-ssRNA or -dsDNA virus must carry a RNA-dependent RNA polymerase

associated with or within capsid

a) Attachment (basis of specificity)

b) Penetration (receptor-mediated endocytosis and membrane fusion)

c) Uncoating (location and mechanism)

d) Replication (location of viral protein and of viral nucleic acid biosynthesis)

e) Assembly (location)

f) Release (cell lysis vs budding)

(most replicate within nucleus, synthesize early and late mRNAs, and encode a DNA-dependent DNA polymerase, but not a DNA-dependent RNA

polymerase). Notable exceptions on next slide

i) Papillomaviruses and Polyomaviruses - does not encode a viral DNA-dependent DNA

polymerase

ii) Parvoviruses - does not encode a viral DNA-dependent DNA polymerase; no temporal

control of translation of viral proteins

iii) Poxviruses - core contains a DNA-dependent RNA polymerase, replicates within core and in

cytoplasm

iv) Adenoviruses - no exceptions

v) Herpesviruses - encodes a thymidine kinase, three classes of RNA transcripts - alpha, beta

and gamma transcripts.

vi) Hepadnaviruses - replicates in cytoplasm, contains a reverse transcriptase, DNA genome is

replicated via a RNA intermediate, DNA replication occurs within cores, no temporal

control of translation of viral proteins.

i) Double-stranded RNA viruses - early and late transcripts, replication of genome occurs

within cores using positive-strand RNA as template.

ii) Positive-stranded viruses - genome is synthesized using negative strand viral RNA as a

template; translation results in polyproteins which are cleaved to form RNA polymerases

and viral proteases. Togaviruses synthesize early and late RNA transcripts.

iii) Negative-stranded viruses - nucleocapsid contains a RNA-dependent RNA polymerase

which synthesizes a positive strand RNA for translation and as a template for synthesis of

genome. Orthomyxoviral genomes replicate in nucleus using cellular RNA as primer and

virions assemble in cytoplasm

iv) Retroviruses - nucleocapsid contains a RNA-dependent DNA polymerase and an integrase.

The virion RNA is a template for the synthesis of a DNA copy. The viral double-stranded

DNA integrates into the host's chromosome. Transcription of the integrated viral DNA

results in viral RNA that serves as progeny genomes and is used for translation. Viral

polyproteins are cleaved by viral proteases to form virion proteins including the RNAdependent

DNA polymerase and integrase.

(1) Encoded by cellular gene

(2) Transcription occurs upon viral infection, associated with viral nucleic acid replication

(3) Binds to specific receptor proteins on cell membrane, accounting for species specificity

(4) Induction of interferon-inducible proteins by signal transduction and phosphorylation of

cellular transcription factors

(5) Activation and functioning of the interferon inducible enzymes requires viral doublestranded

RNA and ATP

(6) Functions of interferon-inducible 2'-5' adenylate synthetase and of the interferon

inducible protein kinase

Anti-viral inhibits polymerase activity by causing chain termination; nucleoside analog

(derivatives of acyclovir include valacyclovir, penciclovir, famciclovir)

(i) Specifically phosphorylated by herpesvirus thymidine kinase.

(ii) Preferentially inhibits herpesviral DNA-dependent DNA polymerase

nucleoside analog anti-viral inhibits viral polymerase activity by causing chain termination

(i) Used in treatment of cytomegaloviral retinitis in AIDS patients. Specific

inhibition of viral DDDP

(ii)Phosphorylated by CMV protein kinase homologue, then to the triphosphate

form by cellular kinases

anti-viral nucleoside analog inhibits viral polymerase by causing chain termination

(i) Phosphorylated by cellular enzymes

(ii)Inhibits HIV reverse transcriptase

(iii) Other nucleoside analogs that inhibit HIV reverse transcriptase (and in some

cases HBV): dideoxyinosine, dideoxycytidine, lamivudine, emtricitabine, adefovir

nucleoside analog anti-viral inhibits viral polymerase via chain termination

(e.g. cidofovir for CMV, tenofovir for HIV and HBV)

nucleoside analog anti-viral inhibits viral polymerase via chain termination

(i) Phosphorylated by cellular enzymes and inhibits HBV DNA polymerase (for

chronic HBV infection

Causes errors in replication and transcription; nucleoside analog anti-viral

 - inhibits respiratory synctial virus; also inhibits nucleoside biosynthesis

and formation of the mRNA 5' guanosine cap

Trifluridine (trifluorothymidine, TFT)

or Idoxyuridine

nucleoside analog anti-virral causes error in replication and transcription

 thymidine analog, phosphorylated by

cellular enzymes, topical administration

(1) Foscarnet - Binds to the pyrophosphate binding site of the herpesvirus DNA polymerase

and inhibits the viral DNA polymerase activity. Does not require phosphorylation to be

active. Treatment of CMV retinitis in AIDS patients.

(2) Efavirenz, nevirapine, and delavirdine - noncompetitively inhibits HIV-1 reverse

transciptase by binding to the enzyme; does not require phosphorylation to be active

Protease Inhibitors (e.g. saquinavir, indinavir, nelfinavir, ritinavir) - Binds to active site of

the HIV protease inhibiting the cleavage of HIV polyproteins.

ii) Neuraminidase Inhibitors (zanamivir, oseltamivir) - competitive inhibitor of sialic acid

binding, prevents the functioning of neuraminidase and the formation of infectious progeny

virions

(enfuvirtide): blocks HIV fusion with host cell by binding to gp41 (for HIV in

combination with other drugs)

maraviroc [Selzentry]): blocks HIV binding to the chemokine receptor CCR5

(raltegravir [Isentress]): blocks incorporation of HIV DNA into host genome

Characteristics: naked icosahedral capsid (hexon, hexon-associated proteins, fiber [attachment,

hemagglutination] penton base [cytotoxic], core proteins [no enzymes]), genome dsDNA

Replication: in nucleus; early, and late transcripts; release by cell lysis

Pathogenesis: lytic or latent infections; transmission by aerosols, direct contact, fecal/oral; human

reservoir

Infections: acute febrile pharyngitis, atypical pneumonia, acute respiratory disease, pertussis-like

syndrome, pharyngoconjunctival fever, epidemic keratoconjunctivitis, acute hemorrhagic cystitis,

gastroenteritis (diarrhea in infants)

Control/prevention: none

(envelope with 2 types of glycoproteins (G1 & G2);

genome composed of 3 neg pol RNA strands (large [L], medium [M], small [S]); L codes for RNS-dep-

RNA pol (found in nucleocapsid), M codes for envelope glycoproteins and a nonstructural protein, S

codes for nucleocapsid and a nonstructural proteinenvelope; replication in cytoplasm; bud into golgi

(major strains: California encephalitis virus, La Crosse encephalitis virus)

Pathogenesis: Replicates in (transovarian transmission) and transmitted by mosquito (vector); squirrels,

chipmunks major reservoirs

Infections: subclinical, mild febrile disease, meningitis, encephalitis

Control/prevention: control vector

(major strain: Sin Nombre)

Pathogenesis: mice major reservoir (strains are species-specific); transmitted by mouse saliva, urine,

feces

Infections: pulmonary syndrome (pulmonary edema), hemorrhagic fever renal syndrome (not in U.S.)

Control/prevention: control reservoir

Characteristics: enveloped, helical nucleocapsid symmetry; 1 segment pos pol RNA genome; E2 protein

(attachment), E1 protein (matrix for assembly), E3 protein (hemagglutinin on some strains), L protein

(RNA-dependent-RNA polymerase (synthesizes neg pol template RNA; early protein during

replication), N protein (nucleocapsid)

Replication: replication and assembly in cytoplasm; neg pol template strand made from which several

mRNAs and progeny genomes are made; bud into ER for assembly; released through golgi

Pathogenesis: peak late winter through early spring; transmitted by aerosols, hand to hand, object to

hand; infects mostly URT epithelial cells; inflammation and cytokines contribute to pathogenesis.

Reinfections possible

Infections: cold (with pharyngitis), pneumonia, gastroenteritis

Control/prevention: none

(genus

; St. Louis Encephalitis virus, Dengue virus, Yellow Fever virus,

Japanese encephalitis virus, West Nile virus)

except envelope derived from intracytoplasmic membranes

Replication: similar to

except all of genome translated into one protein that is processed into

1.

: transmitted by mosquito; bird reservoir; infects reticuloendothelial

tissue, then viremia and dissemination to CNS

transmitted by mosquito and vertically to neonate; primate and mosquito

reservoir; infects reticuloendothelial tissue, then viremia (virus circulates in blood cells) with

dissemination to many tissues; inflammatory cytokines associated with pathogenesis and

symptoms.

transmitted by mosquito; primate reservoir; pathogenesis similar to Dengue

except hepatitis, nephritis and circulatory failure more prominent.

: transmitted by mosquito; pigs and aquatic birds main reservoir

5.

: transmitted by mosquito; crows and aquatic birds main reservoir

1.

: fever & headache, meningitis, encephalitis

2.

: Dengue fever (self-limited disease), Dengue hemorrhagic fever, Dengue shock

syndrome

: self-limited disease, hemorrhagic form

4.

: asymptomatic or encephalitis

5.

: same as St. Louis encephalitis virus

Control/prevention: control vector; vaccine for Yellow fever virus and Japanese encephalitis virus

(~ 20 strains) (family

Picornaviridae)

Characteristics: like Enterovirus but more resistant

Replication: like Enterovirus but infects hepatocytes

Pathogenesis: fecal/oral and common-source transmission; humans only significant reservoir; incubation

2-6 wks; portal inflammation and periportal necrosis (mediated by virus and CMI); no carriers or

chronic disease

Infections: Hepatitis (acute)

Control/prevention: block transmission; passive or active immunizations; single vaccine or vaccine for

both HAV and HBV (Twinrix)

(family

Hepadnaviridae)

Characteristics: enveloped; circular partially dsDNA genome; Major antigens: HBsAg (envelope

protein), HBcAg (core/capsid protein), HBeAg (truncated core protein); core has reverstranscriptase

Replication: replicates in hepatocytes; dsDNA synthesis completed in core, DNA to nucleus; following

transcription and translation, RNA pregenome enclosed in progeny core; RNA pregenome serves as

template for synthesis of neg pol DNA strand, then partial synthesis of pos DNA strand; buds into golgi

and released by exocytosis

Pathogenesis: blood, sex, direct contact, transplacental or during birth transmission; portal and periportal

necrosis (mediated mostly by inflammatory infiltrate) that may lead to fibrosis and cirrhosis; estimated

that 1 million are carriers; humans most significant reservoir; incubation 1 to 4 months (avg 8 wks)

Infections: Hepatitis (subclinical; acute, self-limited; chronic persistent; chronic active; cirrhosis;

hepatocellular carcinoma)

Control/prevention: block transmission; passive or active immunizations (see HAV above); α IFN plus

reverse transcriptase inhibitor (adefovir, lamivudine, entecavir, or tenofovir) or telbivudine for chronic

infection

21

(genus

)

Characteristics: satellite virus that co-infects with HBV; enveloped; circular ssRNA genome; HDVAg is

core protein; requires HBsAg for replication

Replication: replication in hepatocytes completed only in presence of HBV

Pathogenesis: exacerbation of HBV infection

Infections: coinfection with HBV yielding fulminant hepatitis with death (~4%) or recovery with

immunity (~90%); superinfection of HBV carriers yielding fulminant hepatitis with death (~10%), acute

hepatitis with recovery (~10%), or chronic HBV/HDV hepatitis with cirrhosis (~80%)

Control/prevention: block transmission; α IFN

(family

Flaviviridae)

Characteristics: enveloped; pos pol RNA genome; E1 and E2 envelope proteins; genome codes for 2

proteases and a RNA-dep-RNA-pol

Replication: similar to other Flaviviruses; genome encodes for a polyprotein that is cotranslationally

processed into at least 10 proteins; may replicate in cells other than hepatocytes; multiple genetic

variants recovered from single individual

Pathogenesis: transmitted predominantly by blood (transfusions, iv drug use); high percentage (~80%)

of infections become chronic; incubation 2-26 wks (avg 6-12 wks); characterized by inflammation with

fibrosis

Infections: Hepatitis (acute with resolution [~15%], chronic [~85%] that is stable [~80%] or results in

cirrhosis [~20%][stable, progressive with death, or hepatocellular carcinoma])

Control/prevention: block transmission; chronic treated with α IFN or α IFN + ribavirin

(genus

)

Characteristics: non-enveloped; pos pol ssRNA genome

Pathogenesis: pathogenesis and transmission like HAV; incubation 4-8 wks; infects a number of

mammals but humans probably main reservoir for human strain-associated infection

Infections: Hepatitis (acute) with a high mortality in pregnant women (~20%)

Control/prevention: block transmission

(enveloped [from nucleus], icosahedral capsid, dsDNA genome, no core enzymes,

replication in host nucleus, three phases of protein synthesis: immediate early [alpha proteins], early

[beta proteins], late [gamma proteins]; viral-encoded DNA polymerase [a beta protein] replicates the

genome; viruses released by budding or cell lysis; human reservoir; envelope proteins for attachment,

fusion, and cell trophism)

(Human Herpes virus -1 & -2;

)

Pathogenesis: lytic and latent (in neurons) infections; transmission by saliva, sex, and vesicle fluid;

syncytia and intranuclear inclusions occur

Infections: gingivostomatitis, pharygotonsillitis, vulvovaginitis, skin infections (whitlow, gladiatorum),

eye infections, genital herpes, meningitis, encephalitis, neonatal infection, infection in the

immunocompromised, recurrent infections

Control/prevention: acyclovir, famciclovir, penciclovir,valacyclovir; topical preparations; cesarean

section for overt disease in genital tract

(Human Herpes virus -3)

Pathogenesis: lytic and latent (in neurons) infections; transmission by aerosols (RT droplets) and vesicle

fluid; rarely transplacental; syncytia and intranuclear inclusions occur; infects reticuloendothelial tissue

then mucous membranes and skin following viremia

Infections: chickenpox (varicella), shingles (zoster)

Control/prevention: varicella Ig (VariZIG) and vaccines for varicella and zoster, acyclovir for varicella;

famciclovir or valacyclovir for zoster

Pathogenesis: cellular receptor is CD21 (CR2), MHCII are coreceptors; productive (EBNA, VCA),

transforming and latent infections (EBNA, LMPs); transmission by intimate contact (saliva); B cell

activation and proliferation (heterophile Abs), 2 phases of lymphocytosis (B cells and Downey cells);

IL-10-like protein inhibits Th1 response

Infections: heterophile positive mononucleosis (complications), lymphoproliferative disease, neoplastic

diseases (Burkitt's lymphoma, Hodgkin's lymphoma, nasopharyngeal carcinoma)

Control/prevention: none

Replication: large nuclear inclusions occur (Owl's eye inclusion bodies); human CMV grows only in

human cells

Pathogenesis: inhibits expression of MHCI proteins; productive and latent (in many cell types)

infections; congenital, perinatal, oral, sexual, blood, and transplants route of transmission

Infections: congenital infection (cytomegalic inclusion disease), perinatal infection, heterophile-negative

mononucleosis, hepatitis, infection in immunocompromised (pneumonia, chorioretinitis,

colitis/esophagitis, CNS)

Control/prevention: ganciclovir, valganciclovir, foscarnet, or cidofovir

Pathogenesis: transmitted by saliva; productive and latent infections; infects mononuclear cells;

downregulates MHCI and CD3 expression

Infections: Roseola (6th disease, exanthem subitum) in children; adult infection (lymphadenopathy,

hepatitis, mono-like syndrome); in immunocompromised (pneumonitis, encephalitis, hepatitis); HHV-7

may cause second cases of roseola

Control/prevention: none

Pathogenesis: latent and lytic infections; latency-associated nuclear antigen important in neoplasia and

during latent genome replication

Infections: Kaposi's sarcoma

Control/prevention: none

Characteristics: helical symmetry, enveloped, 7-8 negative polarity ssRNA genome; NA (N) and HA (H)

envelope proteins (antigenic drifts and shifts)

Replication: replicates in nucleus, assembles in cytoplasm; viral RNA-dependent RNA Pol synthesizes

pos pol RNA for translation and templates for genome replication

Pathogenesis: birds and other animals reservoirs for Inf A; human reservoir for B and C; aerosol

transmission; NS1 inhibits antiviral effects of interferons; replication in RT induces desquamation with

loss of ciliated epithelium; cytokines and T cells responses contribute to pathogenesis

Infections: influenza (complications: influenza pneumonia, bacterial pneumonia, myositis, meningitis,

aspirin-associated Reye syndrome), common cold

Control/prevention: vaccines; amantadine, rimantadine, zanamivir, oseltamivir

Characteristics: enveloped, helical nucleocapsid symmetry; 1 segment neg pol RNA genome;

filamentous and pleomorphic

Replication: similar to Rabies; genome codes for 7 proteins

Pathogenesis: reservoirs and routes of spread uncertain; probably spread by direct contact or vectors;

massive tissue necrosis and hemorrhage; cytokines contribute to pathogenesis

Infections: hemorrhagic fever

Control/prevention: Possible use of hyperimmune serum

(helical symmetry, enveloped, 2 cirular ssRNA segments as genome; rodent reservoir,

rodent urine transmission)

spongiform encephalopathies associated with the accumulation of insoluble prion proteins

leading to progressive dementia and death (Kuru, Crueutzfeldt-Jakob disease variants, Mad

cow disease)

Human Astrovirus

8 serogroups

family Astroviridae

Characteristics: non-enveloped, icosahedral nucleocapsid symmetry; 1 segment pos pol ssRNA genome

filamentous and pleomorphic

Replication: similar to Noroviruses

Pathogenesis: fecal/oral transmission; peak in winter; mostly infects children under 3yr but all can be

infected; estimated 4 million cases per yr

Infections: gastroenteritis (nausea and diarrhea)

Control/prevention: block transmission

Norovirus (5 serogroups)

family Caliciviridae

Characteristics: non-enveloped, icosahedral symmetry; genome pos pol ssRNA

Replication: replicates and assembles in cytoplasm

Pathogenesis: transmitted by fecal/oral, aerosol, common source, human to human; many animal

reservoirs; estimated 20 million cases per year; infects epithelial cells in jejunum and prevents

absorption; peaks in fall and winter; all ages infected

Infections: gastroenteritis (vomiting and diarrhea)

Control/prevention: control transmission

Human Papillomavirus

Family Papillomaviridae

Characteristics: non-enveloped, icosahedral symmetry; circular dsDNA genome

Replication: in nucleus utilizing host enzymes

Pathogenesis: the most common viral STD; transmission by direct contact (lesions or inanimate objects);

long incubation; latent and productive infections occur; infection induces epithelial acanthosis,

parakeratosis, and hyperkeratosis (inhibits apoptosis); the koilocyte is diagnostic

Infections: Papillomas: cutaneous, head and neck, anogenital; cervical cancer

Control/prevention: vaccine; chemicals, surgery, imiquimod

Polyomavirus

family Polyomaviridae

JC and BK viruses

Characteristics: similar to the Papillomaviruses

Replication: similar to Papilloma viruses except prefer to replicate in the respiratory and urinary tracts

(JC and BK) and CNS (JC)

Pathogenesis: multiply in respiratory tract then kidney after viremia; latent infection in kidney

Infections: JC: progressive multifocal leukoencephalopathy; BK & JC: UTI in immunosuppressed

Control/prevention: none

Parainfluenza, Mumps, Measles, Respiratory Syncytial, Metapneumovirus

Characteristics: HN protein (hemagglutinin/neuraminidase for attachment)

Pathogenesis: transmitted by aerosols or direct contact; humans only reservoir; replicates in mucosal

epithelium of URT; immunity short-lived so re-infections common; Th1 response contributes to path;

HPIV-1 and 2 peaks in fall and winter; HPIV-3 all year with peak in spring; HPIV-4 all year

Infections: HPIV-1-3: croup, pneumonia, bronchiolitis/bronchitis; HPIV-1-4: cold, otitis media,

conjunctivitis

Control/prevention: upper airway support

(genus

Rubulavirus)

Characteristics: like Parainfluenza

Pathogenesis: transmitted by aerosols; humans only reservoir; replicates in mucosal epithelium of URT

yielding viremia; infects parotids and submandibular glands; also may infect pancreas, testes, ovaries,

peripheral nerves, eye, inner ear, and CNS; virus occurs in oral secretions and urine

Infections: mumps (parotitis); complications (orchitis, oophoritis, meningitis, encephalitis)

Control/prevention: vaccine

(genus

)

Characteristics: H protein for attachment

Pathogenesis: transmitted by aerosols; humans only reservoir; replicates in URT, then reticuloendothelial

tissue yielding viremia; infects conjunctivae, UT, CNS, RT; infection of endothelial cells results in

vasculitis; virus occurs in RT secretions, urine

Infections: Rubeola (measles); complications (encephalitis, pneumonia, giant cell pneumonia in

immunocompromised, subacute sclerosing panencephalitis)

Control/prevention: vaccine

Pathogenesis: transmitted by aerosols and direct contact (hands); humans only reservoir; replicates in

mucosal epithelium of URT then spreads to LRT; incomplete immunity from infection; pathologic

change associated with syncytia and inflammation-mediated necrosis

Infections: infants and young children: bronchiolitis, pneumonia, tracheobronchitis, croup, otitis media;

older children and adults: cold, pharyngitis, tracheobronchitis, pneumonia

Control/prevention: Ribavirin for certain situations; Palivizumab (humanized Ab to the F glycoprotein)

Characteristics and pathogenesis: like RSV

Infections: bronchiolitis and pneumonia in young children; cough, congestion in older children and

adults

Control/prevention: none

Human Parvovirus (B19)

(genus Erythrovirus)

Characteristics: non-enveloped, icosahedral symmetry; ssDNA genome

Replication: in nucleus

Pathogenesis: aerosol or transplacental routes of infection; infects erythroid precursors; requires

mitotically active cells; humans only reservoir

Infections: Erythema infectiosum (5th disease) in children; mild disease in adults (polyarthritis); fetal

infections and complications (hydrops fetalis); aplastic crisis in those with hemolytic anemias

Control/prevention: none

Enteroviruses, Rhinovirus

positive polarity ssRNA genome; non-enveloped,

icosahedral symmetry; capsid proteins mediate adherence; replication in the cytoplasm, one large protein

processed to structural proteins, polymerase, and protease; release by cell lysis; human reservoir)

Pathogenesis: transmitted by fecal oral, direct contact, or aerosols; initial replication in GIT; humans

only reservoir; resistant to low pH, salt, detergents; final target tissue varies with virus (e.g. skin, heart,

CNS)

Infections: Poliovirus (Poliomyelitis), Coxsackie A (acute febrile disease, meningitis, encephalitis, cold

w/ fever, febrile rash {hand, foot and mouth disease, pericarditis, hemorrhagic conjunctivitis,

herpangina), Coxsackie B (acute febrile disease, meningitis, encephalitis, cold w/ fever, myocarditis,

pericarditis, pleurodynia, transplacental infection), Echovirus A (acute febrile disease, meningitis,

encephalitis, cold w/ fever, febrile rashes, diarrhea w/ fever), Enterovirus (hemorrhagic conjunctivitis)

(IPV now used again in USA, OPV still used in countries with active polio cases)

Pathogenesis: most infections in early fall & late spring; transmitted by direct contact (hand to hand,

object to hand) or aerosols; replication in URT; ICAM-1 host cell receptor; cytokines contribute to

pathogenesis

Infections: cold, lower RT infection, exacerbation of chronic lung and bronchial diseases (e.g. asthma);

recurrent infections

Control/prevention: none

Smallpox, Molluscum contagiosum,

(genus

Orthopoxvirus, species Variola virus)

Pathogenesis: humans only reservoir; transmission by aerosols or direct contact; replicates in

reticuloendothelial tissue then disseminates to skin and mucous membranes

Infections: variola major and minor

Control/prevention: no treatment; vaccine (Vaccinia virus; not available to public)

Pathogenesis: transmitted by direct contact including sexual transmission; self-limiting cutaneous

lesions occur (umbilicated nodule with caseous plug)

Infections: Molluscum contagiosum

Control/prevention: no treatment

Characteristics: enveloped, helical nucleocapsid symmetry; 1 segment neg pol RNA genome

Replication: replication and assembly in cytoplasm; pos pol template strand made from which progeny

genomes are made; several mRNAs made from neg pol strand

Pathogenesis: zoonotic disease (common reservoirs are bats, foxes, raccons, and skunks); transmission

by bite or scratch or aerosols; virus travels by retrograde axonal transport to CNS then via afferent

neurons to eye, skin, salivary glands

Infections: Rabies encephalitis

Control/prevention: vaccine

Rotavirus, Colorado tick fever virus (non-enveloped, dsRNA genome)

(genus

Rotavirus, serogroups A-E)

Characteristics: 3 capsid layers and inner core; outer capsid composed of VP4 (host attachment); core

contains complete transcription system; genome composed of 11 segments of dsRNA

Replication: transcription occurs in inner core, translation in cytoplasm; genome replicated in progeny

core using pos pol RNA template; buds into ER, release by cell lysis

Pathogenesis: estimated 4 million cases/yr; fecal/oral or human to human transmission (virus survives in

environment); humans probably only reservoir; peak age 6mo-2yr but all ages can be infected; infects

villus cells in small intestine preventing absorption

Infections: gastroenteritis (fever, vomiting, watery diarrhea)

Control/prevention: none

Characteristics: like Rotavirus but outer capsid not as organized (2 capsid layers); genome 12 dsRNA

segments

Replication: like Rotavirus

Pathogenesis: transmitted by wood ticks; small mammals are reservoirs; infects erythroid precursors

Infections: Colorado tick fever (relapsing fever, headache, myalgia)

Human immunodeficiency virus 1 & 2, Human T-cell lymphotrophic 1 (enveloped, 2

identical pos pol RNA stands as genome; proviral DNA integrates into host chromosome; core contains

reverse transcriptase, protease, integrase; genome encodes regulator proteins; humans only significant

reservoir; transmitted by sex, blood, perinatal [in utero, at delivery, breast-feeding])

Characteristics: envelope proteins gp 120, gp 41 for attachment/entry; inner core (Gag protein p24)

Replication: attaches via CD4 and chemokine receptor; envelope fuses, core enters cytoplasm, reverse

transcriptase synthesizes DNA; transcripts and progeny genomes synthesized; assembly and buds

through plasma membrane; core maturation occurs after release

Pathogenesis: chronic infection that induces profound immunosuppression resulting in life-threatening

secondary infections; lymphopenia, reduced T-cell activity, and reduced macrophage activity; incubation

1-6 wks before onset of acute retroviral syndrome; routes of transmission like HBV; Infections: AIDS;

CDC classification: acute (acute retroviral syndrome ["mononucleosis-like"]), chronic (asymptomatic

with persistent generalized lymphadenopathy), final crisis (secondary infections, neurologic disease,

secondary neoplastic disease, unexplained constitutional diseases); presentations peculiar to women or

children

Control/prevention: block transmission; nucleoside RT inhibitors, non-nucleoside RT inhibitors (only for

HIV-1), protease inhibitors, fusion inhibitor, integrase inhibitor, and co-receptoer inhibitor (see antiviral

section)

Rubella virus, Alphaviruses

(enveloped [from cytoplasm], icosahedral symmetry, 1

segment pos pol RNA genome; 2/3 of genome translated into early proteins (protease, RNA-dep-RNA

pol); neg pol strand made for genome template and 26S transcript; 26S translated into precursor protein

that is cleaved by protease into structural proteins

Pathogenesis: aerosol transmission; humans only reservoir; infects URT, then 1st viremia, infection of

reticuloendothelial tissue then second viremia (fetal infection possible) and immune complex-mediated

vascultis (rash)

Infections: Rubella (German measles), congenital rubella syndrome

Control/prevention: vaccine

Pathogenesis: transmitted by mosquito; birds (WEE & EEE), rodents reservoirs (VEE) and possibly also

amphibians and reptiles; infection of reticuloendothelial tissue then viremia and CNS infection;

inflammatory neuronal necrosis

Infections: encephalitis

(+ssRNA, mosquito-borne)

oC), petechial or maculopapular rash, then headaches, insomnia,

photophobia, intense joint pain (resembles Dengue fever), severe prostration lasting several weeks to

several months; infection of endothelial cells and macrophages; cytopathic infection results in

apoptosis of host cell

Diagnosis and treatment: Diagnosis usu. by RT-PCR or by ELISA for anti-CHIKV IgM; currently no

vaccine, and no specific treatment; chloroquine may alleviate arthritis symptoms

In the news: Typically an African and Asian virus, CHIKV underwent a mutation around 2005 that

enabled it to use another species of Aedes mosquito as a vector. This new host has a broader range, and

has resulted in primary CHIKV cases in Europe (Italy) and on Reunion Island (France).

(grow as filaments or hyphae [septate or non-septate] and reproduce with specialized structures that bear the conidia or produce conidia within the filament.)

(1) Dimorphism is an important trait in many pathogenic fungi. It means that at one temperature (usually 25C), the fungus grows as a mold, and at another temperature (usually 37C) the fungus grows as a yeast

Usually composed of a mixture of chitin, glucan,

and mannan. Yeasts usually only have chitin at the bud scar. The cell wall

is a potent immunogen, however the role of Abs in protection is limited.

Plasma membrane (Fungal plasma membranes contain the sterols ergosterol & zymosterol. Ergosterol and enzymes that synthesize it are the major targets of antifungal drugs.)

Conidia-free spores not enclosed by a spore bearing sac

Sporangiospores-formed by successive division within a sac like structure called a sporangium, attached to a stalk called a sporangiophore

Arthrospores-block shaped spores formed when a septate hypha fragments at the crosswall

Chlamydospores-thick walled sperical conidium formed by the septate hypha; are resting spores

Blastospores-produced by budding from a parent cell that is a yeast or another conidium

Microconidium and macroconidium-smaller and larger conidia produced by same fungus (micro=short stalk/one celled)

(heterotrophic; utilize a variety of carbohydrates [specific for the species]

some are strict aerobes, some facultative anaerobes)

a.Portals of entry (skin, inhalation, GIT, UT, normal flora)

b. Virulence determinants (predisposing condition [reduced CMI, underlying disease]; filament vs. yeasts; components immunosuppress and/or evade

immune system; extracellular enzymes; induction of proinflammatory cytokines; tissue trophism and adherence; allergic reactions)

Disease Classification

(1) superficial (Pityriasis versicolor, Tinea nigra)

(2) cutaneous (Dermatophytosis)

(3) subcutaneous (Sporotrichosis)

(4) systemic

(a) primary (Coccidioidomycosis, Histoplasmosis,

Blastomycosis, Cryptococcosis)

(b) opportunistic (Candidiasis, Aspergillosis, Mucormycosis

a. Microscopy (cotton blue, KOH, methenamine silver stain, periodic acid-Schiff stain)

Cryptococcus, dermatophyte test medium, Sabouraud dextrose agar, biochemical tests

c. serum antibody detection; complement fixation test, agar diffusion test, PCR

(Nystatin, Amphotericin B [AmB]; bind ergosterol and cause an increase in membrane permeability; nystatin used topically for oral and vaginal candidiasis; AmB used topically and systemically [colloidal complex in desoxycholate or as a lipid complex]; AmB drug of choice for most disseminated fungal infections)

Azoles (Miconazole, Ketoconazole, Clotrimazole, Itraconazole,Fluconazole, Voriconazole, Posaconazole, Terconazole; inhibit cytochrome P-450 and thus block ergosterol synthesis that results in increased membrane permeability

Dermatophytes/

agents causeing superficial infections

(anthropophilic, zoophilic, & geophilic

varieties; routes of transmission usually direct contact with spores or spore-laden hair or skin scales;

pathogenesis: spores adhere to keratinized tissue, germinate, secrete keratinases, and invade and grow;

hair infection may be endothrix or ectothrix pattern; extent of inflammation varies; Th1 response needed

to control)

Dermatophytoses

Tinea Pedis

(infection of foot and toes; "id reaction" (autoeczematization)

or less frequently

Dermatophytoses

Onychomycosis

(Tinea unguium; infection of nails; etiology like T. pedis; treat with terbinafine, fluconazole, griseofulvin

Dermatophytoses

Tinea corporis and Tinea faciei

(infection of the skin and face, respectively;

T.verrucosum; treat topical, terbinafine, fluconazole, itraconazole

Dermatophytoses

Tinea barbae

(infection of the beard; etiology:

T. verrucosum, T. mentagrophytes

treat topical, terbinafine, fluconazole, itraconazole)

Dermatophytoses

Tinea cruris

(infection of the groin; etiology:

T. rubrum, E. floccosum; treat topical, terbinafine, fluconazole, itraconazole

Dermatophytoses

Tinea capitis

(infection of the scalp; etiology

T. tonsurans

(most common in this country), M. canis, M. audouinii, T. verrucosum; treat griseofulvin, terbinafine, itraconazole

(1)Tinea nigra (infection of the epidermis, usually hands; etiology:

Exophiala werneckii; treat topical, ketoconazole, itraconazole)

(2) Tinea versicolor (infection of the skin, trunk common; etiology:

Malassezia furfur; treat topical selenium sulfide, ketoconazole, fluconazole,

Characteristics: ubiquitous (especially soil and vegetation) dimorphic fungus; at ambient

temps grows as branching septate hyphae with single or clusters of microconidia;

at 37C grows as elongated yeasts

Pathogenesis: traumatic inoculation of skin with conidia or hyphae; inflammation,

induration at site; asending lymphangitis may occur; pulmonary infection initiated

by inhaling conidia

Infections: lymphocutaneous sporotrichosis, pulmonary sporotrichosis, osteoarticular

sporotrichosis, disseminated in AIDS

Control: cutaneous with itraconazole; disseminated with amphotericin B

Characteristics: found in desert soil (endemic in southern Texas, New Mexico, Arizona,

and California); at ambient temps grows as branching, septate, hyphae that forms

arthrospores; at 37C forms spherules containing endospores

Pathogenesis: ~60% of the infections are asymptomatic; infection initiated by inhalation

of arthrospores; pulmonary symptoms generally mild and are associated with

inflammatory reaction to spherules; may form cavity or nodular granuloma; may

disseminate to skin, bone and joints, and CNS

Infections: primary pulmonary coccidioidomycosis, disseminated coccidioidomycosis,

primary cutaneous coccidioidomycosis

Control: ketoconazole, fluconazole, itraconazole, or amphotericin B for severe infection

(var

capsulatum and var duboisii) (Histoplasmosis)

Characteristics: grows in rich, acidic soil enriched by bird and bat feces (endemic in the

Ohio-Mississippi valleys); at ambient temps grows as branching, septate hyphae

that form microconidia and tuberculate macroconidia; at 37C grows as small, oval

yeasts

Pathogenesis: ~90% of cases asymptomatic or mild influenza-like; inhale microconidia,

ingested by macrophages, undergoes dimorphic transition; disseminates to

reticuloendothelial tissue; a facultative intracellular parasite (in macrophages)

Infections: acute primary pulmonary histoplasmosis, chronic (cavitary) pulmonary

histoplasmosis, progressive disseminated histoplasmosis (acute and chronic),

H. capsulatum  var duboisii)

Characteristics: epidemiology similar to

H. capsulatum except endemic area larger;

grows in rich soil contaminated with bird feces or decaying vegetation; at ambient

temps grows as branching, septate hyphae that produce microconidia; at 37C

grows as a thick-walled yeast with large-pore buds

Pathogenesis: ~50% of infections are asymptomatic; inhale microconidia, dimorphic

transition, WI-1 cell wall protein mediates adherence to host cells; yeast cell wall

may be antiphagocytic; tissue damage mediated by inflammatory infiltrate;

lesions may become granulomatous

Infections: primary pulmonary blastomycosis (course may invole complete recovery or

become progressive with or without dissemination), chronic pulmonary

blastomycosis, disseminated blastomycosis, cutaneous blastomycosis

Control: itraconazole or amphotericin B for severe infection

Cryptococcus neoformans (serotypes D and A)

and

C. bacillospora (sero B&C)

cryptococcosis

Characteristics: sero A has worldwide distribution, found in areas contaminated with

C. bacillospora restricted to

regions with eucalyptus trees, infects the immunocompetent; grows as a yeast at

all temps; prominent polysaccharide capsule; deposits melanin in cell wall when

grown on catecols

Pathogenesis: capsule is antiphagocytic and immunosuppressive; melanin protects from

oxidative damage; small-capsule yeasts inhaled, primary infection established in

lung, disseminates to CNS

Infections: pulmonary cryptococcosis (acute and chronic), disseminated cryptococcosis

(skin, CNS)

Control: fluconazole, amphotericin B, or amphotericin B +flucytosine

(

C. tropicalis, parapsilosis, glabrata) (Candidiasis)

Characteristics (C. alb): grows as yeasts at all temps; at 37C in the presence of inducers

forms germ tubes and eventually hyphae (dimorphic transition); on special media forms

pseudohyphae and chlamydospores; C. albicans causes ~70% of the candidiasis

cases; normal inhabitant of the GIT

Pathogenesis: usually requires predisposing condition to cause infection;

attachment followed by release of proteases and tissue invasion associated with acute

infection; chronic infection often involves formation of granulomas

Infections: oral and vaginal candidiasis, intertriginous candidiasis, paronychia, onychia,

generalized cutaneous, chronic mucocutaneous, esophagitis, gastrointestinal

candidiasis, bronchopulmonary candidiasis, UTI, fungemia, endocarditis,hepatosplenic candidiasis

Control: topical (e.g. nystatin, miconazole), fluconazole, posaconazole, amphotericin B,

amphotericin B + flucytosine, or echinocandin

(A. fumigatus and A. flavus) (Aspergillosis)

Characteristics:

A. fumigatus causes ~90% of the infections; common soil fungus,

worldwide distribution; thin septate hyphae that typically branch at 45 degree

angles; asexual cycle involves formation of conidia on complex conidiophore

Pathogenesis: inhale conidia, germinate, hyphae adhere to extracellular matrix proteins,

secrete enzymes and toxic secondary metabolites, hyphae invade tissue or grow in

cavities; Th1 response induced; immunocompromised at greatest risk

Infections: allergic bronchopulmonary aspergillosis, aspergilloma (fungus ball), invasive

sinusitis, invasive pulmonary aspergillosis, disseminated aspergillosis

Control: voriconazole (drug of choice for invasive disease), amphotericin B, itraconazole,

or echinocandin

(

Rhizopus, Absidia, Mucor, Rhizomucor)

Characteristics: ubiquitous soil fungi; grow as irregularly shaped, non-septate hyphae

with right-angle branches; sporangiospores contained in sporangia

Pathogenesis: infections limited to the immunocompromised, diabetics, and trauma;

inhale spores, germinate, invade tissue and blood; results in tissue necrosis,

thrombosis

Infections: rhinocerebral mucomycosis (most in poorly managed diabetics), pulmonary

mucormycosis (neutropenia), cutaneous mucomycosis (trauma)

Control: amphotericin B or posaconazole

pneumocystis jirovecii (formerly P. carinii)

pneumocystosis

Characteristics: complex sexual cycle, simple asexual cycle involving yeast-like trophic

form

Pathogenesis: transmitted by aerosols; trophozoite or sporozoite infectious form inhaled,

adheres to type I epithelial cells, proliferates, and induces inflammatory exudate

resulting in hypoxemia; immunosuppression required for infection

Infections: pneumonia (disseminates to reticuloendothelial tissue in advance AIDS

patients)

Control: trimethoprim+sulfamethoxazole

(size 2-100

m, cytoplasm often composed of inner endoplasm

[nutrition] and outer ectoplasm[organelles of locomotion])

(1) Rhizopods (amebas; reproduce by binary fission)

(2) Ciliates (reproduce by binary fission)

(3) Flagellates (reproduce by binary fission)

(4) Sporozoans (reproduce sexually [sporogony] and asexually

[shizogony])

(5) Physiology (most fac. anaerobes; heterotrophic; engulf food by

pinocytosis or phagocytosis; some have specific site for ingestion

[the peristome or cytostome]; many can form resistant cysts)

(elongated, bilaterally symmetric, length varies from <1mm to

>1m; body wall covered with cuticle; anterior end may possess suckers,

hooks, teeth, etc. for attachment; all have differentiated organs [primitive

nervous and excretory systems and well developed reproductive systems

(1) Roundworms (nematodes; have cylindrical bodies, tubular

alimentary track, and the sexes are separate)

(2) Tapeworms (cestodes; have flattened bodies; the anterior end

[scolex] has suckers and or hooklets for attachment; reproductive

segments are called proglottids and each contains both male and

female gonads; no digestive tract)

(3) Flukes (trematodes; flat with branching alimentary tracts;

particulate wastes are regurgitated through the mouth; have two

S.mansoni))

4) physiology (ingest or absorb body fluids, etc.; usually anaerobic respiration)

(all aspects of the immune system important; eosinophils directed at

worms; IgE made to many; acquired resistance often absent or incomplete;

effector mechanisms usually directed at surface antigens of the parasite)

3. Diagnosis (direct examination of specimens [microscopy], serology [ELISA, IF,

CF], molecular probes)

Drugs for luminal protozoa

 (aemae, flagellates, ciliates)

(1) Metronidazole and tinidazole

Cryptosporidium)

(3) Paromomycin

(4) Iodoquinol

(5) Furazolidone

(6) Pentamidine

Naegleria and Leishmania)

(1) Chloroquine

(2) Primaquine

(3) Quinine

(4) Quinidine

(5) Mefloquine

(6) Atovaquone/proquanil (malarone)

(7) Doxycycline

(8) Artesunate (for severe malaria; only available from the CDC)

(1) Albendazole

(2) Mebendazole

(3) Pyrantel pamoate

(4) Ivermectin

1) praziquantel

2) Albendazole

1) pyrimethamine/sulfadiazine (for Toxoplasma gondii)

2)Trimethoprim/sulfamethoxazole (for Cyclospora cayatamensis)

(

)

Characteristics/life cycle: sporogeny in mosquito (gametocytes, ookinete, oocyst,

sporozoites), schizogony in human (sporozoite, merozoite [liver & RBC],

trophozoite, schizont, gametocyte

; symptoms associated with RBC rupture

and proinflammatory cytokines; anemia associated with depression of marrow

function; RBCs sequestered in spleen

most prevalent worldwide, invades immature RBC, may

cause chronic infection;

invades any RBC, associated with microvascular disease as a result of mature trophozoite-infected RBC adhering to microvascular endothelium

Control: chloroquine, mefloquine, primaquine, atovaquone/proquanil, quinine

Characteristics/life cycle: schizogony and sporogeny in cat GIT (trophozoites,

merozoites, gametocytes), oocyst released in feces that mature to contain

sporozoites; oocyst ingested by intermediate host (humans), intracellular

schizogony occurs yielding tachyzoites that encyst; cyst produces sporozoites and

bradyzoites that are passed in feces and infect definitive host

Pathogenesis: transmitted by fecal-oral route or from ingesting undercooked infected

meat; various sizes cysts occur in tissue with varying degrees of inflammation

Infections: acute and chronic toxoplasmosis, congenital toxoplasmosis, toxoplasmosis in

the immunocompromised

Control: pyrimethamine + sulfadiazine or clindamycin

Characteristics/life cycle: acid fast oocysts containing 4 sporozoites ingested, sporozoites

released and attach to microvilli in GIT; become schizonts that release merozoites

that become gametes that mate and become oocyst that is released in the feces

Pathogenesis: many animals serve as reservoirs; transmitted by fecal/oral and person to

person; oocyst resistant to chlorination

Infections: Cryptosporidiosis (noninflammatory, watery diarrhea); may be prolonged in

immunocompromised

Control: avoid contaminated water; Nitazoxanide (Alina)

Characteristics/life cycle: like

C. parvum

but oocyts (fluoresce under UV light) contain 2

sporocysts that each contain 2 sporozoites

C. parvum

except oocyts mature in the environment

Infections: like

C. parvum

Control: trimeth-sulfameth

Characteristics/life cycle: trophozoite with ameboid morphology; forms cyst with

chromatoidal body

Pathogenesis: transmitted by anal sex, fecal/oral, fomites; ingest cyst, gastric acid induces

release of trophozoites, adhere to epithelial cells in colon via galactose-specific

lectin, release pore-forming protein, invade, and multiply; kill epithelial cells

resulting in a loss of fluid uptake and inflammatory diarrhea

Infections: amebiasis (inflammatory diarrhea), may be asymptomatic (carriers), may

disseminate in immunocompromised

Control: metronidazole or tinidazole followed by paromomycin to eliminate cysts

Characteristics/life cycle: flagellate morphology (flagella, axostyle, undulating

membrane); exists only as trophozoite that divides by binary fission

Pathogenesis: transmitted by sexual contact; infects urethra, vagina, prostate; serious

infections involve necrosis and inflammation; men mostly asymtomatic and the

predominant reservoirs

Infections: women: asymptomatic, vaginitis; men: asymtomatic, urethritis, prostatitis

Control: safe sex; metronidazole or tinidazole

Characteristics/life cycle: flagellate morphology (flagella, sucker [adhesive disk], 2

nuclei); trophozoite and cysts occur; trophozoites multiply by longitudinal binary

fission

Pathogenesis: transmitted by fecal/oral or contaminated food or water; ingest cyst,

trophozoites released and attach to epithelial cells in duodenum; attachment

induces inflammation, tissue damage, and reduce absorption

Infections: acute or chronic noninflammatory diarrhea; may be asymptomatic

Control: metronidazole or tinidazole

(

L. tropica, L. mexicana, L. braziliensis, L. major, L. donovani)

Characteristics/life cycle: hemoflagellate morphology of free-living promastigote,

intracellular amastigote

Pathogenesis: numerous animal reservoirs; transmitted by the bite of female sandfly;

promastigote invades reticuloendothelial tissue and becomes the intracellular

amastigote; replicates and invades other tissue, resulting in inflammation and

necrosis

Infections: cutaneous, mucocutaneous, and disseminated (visceral) leishmaniasis

Control: amphotericin B or pentamidine

Characteristics/life cycle: epimastigote in insect gut, trypomastigote free-living in host

(hemoflagellate morphology), amastigote intracellular

Pathogenesis: numerous animal reservoirs; transmitted by feces of reduviid (kissing) bug;

trypomastigote invades tissue, becomes intracellular amastigote that replicates

and lyses cell; trypomastigote released into blood; tissue inflammation and

necrosis

Infections: American trypanosomiasis (Chagas’ disease)

Helminths:

Enterobius vermicularis (pinworm)

Characteristics: nematode morphology (cylindrical body, tubular alimentary tract, separate sexes)

Pathogenesis: humans only reservoir; hand to mouth or fecal/oral transmission; ingest

eggs, hatch, larvae penetrate mucosa of large intestine, mature into different

sexes, mate, female lays eggs in perianal area; eggs induce allergic reaction

Infections: Pinworm disease (Enterobiasis)

Control: mebendazole or albendazole; pyrantel pamoate is an alternative

Characteristics: nematode morphology (cylindrical body, tubular alimentary

tract, separate sexes)

Pathogenesis: humans only reservoir; fecal/oral transmission; ingest embyonated egg,

larvae penetrate mucosa of large intestine, sexes mature, mate, female releases

eggs in feces; larvae develop in moist, dark environment; whip penetrates and

damages mucosa; symptoms related to worm burden

Infections: Whipworm disease (Tricuriasis)

Control: mebendazole or albendazole

Characteristics: nematode morphology; worms may reach 1 m in length

Pathogenesis: humans main reservoir; fecal/oral, hand to mouth transmission; ingest

embyonated egg, larvae penetrate duodenal wall, enter blood then lung, grow in

alveoli, coughed up and swallowed, mature in small intestine, mate, female

produces eggs that are passed in feces; larvae in fertilized eggs mature in moist

dark environments; symptoms related to worm burden

Infections: Ascariasis

Control: mebendazole or albendazole; pyrantel pamoate is an alternative

(Ancylostoma duodenale)

(Hookworm)

Characteristics: nematode morphology; 2 larval morphologies (rhabditiform

[free-living], filariform [infective])

Pathogenesis: transmitted by contact with contaminated soil; filariform larvae penetrate

skin, enter blood, then lungs, coughed up, swallowed, attach to mucosa of small

intestine, induces inflammation and necrosis; mate, eggs pass in feces, mature in

soil, rhabditiforn larvae released, free-lining, develop into infective filariform

larvae

Infections: Hookworm disease (hypersensitive pneumonitis, GIT symptoms); cutaneous

larval migrans caused by non-human hookworms

Control: albendazole, mebendazole, or pyrantel pamoate

Characteristics: like

Necator

Pathogenesis: transmitted by contact with contaminated soil; filariform larvae penetrate

skin, enter blood, then lungs, coughed up, swallowed, mate in small intestine,

males ejected, female burrow into mucosa and produce eggs; hatch liberating

rhabditiform larvae, some pass in feces, some develop into filariform and

continue the infection; pathogenesis dependent on worm burden

Infections: Strongyloidiasis (acute [hypersensitive pneumonitis, GIT asyptomatic to

inflammatory diarrhea], hyperinfection syndrome in immunocompromised)

Control: ivermectin or albendazole

Characteristics: eggs of non-human ascarid hatch in GIT and undergo limited

development

Pathogenesis: ascarids migrate into tissue; symptoms and pathogenesis related to

migration (eosinophilia and hepatomegaly common)

Infections: Toxocariasis (Visceral larva migrans); Ocular larval migrans associated with

infection by larvae

Control: usually self-limited; albendazole or mebendazole for severe disease

Characteristics: nematode morphology

T. spiralis worldwide, T. murrelli in North American

bears); transmitted by eating undercooked meat; ingest cyst, larvae released,

develop in intestinal mucosa of small intestine (intracellular parasites), mature,

mate, females produce larvae that enter the blood, then muscle where the coil and

encyst; pathogenesis depends on worm burden; myositis and vasculitis occur

Infections: Trichinosis (symptoms depend on worm burden and location of cysts)

Control: mebendazole or albendazole stops development of new larvae

Characteristics: cestode morphology and life cycle (proglottids, scolex,

resistant cuticle)

Pathogenesis: pig ingests embryophores, cattle ingest gravid proglottids and embyonated

T. solium embryophore (Cysticercosis)

Infections: tapeworm disease (GIT symptoms depend on worm burden); Cysticercosis when T. solium embryophore is ingested

Control: avoid undercooked meat; praziquantel or niclosamide

diphyllobothrium latum

(freshwater fish tapeworm)

Characteristics: cestode morphology; crustaceans and fish intermediate hosts; prevalent

in cool lake water

Pathogenesis: humans ingest undercooked fish infected with sparganum larvae, attach to

mucosa of small intestine, mature, eggs in feces, eggs released into freshwater

develop into coracidium that infects crustaceans

Infections: Fish tapeworm disease (GIT symptoms depend on worm burden)

Control: praziquantel or niclosamide

Characteristics: trematode morphology; unlike most trematodes sexes are separate; eggs

have characteristic lateral spine; adults are obligate intravascular parasites; aquatic

snail intermediate host

Pathogenesis: cercaria penetrate skin, enter blood, develop in portal circulation (inferior

mesenteric vein near lower colon), coat themselves with host proteins, mate, eggs

produced; eggs pass into GIT and released in feces

Infections: Schistosomiasis (blood fluke infection; hypersensitive skin reaction at sites of

skin penetration; hepatic and GIT symptoms depend on worm and egg burden)

Control: praziquantel

A.

A.