of "clue cell" on microscopic examination of vaginal smear wet mount
• 2. adherent grayish discharge
• 3. production of volatile malodorous amines on addition of KOH (whiff test)
• 4. vaginal pH > 4.5 (e.g. Femexam pH and amine test card)

• antibiotics active against microbes
• e.g. clindamycin
• e.g. metronidiazole

• intact epithelium
• phagocytic cells (neutrophils, macrophages, monocytes)
• antibacterial secretions: fatty acids (skin) (seminal fluid)
• desquamation (skin)
• lysozyme (conjunctiva)
• normal microbiota
• mucociliary clearance (respiratory epithelium)
• alveolar macrophages (respiratory epithelium)
• secretory IgA (respiratory epithelium, gut epithelium, urogenital epithelium)
• peristalsis (esophagus, intestines)
• acidity (stomach)
• urine flow
• ciliated epithelium of fallopian tubes

• The phagocytic cell - monocytes, macrophages, dendritic cells, neutrophils
• Inflammation: recruitment of opsonins, phagocytic cells to site of infection
• Complement: opsonization (most important), direct lysis (less important)
• Phagocytosis: killing of bacterial cell (oxidative processes and antibacterial peptide-mediated membrane damage); processing and presentation of bacterial antigens

• Innate Immunity
• Alternative pathway of complement fixation
• Mannan-binding lectin (MBL) pathway of complement activation
• Pattern recognition of microbial components triggers innate immune responses
• Toll-like receptor (TLR) – cell surface receptors
• Nod-like receptor (NLR) – intracellular receptors

• Acquired Immunity
• Humoral: (antibody mediated)more efficient opsonization, complement fixation; neutralization of toxins; prevention of adherence to mucosal surfaces
• Cellular: activation of monocytes/macrophages; killing of intracellular bacteria

• toxins may act locally with tissue damage
• toxins may act locally and directly affect epithelial function without tissue damage
• toxins may be disseminated with systemic effects

• non-invasive pathogens
• invasive pathogens (routes of tissue invasion; strategies against phagocytic cells)
• Mucosal Surface Colonization and Production of Toxins
• Tissue Invasion
• Penetration of intact epithelium
• Penetration of compromised epithelium (physical trauma; arthropod vector)
• Inflict damage to tissue prior to phagocytosis
• Avoid phagocytosis
• destroy phagocyte
• antiphagocytic surface properties
• inhibit phagocytic function by “injection” of effector proteins
• Survive phagocytosis (escape from phagosome, prevent lysosomal fusion, survive in phagolysosome)
• Escape from neutrophil extracellular traps (NETs) (dissolution of NETs by bacterial DNases)

Blood, throat swab, sputum, urine, STD (cervical, urethral) CSF, other body fluids (pleural, ascitic, synovial, etc.)

• Direct microscopic examination
• Direct antigenic detection techniques
• Molecular diagnosis - Nucleic acid amplification/hybridization
• Selection of appropriate media and conditions (Differential, selective media; Aerobic, microaerophilic, anaerobic incubation)
• Isolation and microscopic examination
• Antigenic tests
• Molecular analysis
• Biochemical analysis
• Serology

• N. gonorrhoeae
• Chlamydia
• Mycobacteria
• Rickettsia
• Viruses

• syphilis
• Lyme disease
• leptospirosis
• Mycoplasma pneumoniae
• Rickettsia sp.
• viral (e.g. HIV, hepatitis)

• Mycobacterium tuberculosis
• certain fungal pathogens

NO: even though they contain matter capable of self-replication (i.e. nucleic acids), viruses do not independently self-replicate

• not synthesized by mammals
• bag-shaped mesh-like structure
• surrounds cell membrane
• single cross-linked macromolecule
• provides rigidity
• glycan strings (backbone): muramic acid, glucosamine
• (tetra)peptide side chains
• inter-peptide cross-links

• Spheroplasts (partial removal)
• Protoplasts (complete removal)
• (both are stable only in highly osmotic solutions)

• Cell membrane
• + Peptidoglycan cell wall
• (+ Outer membrane)
• Anything else associated with the above

• 1. heat/dry
• 2. crystal violet stain
• 3. iodine fix
• 4. alcohol de-stain
• 5. safranin stain

• lipoteichoic acid (serves as adhesin)
• teichoic acid (defines serotype; recognized by antibodies; cell wall digestion/synthesis)

• Mycoplasma
• Chlamydia

• they are gram (+) bacteria but possess an outer cell membrane (arabinogalactan +; mycolic acid layer)
• e.g. Mycobacterium
• e.g. Nocardia

• a capsule is covalently attached and makes agar colonies appear smooth
• a slime layer (or glycocalyx) is non-covalently attached

• Bacillus
• Clostridium

• Sterilization: killing of all microorganisms in a material or on the surface of an object.
• Disinfection: reducing the number of viable microorganisms present in a sample
• Sanitization: cleaning of pathogenic microorganisms from public eating utensils and objects

• Disinfectant: a chemical or physical agent that is applied to inanimate objects to kill microbes (e.g. sink surface, dental tools)
• Antiseptic: a chemical agent that is applied to living tissue to kill microbes (e.g. skin, oropharynx, conjunctiva)

• Protein denaturation (heat; moist heat esp. for spores; alcohols, oxidizing agents, halogens
• Membrane disruption (surfactants, organic acids, alcohols, phenolics
• Nucleic acid damage (UV radiation, oxidizing agents
• Inhibition of metabolism (ionizing radiation, heavy metals, oxidizing agents, alkylating agents)

The killing of microorganisms occurs exponentially

• spores
• mycobacteria
• gram (-) bacteria
• gram (+) bacteria

increases resistance

• Plasmid-encoded resistance:
• Inactivation (enzymes, e.g. formaldehyde dehydrogenase)
• Decreased uptake (resistant LPS or porins structure)
• Efflux (pumping out)

• Mutation-acquired resistance:
• Optimizing the ways to inactivate, decrease uptake or pump out.

• Bacillus
• Haemophilus
• Neisseria
• Streptococcus
• S. pneumoniae

• adhesins, fimbriae (binding to human tissues)
• capsule (protection from immune system)
• siderophores (iron acquisition - growth rate)
• flagella (spread into new compartments)
• TOXINS (damage to human cells)

• Endotoxins – usually released by dead bacteria (LPS)
• Membrane-bound toxins - act from the bacterial surface
• Exotoxins – secreted out by live bacteria (mostly proteins)

• gram (-) bacteria only
• Salmonella
• Shigella
• Diarheal E. coli
• Yersinia
• Pseudomonas

• Staphylococcus aureus
• Enteric bacteria
• Neisseria gonorrhoeae
• Haemophilus influenzae

• Streptococcus pneumoniae
• Staphylococcus aureus (MRSA)
• Neisseria meningitidis

Pseudomonas aeruginosa

• Staphylococcus aureus
• Enteric bacteria
• Neisseria gonorrhoeae
• Haemophilus influenzae
• Pseudomonas aeruginosa
• Streptococcus pneumoniae
• Staphylococcus aureus (MRSA)
• Neisseria meningitidis

• beta lactams (e.g. penicillin, ampicillin, cephalosporins, etc.)
• glycopeptide antibiotics (vancomycin, telavancin)

vancomycin

• macrolides
• mupirocin
• linezolid
• aminoglycosides
• tetracyclines
• clindamycin
• retapamulin
• synercid

• pneumonia
• sinusitis
• Chlamydia
• atypical mycobacteria
• Toxoplasma (parasite)
• Streptococcus pneumoniae
• acne (erythromycin)

• e.g. streptomycin, gentamicin, tobramycin, neomycin
• Synergistic with ß-lactam antibiotics for serious Gram-positive infections
• Useful against Pseudomonas aeruginosa
• Inactive against anaerobes
• the most toxic of currently used antibiotics

• e.g. doxycycline, minocycline
• Effective for intracellular pathogens (e.g. Chlamydia, Rickettsia)

• quinolones: ciprofloxacin (gram (-)); levofloxacin (levaquin) (gram (+)); moxifloxacin (gram (+), gram (-) anaerobes)
• rifampin
• metronidazole

• disrupt topoisomerases and DNA gyrase of bacteria
• useful against community acquired pneumonia

quinolones

• disrupts nucleic acid synthesis: binds to bacterial RNA polymerase
• useful only in prophylaxis or in combination
• important in treatment of tuberculosis
• prophylaxis of menigococcal disease

• DNA disruption
• useful against all anaerobes
• Trichomonis vaginalis
• Entamoeba histolytica (protozoa)

Trimethoprim sulfamethoxazole

• sulfanamides
• Trimethoprim
• Trimethoprim sulfamethoxazole (Bactrim, Septra)

• ß-lactam + aminoglycoside for Pseudomonas
• Trimethoprim + sulfamethoxazole for Enterococcus

• In some cases synergy offers clear advantage.
• (ß-lactam + aminoglycoside for Pseudomonas, EnterococcusTrimethoprim + sulfamethoxazole)
• To prevent emergence of resistance by mutation (e.g. tuberculosis).
• To treat polymicrobial infections.
• In empiric therapy to cover multiple pathogens (e.g. STDs)

• Appropriate when a specific antibiotic has been demonstrated to prevent a specific infection for which there is high risk.
• Early treatment of asymptomatic infection, e.g. tuberculosis.
• Recurrent urinary tract infections.
• Prior to and following surgical procedures with high risk of infection.
• Control of outbreaks of meningococcal disease
• Travel

• Daptomycin
• Clindamycin
• Linezolid
• Tigecycline
• Synercid
• Mupirocin
• Retapamulin

• membrane depoloarization
• useful for skin and subcutaneous infections caused by Gram-positive organisms
• Staphylococcus (MRSA),
• Streptococcus,
• Entercoccus (VRE)
• Staphylococcus aureus,
• E. faecium bacteremia,
• endocarditis

• inhibits protein synthesis
• useful against community acquired MRSA, anaerobic infections

• inhibits protein synthesis
• Broadest spectrum drug available against Gram-positives
• useful against MRSA, penicillin-resistant Streptococcus pneumoniae, and vancomycin-resistant enterococci (VRE)

• arthralgia
• myalgia

• inhibits protein synthesis
• Useful for eradication of nasal carriage of MRSA
• treatment of skin infections caused by Staphylococcus aureus and Streptococcus pyogenes
• topically applied

• Isoniazid – (mycolic acid synthesis) used for treatment of active tuberculosis in combination with other drugs, and alone for chemoprophylaxis
• Pyrazinimide
• Ethambutol
• Rifampin (targets RNA polymerase)

• rifampin
• isoniazid
• resistance acquired by mutation

Used for single dose oral therapy of E. coli urinary tract infections

• Gram (+) spherical/ovoid cocci, usually in chains
• Form significant portion of normal flora
• non-spore forming
• Metabolism is anaerobic: some strict, some oxygen-tolerant
• Most species rarely cause disease

• Significant human pathogens:
• Streptococcus pyogenes (GAS, group A strep)
• Streptococcus agalactiae (GBS, group B strep)
• Viridans streptococci
• Streptococcus pneumoniae

• 1. hemolysis on blood agar (complete = beta; partial = alpha; none = gamma)
• 2. serologic properties based on cell wall polysaccharides (Lancefield groups)
• 3. biochemical/physiological properties

enterococci

• S. pyogenes (GAS)
• S. agalactiae (GBS)
• Groups C and G

• S. pneumoniae (pneumococcus)
• S. bovis (GDS)
• Groups C and G
• Viridans group
• Milleri group

• Groups C and G
• S. bovis (GDS)
• Viridans group
• Milleri group

• exudative pharyngitis
• palatal petechiae
• "beefy" red throat
• fever
• sore throat, malaise
• absence of cough
• lymphadenopathy
• lasts about 1 week

• Onset acute
• severe pain out of proportion to exam findings
• fever and chills
• Rapid progression over hours - life-threatening

• Prompt, aggressive surgical debridement of necrotic tissue
• may require plastic surgery later
• Intensive care: antibiotics, IV fluids, inotropic support

• Joint involvement: Migratory arthritis, large joints
• O (♥): Carditis - inflammation of cardiac connective tissue, enlargement, heart failure; prolonged PR interval on EKG; valvular damage
• Nodules, subcutaneous: bony surfaces, prominences
• Erythema marginatum: advance at margins, clear at center
• Sydenham’s chorea (St. Vitus’ dance): emotional lability, purposeless movements

• onset 3 weeks post pharyngitis
• recurs with repeat GAS infection
• autoimmunity due to molecular mimicry

pneumonia by S. pneumoniae

Streptococcus pneumoniae

• 1. hyaluronic acid capsule (antiphagocytic, adhesion, camoflauge)
• 2. M protein (adhesion, antiphagocytic)
• 3. lipoteichoic acid (adhesion)

• Gram-positive, non-motile, non-spore forming
• 0.5-1 μm diameter
• Lab isolates grow in clusters (staphylo = bunches of grapes) - but not always seen in clinical specimens
• Aerobes or facultative anaerobes
• Grow best on blood-enriched media
• β-hemolytic
• Grow at 18-40 C
• Can grow in 10% NaCl
• Catalase-positive; S. aureus coagulase-positive

• Coagulase positive: S. aureus
• Catalase positive: S. aureus, S. epidermidis, S. saprophyticus

• S. aureus: most virulent
• S. epidermidis: foreign body infections
• S. saprophyticus: UTI

neutralizes oxidative burst of phagocytes

converts fibrinogen to fibrin by binding prothrombin

• superantigen:
• Distinct class of bacterial (or viral) antigens that bind to MHC class II receptors in a distinctive way
• Activate T cells without processing by antigen-presenting cell
• Stimulates massive cytokine production by CD4+ cells
• resulting in toxicityIL-1:
• high feverTumor necrosis factor
• interferon gamma
• associated with staphylococci

• Pelvic syndrome: arthritis + osteomyelitis + myositis + septic thrombophlebitis + necrotizing pneumonia + sepsis
• associated with S. aureus

• Pseudomonas aeruginosa (#1)
• S. aureus

associated with IVDU

• gram (+) cocci:
• S. aureus
• S. epidermidis
• Viridans strep
• Groups C and D strep
• enterococci

• gram (-):
• Haemophilus aphrophilus
• Actinobacillus actinomycetemcomitans
• Cardibacterium hominus
• Eikenella corrodens
• Kingella kingae

other random bacteria: chlamydia, legionella, etc.

(fungi)

• Entamoeba coli (protozoan; GI tract)
• Giardia lamblia (can be commensulate or pathogenic)

Giardia lamblia

human body louse (Pediculus humanus)

Strongyloides stercoralis

• definitive host = human
• intermediate host = snail

• definitive host:
• Leishmania spp. (also reservoir host)
• Toxocara canis
• Echinococcus spp.

• incidental host:
• Trichenella spiralis (muscle)

• carrier host:
• Cutaneous Larva migrans

malaria vector = female anopheles mosquito = biological vector

Entamoeba histolytica vector = housefly = mechanical vector

• Giardia
• Entamoeba histolytica
• Toxoplasma
• Cryptosporidia
• Cestodes
• some Nematodes
• Trematodes (except Schistosomes)
• Taenia solium (cystercerci in measly pork)

• Malaria
• Babesia
• Filaria
• Leishmania
• Trypanosomes

• Hookworm
• Strongyloides
• Schistosomes (Cercaria)

Trichomonas

• Anasakiasis
• schistosome cercariae
• hookworms

Entamoeba histolytica

• African Trypanosomes
• malaria

Trypanosomes

• Ascaris (appendix)
• tapeworms
• schistosomes
• filaria

• Echinococcus spp. (liver)
• Cysticerci (measley pork)

Helminth larvae (Toxocariasis)

helminthic infections

Trypanosoma cruzi

• malaria
• schistosomiasis

• leishmania
• schistosomiasis

• Antigenic Variation: African trypanosomes, malaria
• Molecular Mimicry: trypanosomes, schistosomes
• Concealment of antigens: schistosomes, hydatid cyst
• Intracellular location: malaria, toxoplasma, leishmania, Trypanosoma cruzi
• Immunosuppression: trypanosomes, malaria

• malaria kills the most people every year
• common mechanisms: anemia, immune system evasion

• immune system evasion: constant rearrangment of PfEMPs on infected RBC
• partial immunity: PfEMP antibodies; G6PD deficiency; no Duffy-blood (FyFy) markers; sickle-cell trait

• Toxoplasma gondii causes the most common protozoan infection (toxoplasmosis) world-wide
• acquisition: (feline) fecal oocysts; oocysts in raw meat (lamb, pork, some beef); transplacental
• pathogenicity: fecal/tissue oocysts --> trophozoites --> disemmination: lympthadenopathy, inflammation

• microspora
• Coccidia:
• Cyclospora
• Crytposporidium
• Isospora belli

• Apicomplexa
• Coccidia

• Plasmodia
• Toxoplasmodia
• Cryptosporidia
• Isospora
• Cyclospora

• Plasmodium falciparum: causes most fatalities, drug resistance common, predominant in tropics
• Plasmodium vivax: relapsing, common in subtropics and temperate
• Plasmodium ovale: relapsing, found in W. Africa
• Plasmodium malaria: uncommon, temperate or subtropics
• Plasmodium knowlesi: primate malaria in SE Asia (Malaysia), now in humans, appearance like P. malaria, but more serious/fatal

• P. falciparum: rings in early trophozoite; high parasitimia; banana gametocyte
• P. vivax: rings and schizont; no need for Duffy-blood; hypnozoites
• P. ovale: lots of merozoites in late trophozoite; no need for Duffy-blood; hypnozoites
• P. malaria: line through cell; rosette schizont
• P. knowlesi: primate malaria --> human (severe) malaria

• P. vivax, P. ovale: reticulocytes
• P. malaria: senescent cells
• P. falciparum: all stages

Cryptosporidium

• Cyclospora cayatanensis
• Cryptosporidium (superficial parasitopherous)

• coccidia that infect upper small bowel
• cause diarrhea
• oocysts in stool (AFS)

Entamoeba histolytica

Acanthameba

Naeglaria fowleri

Trichomonas vaginalis

• same host: Toxoplasma gondii; Isospora spp.
• different host: Plasmodium spp.

• a. Trichomonas vaginalis
• b. Direct (venereal) spread
• c. Trophozoite infective agent
• d. Worldwide

• a. Entamoeba histolytica, Giardia lamblia, Balantidium coli
• b. Indirect (fecal-oral) spread
• c. Cyst infective agent
• d. Found in areas of poor sanitation

• a. Plasmodium sp., Trypanosoma sp., Leishmania sp.
• b. Arthropod vector
• c. Tropical and subtropical areas

• proteases
• amoeba pores
• phospholipases
• release of toxic PMN contents

Galactose-inhibitable adherence protein (GIAP lectin)

• Luminal Flagellates:
• Trichomonas vaginalis
• Giardia lamblia

• Hemoflagellates (Trypanosomatids):
• Trypanosoma brucei (African trypanosomiasis)
• Trypanosoma cruzi (American trypanosomiasis)
• Leishmania spp

• encephalitis in normal hosts: Naeglaria fowleri
• encephalitis in immunocompromised: Acanthameba

filtration

Balantidium coli

presence of GIAP lectin

L. braziliensis

• Leishmania vector = sandfly
• T. cruzi vector = reduviid bug
• T. brucei vector = tsetse fly

T. cruzi: transmitted by vector's urine/feces contaminating a wound/mucosa (not direct infection by bite)

Chiga's disease (Trypanosoma cruzi infection)

Trypanosoma brucei (rhodesiense, gambiense)

visceral: L. donovani

• cutaneous:
• L. tropica
• L. major
• L. mexicana
• L. braziliensis

• mucosal:
• L. braziliensis

• Blood Trematodes (Blood Flukes):
• Schistosoma spp.

• Tissue Trematodes (Tissue Flukes):
• Paragonimus spp. - lung
• Clonorchis/Opisthorchis spp. - liver
• Fasciola spp. - liver

• Intestinal Trematodes (Intestinal Flukes):
• Fasciolopsis spp.

• Schistosoma mansoni
• Schistosoma haematobium
• Schistosoma japonicum
• (S. mekongi [SE Asia], S. intercalatum [C&W Africa])

• Schistosoma dermititis
• reservoir host = water fowl, migratory birds, muskrats
• (other hosts: snails, humans)

• Africa, S. America; ova large lateral spine
• Infects inferior mesenteric vein, perirectal area
• Colitis, liver disease (pipestem fibrosis), all above

• Africa, Middle East; ova terminal spine
• Infects peri-vesicular (around bladder) veins
• Bladder damage, obstruction, bleeding, bladder transitional cell cancer

• Asia; produces most ova, diminutive lateral spine; water buffalo reservoir host
• Infects superior mesententeric veins, small bowel

• Eosinophilia
• serology
• ova in biopsies or stool (mansoni or japonicum) or urine (haematobium)

• Schistosomiasis
• Clinical: Early: ‘swimmers itch’; 6 weeks: Katayama fever @ oviposition (serum sickness/allergic); Late: bowel, bladder damage, liver disease (eggs swept to liver, pipestem fibrosis), portal hypertension, hepatosplenomegaly, GI bleeds, pulmonary fibrosis and pulm. hypertension, rarely perispinous vein infection gives transverse myelitis and LE paralysis

Schistosomas

Schistomiasis mansoni

Schistosomiasis haematobium

Clonorchis sinensis (clonorchiasis)

Paragonimus spp.

• bees: lose their venom apparatus in act of stinging then die
• wasps: can sting repeatedly without dying, also can bite

• Black widow sting: neurotoxic venom
• Hobo (recluse) spider sting: necrotic venom

mites (Scabies: Sarcoptes scabei, Chigger: Tunga penetrans)

lice

• Dermatobium hominis
• Cordylobia anthropophaga (Tumbu fly)

• tsetse fly: Trypanosoma brucei (African Sleeping Sickness)
• mosquito: Malaria, lymphatic filariasis, yellow fever, dengue fever, numerous other viruses (JEV, EEV, VEV, etc)
• reduviid bug: Chiga's disease (T. cruzi)
• Lutzomyi phlebotomine fly: leishmaniasis, bartonellosis, viruses
• simulian (deer) fly: loiasis
• louse: relapsing fever, ricketsial disease
• Ioxodes (soft) tick: Lyme disease, babesiosis, anaplasmosis (HGA)
• Hard tick: RMSF, ehrlichiosis (HME), colorado tick fever
• flea: Yersinia Pestis

• Hard ticks: RMSF, (HME) ehrlichiosis, colorado tick fever
• Soft ticks (Ornithodorus): relapsing fever

• by increased blood supply
• increased capillary permeability
• leukocyte ingress
• hypersensitivity reactions: immediate or delayed
• neurotoxic venoms (e.g. Widow spiders [Latrodectus spp.] and scorpions)
• necrotic venoms (e.g. recluse and hobo spiders)

• bees
• wasps, hornets, yellow jackets
• stinging fire ants (S.E. USA)
• harvester ants (W. USA)

pruritis ani: Enterobius Infections: Enterobius vermicularis (Pinworms)

(larva currens: Strongyloides stercoralis)

• Trichuris trichuria, whipworm, small nematodes, widespread in warm places, disproportionately affect children
• Transmitted through fecal contamination of ova in soil, 1-3 week embryonation period required, then contamination of food or water
• Clinical: generally symptomatic only in children, then abd pain, diarrhea, rectal prolapse
• Therapy: albendazole, mebendazole

• Necator americanus, Ancylostoma duodenale:
• Infection by larvae penetrating skin in fecally contaminated areas, warm, poor-sanitation
• Pass through lungs (loeffler’s pneumonia) and move to small bowel where attach and suck blood
• Clinical:Anemia (iron-deficiency)
• Less common: abd pain, protein loss
• Diagnosis: O&P of stool: ova 40x80 uM, thin shell, 2-4 cells
• Therapy: albendazole, mebendazole, pyrantel pamoate

DRACUNCULIASIS (Guinea Worm Infection): Dracunculus medinensis


(hookworm: causes iron deficiency anemia)

• Trichuriasis
• Trichuris trichuria (whipworm)

• Trichinella spiralis:
• Acquired by eating undercooked meat of carnivores (in past, pigs, recently bear/cougars)
• Clinical: Replicate in intestine, sometimes GI symptoms
• Release larvae that disseminate to muscles, causing edema (periorbital), myalgias, encephalitis, eosinophilia about 1-3 wks after ingestion
• Diagnosis: eosinophilia, serology, muscle bx.
• Treatment: Steroids for severe symptoms; Mebendazole, Albendazole (esp. if still in intestinal phase)

Ascaris lumbricoides

• Ascaris lumbricoides
• Ascaris suum

Hookworms (Ancylostoma duodenale, Necator americanus, A. ceylanicum)

Strongyloides stercoralis

Toxocara canis or T. cati

Strongyloidiasis (rhabditiform larvae)

• Strongyloides stercoralis:
• Found in warm, poor-sanitation areasAcquired by penetration of filariform larvae from fecally-contaminated soil
• Larvae pass through to lungs, breakout, up trachea and swallowed into small bowel where 1-2 mm adults find each other and start producing rhabditiform larvae, small % autoinfect making infection persistent for decades
• Clinical: Early: rarely ground-itch at penetration and loeffler’s
• Later: Abdominal discomfort, skin manifestations (hives, etc), larva currens (track like movement that may start in peri-rectal region
• Immunocompromised: hyperinfection syndrome, fever, pulmonary infiltrates, sepsis (often polymicrobial) due to increased invasion of larvae
• Diagnosis: rhaditiform larvae in stool, filariform larvae in sputum in hyperinfection, eosinophilia unless steroids/cytotoxic agents given, serology
• Therapy: Ivermectin, Albendazole

Strongyloidiasis (rhabditiform larvae)

• hookworms:
• Ancylostoma duodenale
• Necator americanus
• A. ceylanicum

• Toxocara canis & cati:
• Caused by accidental ingestion of ova from dog and cat ascariids in fecally contaminated soil (e.g. sandbox ingestion)
• Larvae migrate in tissues, without proper development, causing eosinophilic inflammation
• Clinical:
• Visceral (Age 1-4)Fever, enlarged liver and spleen, skin rash, pneumonia, convulsions, neurologic defects
• Ocular (Age 7-8)Exudative endopthalmitis, mimics retinoblastoma
• Diagnosis: eosinophilia, serology, occ. Biopsies
• Therapy: Albendazole + corticosteroids

Toxocara canis & cati

• Ancylostoma braziliense:
• Caused by dog and cat hookworm larvae
• Humans carrier host (carry larvae without further development)
• Filariform larvae penetrates skin and crawls, leaving red linear rash
• Skin exposure in warm damp areas where pet feces soil environment, e.g. beach in Jamaica, crawling under houses in Fl.
• Diagnostic: no specific diagnosticTherapy: Ivermectin, albendazole

• Onchocerciasis (river blindness): Onchocerca volvulus
• Vector: blackflies (Simulium spp.): Africa, C/S America
• Eosinophilia, nodules, skin changes, microfilariae in eye and skin, blindness
• Dx: skin snips, serology, Mazzotti reaction
• Rx: ivermectin every six months

• Lymphatic filariasis (elephantiasis): Wucheria & Brugia
• Vector: mosquitos (often night biting): much of the tropics
• Clinical: nocturnal fevers, pulmonary symptoms, retrograde lymphangitis, lymphedema
• Dx: blood microfilaria at night or after DEC
• Rx: diethylcarbamazipine

• Loaiasis: Loa loa
• Transmitted by deer flies (Chrysops): West Africa ONLY
• Conjunctival or dermal migration (Calabar Swellings)
• Dx: demonstration of worm or serology
• Rx: diethylcarbamazipine

Onchocerciasis (filariasis)

Filariasis: onchocerciasis (river blindness)

Filariasis (lymphatic): Wucheria bancrofti

Anisakiasis (nematode)

(Diphyllobothriasis (tapeworm); Nanophyetiasis (trematode))

• nematodes (round worm)
• cestodes (tapeworms)
• trematodes (flukes)

Filariasis: Loaiasis

Intestinal Nematodes: Presence of the adult worm in intestine responsible for major disease manifestation(s)

Tissue Nematodes: Produce disease by migration of larvae or adult worms through tissues of definitive host

• Pinworms (Enterobius vermicularis): 1-2 mm nematodes, worldwide, esp. children, oral-fecal transmission
• Auto-reinfection and group infections common
• Clinical: Pruritis ani
• Diagnosis: perirectal cellophane tape test in AM
• Therapy: Albendazole, Mebendazole, Pyrantel pamoate

• Ascaris lumbricoides, transmitted by fecal ova, embryonated in soil >3 wks, contaminating food or water, large nematode adults (15-40 cm)
• Larvae from ova hatch in intestine, move through circulation to lungs, break into alveolae, crawl up to trachea, swallowed back down and 2 mos after infection adults reside in upper intestine by muscular force (6-18 mo life span)
• Clinical: Early: loeffler’s eosinophilic pneumonia; Later: abdominal pain, worm obstruction of orifice
• Diagnosis: ova (mammilated) in stool, adult worm passed
• Therapy: Albendaole