Zoonotic infections Flashcards

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1
Q

Animal bites and scratches transmission

A
  • Bacterial; Pasteurellosis*, Cat scratch fever*
  • Viral; Rabies
  • Fungal; Blastomycosis
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2
Q

Inhalation transmission

A
  • Bacterial; Anthrax*, Ornithosis, Plague*, Q fever,Tuberculosis*, Tularemia*
  • Viral; Lymphocytic choriomeningitis, Hantavirus pulmonary syndrome
  • Fungal; Histoplasmosis
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3
Q

Ingestion transmission

A
  • Bacterial; Brucellosis*, Campylobacter, Listeriosis*, Salmonelosis, Tuberculosis*, Yersiniosis
  • Viral; Norovirus, (Ebola and Marberg HF?)
  • Parasitic; Many parasites (refer to Parasitology notes)
  • Other; Variant Crutzfeldt-Jakob disease (vCJD)
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4
Q

Fecal-oral transmission”

A
  • Bacterial; Salmonellosis, Leptospirosis
  • Viral; Norovirus, Hepatitis A & E
  • Parasitic; Toxoplasmosis, Crytosporidiosis
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5
Q

Arthropod bites transmission

A
  • Bacterial; Lyme disease, Plague*,Relapsing fever, Tularemia*, RMSF, Scrub Typhus, Rickettsial pox, Ehrlichiosis
  • Viral; Yellow fever, Viral encephalitides, Crimean- Congo, Yellow Fever and Dengue hemorrhagic fevers.
  • Parasitic; Babesiosis, Kala azar, Trypanosomiasis
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6
Q

ANTHRAX

A
  • Bacillus anthracis: large, box-car, gram-positive rod; aerobic and spore forming
  • Non-hemolytic
  • Nonmotile
  • Native to hoofed domestic herbivorous animals: cattle, horses, etc.
  • Human Anthrax is endemic in sub-Saharan Africa, Asia, South and Central America, Southern and Eastern Europe
  • Mostly inhalation; Person-to-person transmission is very rare: cutaneous Anthrax

Virulence factors

3 proteins produced by genes carried by a large plasmid pXO1; non-toxic individually, but when combined they become toxic.

  • Lethal Factor (LF)
  • Edema Factor (EF)
  • Protective Antigen(PA)

PA+EF = edema toxin

PA+LF = lethal toxin

  • Polypeptide Capsule (Poly-D-Glutamic acid)
  • Observed in clinical samples only (not in vitro, without special conditions)
  • Three genes (CapA, CapB & CapC) on plasmid pXO2
  • Only one serotype known- probably because of the glutamic acid polymer

Anthrax Pathogenesis

  • Exotoxin mediates all the damage
  • Capsule inhibits phagocytosis of replicating cells
  • Edema toxin cAMP allows accumulation of fluid in the tissue
  • Lethal toxin stimulates macrophages to release TNF-α, IL-1β and other inflammatory cytokines.
  • Both LF & EF inhibit the host innate immunity
  • Germinate, multiply, and release toxins, causing hemorrhagic mediastinitis

Cutaneous Anthrax Pathogenesis:

  • Begins at site of 1° infection as a papule; progresses through a vesicular stage to a painless depressed black necrotic ulcer (eschar)
  • Edema, redness, and/or necrosis without ulceration may occur
  • Form most commonly encountered in naturally occurring cases
  • Incubation period: 1–12 days
  • Case-fatality:
    • Without antibiotic treatment—20%
    • With antibiotic treatment—1%

Sx

  • Cutaneous: the most common in humans, least life- threatening
  • Septicemic- high mortality
  • Pulmonary: highest mortality in humans; rare under natural circumstances: “Wool- Sorter’s Disease
  • Inhalation anthrax sx:
  • Prodrome resembling “Flu-like” illness, characterized by myalgia, fatigue, fever, with or without respiratory symptoms, followed by hypoxia and dyspnea, often with radiographic evidence of mediastinal widening (due to hemorrhagic mediastinitis).
  • Meningitis in 50% of patients
  • Rhinorrhea (rare)

Dx:

  • Gray, opaque, granular, spreading colonies with irregular perimeters growing on 5% sheep blood agar.
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7
Q

Brucella spp

A
  • Gram -ve short rods
  • non-motile
  • facultative intracell
  • Nutritionally fastidious
    • – Facultative Intracellular -> granulomatous response
    • – Require complex artificial media in-vitro
    • – Slow growing (up to 10 days on Blood agar)
  • Enzootic: 4 pathogenic spp in humans
    • B. melitensis- goats, sheep, camels [Europe, Asia, Middle East, South & Central America]
    • B. abortus- cattle [Africa, Asia, South America]
    • B. suis- pigs [South Asia]
    • B. canis-dogs

Epidemiology

Reservoir: Infected animals excrete organisms for prolonged periods in milk, animal urine, feces, vaginal discharge and uterine products -> farm animal ST; California & Texas

Transmission

  • Direct occupational contact: Butchers, Veterinarians.
  • Access through skin breaks, mucus membranes, aerosols, splashes.
  • Ingestion of unpasteurized dairy products.
  • Organism is killed by pasteurization.

Pathogenesis

  • Once skin or mucous membranes are penetrated by organisms they are carried to lymphatics by PMNs
  • Cells multiply within macrophages by inhibiting lysosome- phagosome fusion
  • Humoral response is ineffective; T-cell response required.
  • Failure of T-cell control results in granulomatous inflammation with bacterial multiplication within the RES
  • Waves of bacteria are released into the circulation from these sites resulting in recurrent bacteremia.

Chronic Sx

  • Chronic episodes of nocturnal fever may persist for months to years -> undulating fever w profuse sweating
  • Prolonged cases show marked weight loss
  • Few other physical findings or signs: sometimes glandular or hepatic & splenic symptoms
  • Sacro-ileitis
  • Depression
  • osteomyelitis

Acute Sx

  • Incubation: 7 to 21 days
  • Onset with drenching sweat with high fever (up to 40°C.); then a swinging fever, rigors, lethargy, headache, musculo-skeletal pain; scrotal pain
  • B.melitensis infection is most severe; B. suis : abscess formation
  • Occasionally delirium, abdominal pain, constipation
  • Lymphadenopathy & splenomegaly (DDx for splenomegaly: CMV & HSV also)
  • Infection is localized in 30% of cases especially with delayed diagnosis and treatment

Dx

  • Isolation from blood cultures; positive in 75% of cases with B. melitensis and 50% with B. abortus
  • BM may be useful in more chronic state
  • CSF in neuro-infection : 30% culture positive
  • serology

Rx:

  • Rifampin (1o)
  • Doxycycline
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8
Q

Leptospirosis

A

Leptospira interrogans is ubiquitous in wildlife and domestic animals

  • Tight spiral or Question mark ? shape
  • Sensitive to heat, drying and most chemicals
  • Survives well ( 1 to 2 weeks) in slightly alkaline ground water or soil, but does not multiply.
  • Enters susceptible host by penetrating skin and/or mucus membranes
  • L. ictero-haemorrhagiae is a classical parasite of rats, L. canicola of dogs, L. hebdomadis of cattle, L. pomona of pigs.
  • Epi: Water sports in tropics, Ex. Hawaii
  • 3 types
      1. anicteric
      1. Weil disease: lung involvement -> poor prognosis
      1. fulminant

Pathogenesis

  • Multiply rapidly -> hematogenous spread -> damage the endothelium of small blood vessels resulting in major clinical syndrome -> Weil Disease
  • Organisms are found in the CSF and blood early in infection. Found in urine during the later stages of disease.

Sx

  • Conjunctival suffusion
  • Initial blood stream invasion with localization in kidneys, liver, meninges and brain.
  • Incubation period is 1-2 weeks with 4 syndromes:
  • Bacteremic: flu-like, diarrhoea and vomiting; conjunctival congestion
  • Viral meningitis-like
  • Icteric: fever, hemorrhages, hepatic and renal impairment leading to jaundice & kidney dysfunction (azotemia)
  • Pulm: ARDS

Dx Labs:

  • PMNs rise,
  • liver enzymes rise,
  • CK rise
  • PLT fall
  • CSF shows a “viral pattern”; i.e. CSF Glucose nl
  • Isolation from blood/ urine- special media & prolonged incubation
  • Serology
  • PCR
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9
Q

Tularemia

A

Francisella tularensis

  • Gram negative short rods/coccobacilli
  • Facultative intracell organism
  • not spore forming
  • Nutritionally fastidious: will not grow on blood or other common media; requires supplemental compounds
  • Grown with Cysteine-Glucose Blood Agar (Aerobic), i.e. modified Thayer-Martin
  • Slow growing: Requires 2 to 10 days for visible growth

Epidemiology Enzootic in (small) wild mammals:

Rabbits, beavers, deer (can be found in cats and dogs)

– Ticks : dog tick (Dermacentor variabilis), wood tick (Dermacentor andersoni), lone star tick (Amblyomma americanum), deer flies (Chrysops spp.)

– A northern hemisphere disease (Southwest to Central U.S. is focus); Arkansas or Missouri hunters

Pathogenesis

  • Entry through inhalation, ingestion, or injection
    • – Minimum Infectious Dose < 100 cells
    • Ulcerated lesion develops at injection site -> bacteria may replicate in macrophages -> Bacteremic spread via lymphatics –> seeds RES > caseous granulomatous inflammation
  • Recovery confers long lasting immunity

Sx

  • Incubation: 2 to 5 days> fever, chills & malaise
  • Syndromes depend on site of infection:
    • – Skin ulcers & Ulcero-glandular (from injection: lowest mortality)
    • – Typhoidal (resulting from ingestion)
    • – Pneumonia (from inhalation: highest mortality)
  • Mortality from 5% to 30% depending on form

Rx: aminoglycosides

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10
Q

Pasteurellosis

A

Pasteurella multocida

  • Gram -ve short rods/short bacilli
  • Facultative; ferments carbohydrates
  • Oxidase +
  • Catalase +
  • encapsulated
  • Grows readily on enriched media like 5% Sheep Blood Agar, but not on media selective for Gram negatives (MacConkeys)
  • Bipolar staining aka “Safety-pin staining”
  • Sensitive to penicillin

Epidemiology

  • Normal respiratory biota of many lower animals, including cats and dogs.
  • Human is infected by bite (dogs and cats) or scratch
  • Sometimes also found in human sputum>> so human bite could transmit.

Sx

  • Local infection at site of inoculation e.g. bite
  • Associated cellulitis w/in first 24 h of infection
  • Systemic infection is uncommon but can be quite severe
  • Osteomyelitis
  • Confirm diagnosis by culture from aspirated pus

Rx:

  • Penicillin
  • Amoxicillin
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11
Q

Cat Scratch Disease

A

Bartonella;

  • Gram -ve bacteria; Facultative intracellular pathogens
  • Warthin-Starry Silver stain visualizes better

Transmission vectors include ticks, fleas, sandflies, mosquitoes

Sx B. henselae

  • Cat scratch disease (CSD) in immunocompetent
  • Papule/pustule 3 - 10 days post cat-scratch, lick or bite.
  • Fever and with regional lymphadenopathy (head, neck, axilla)
  • Most cases recover completely & spontaneously
  • Complications in children and immucompromised hosts; needs treatment with ciprofloxacin or other antibiotic for 1-3 months

Sx B. henselae

  • Bacillary angiomatosis in HIV +
    • multiple subcutaneous enlarging rasied red papules, resembling cranberries.
    • Occur in viscera as well.
  • Infectious endocarditis
  • Chronic bacteremia

Sx B. quintana

  • Bacillary angiomatosis,
  • Trench fever
  • Infectious endocarditis
  • Chronic bacteremia

Sx B. bacilliformis

  • Carrion disease (verruca peruana)
  • Oroya fever
  • Acute and Chronic phase

Rx:

  • Macroglide
  • Tetracycline
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12
Q

Ornithosis

A

Species: Chlamydophila psittachi

Round with narrow periplasmic space

No peptidoglycan in the cell wall, instead it contains LPS with weak endotoxicity

Major Outer Membrane Protein (MOMP) is major cell wall component and unique to each species

Outer Membrane Protein (OMP) is common to all chlamydia

Pathogenesis

  • Spreads to the RES of liver and kidneys producing necrosis
  • Seeded in the lung through blood causing lymphocytic inflammation in the alveoli
  • Edema, thickening of the alveolar wall, infiltration of macrophages, necrosis and occasional hemorrhages
  • Mucus plugs the bronchioles causing cyanosis and anoxia

Epidemiology

  • Transmitted to humans through inhalation of waste products of birds
  • Person-to-person transmission is rare
  • Veterinarians, zookeepers, pet shop owners and employees of poultry-processing plants are high risk** **

Sx:

  • very severe RTI
  • Incubation 5-14 days
  • Headaches, high fever, chills, myalgias
  • Pulmonary symptoms include nonproductive cough and consolidation
  • CNS involvement common, encephalitis, convulsions, coma and death
  • GI symptoms, nausea, vomiting and diarrhea
  • Other sx include hepatosplenomegaly and follicular keratoconjunctivitis
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13
Q

Yersiniosis

A

Plague: Yersinia pestis

  • Common features of Yersinia (repeated from GIT)*
  • Gram negative short rods/bacilli
  • Member of the Enterobacteriaceae:
  • Encapsulated
  • Resistant to cold
  • bipolar staining “safety pin”
  • non-motile

Unique features of Y. pestis

  • YOPS secreted via type III system
  • Glucose fermenter
  • Grows readily in standard media
  • Rich polysaccharide capsule present in virulent strains

Reservoirs

  • Sylvatic Plague: Rural reservoirs of Y. pestis still exist in several areas of the world,
    • – Semi-arid regions of the Southwestern U.S.A.
    • – Southeast Asia & Grasslands of Central Asia (the original homeland of Y. pestis)
  • Not found (in significant numbers) in: Western Europe, Africa or Australia
  • A disease of small rodents: Prairie dogs, Voles, Rats, Ground Hogs, Rock Squirrels

Vector

  • Xenophylla cheopis the Rat Flea
  • Flea acquires Y. pestis when it takes a blood meal from an infected rodent host.
  • Infection by reugurg: Organism multiplies in proventriculus of the flea, eventually blocking the flea’s GI tract.
  • Starving flea regurgitates infectious material when attempting to take another blood meal.
  • Flea eventually dies of the infection

Incubation

  • Bubonic form is 4 to 7 days
  • Pneumonic form is 18 to 36 hours -> more severe

Pathogenesis: Flea bite & reaches LN

  • Higher temperature induces formation of virulence factors.
  • Rapid multiplication.
  • Infected lymph node swells and becomes painful: a Bubo
  • Progresses to bacteremia which seeds liver, spleen lungs and sometimes meninges
  • Pulmonary infection can then be transmitted by respiratory droplets: Pneumonic Plague

Sx

  • Bubonic plague: swollen, painful bubo -> inguinal lymph and axial nodes;
  • increasing fever, pooling of blood and microhemorrhages in face and extremities.
  • Pneumonic: violent and fulminating bacterial pneumonia; bloody sputum; nearly always fatal.
  • Uncontrolled spread -> abscess, cutaneous hemorrhage, necrosis

Dx

  • LN aspirate: An affected bubo should contain numerous organisms that can be evaluated microscopically and by culture.
  • Blood cultures: Organisms may be seen in blood smears if the patient is septicemic.
  • sputum
  • Bronchial/tracheal washing
  • Stain: Wayson stain or Bipolar staining
  • LN, spleen, lung, liver tissue, BM samples for EIA or PCR
  • CCR-5 mutations may confer dual resistance to HIV and bubonic plague

Rx: doxycycline

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14
Q

Q Fever

A

Caused by Coxiella burnetti

  • Obligate intracellular Gram -ve
  • spore-forming
  • Can survive in extracellular environment for a long time
  • Cattle, sheep, goats are important reservoirs (ticks are important for animal cycle) -> spores in animal feces
  • Transmission: inhalation of aerosolized particles ( important for humans)
  • C. burnetti shows phase variation
    • Infected source isolates – phase I, highly infectious with intact LPS;
    • phase II within in-vitro culture; not infectious, with truncated LPS
  • Incubation: period 3-4 weeks

Sx:

  • Most infections are asymptomatic. Influenza-like symptoms during an acute infection.
  • Fever, headache, chills;
  • No Rash! (20% rash)
  • pneumonia,
  • hepatitis
  • Osteomyelitis, encephalitis, endocarditis is most common in chronic cases.

Dx: serological; phase I and II, IgM peak at 4-6 weeks

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15
Q

Korean Hemorrhagic Fever (Hantaan virus)

A

Genus: Hantavirus

– Hemorrhagic Fever with Renal Syndrome

– Deer Mouse, rats

– far east, Scandinavia, E. Europe,

– severe pulmonary syndrome in SW US (Sin Nombre)

– no vaccines

Sx: fever and muscle ache followed rapidly by interstitial edema, respiratory failure and death within days

Dx: RT-PCR

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16
Q

C. jejuni (additional Notes)

A
  • Most infections are self limiting but may persist longer
  • Guillain-Barre (GBS) is due to cross-reactivity between capsular oligosccharides and glycosphingolipids on nerve surface (autoimmune disease).
  • Culturing requires Low O2 tension and higher incubation temperature ( 42oC)
17
Q

Lyme Disease

A
  • B. burgdorferi has same range as Ixodes sp. ticks
  • spirochete
  • require Wright-Giemsa stain

Ixodes sp. ticks Life Cycle

  • Eggs hatch to larvae (spring to summer)
  • Larvae require a vertebrate blood meal to develop into nymphs (early fall)
  • Nymphs become dormant in winter; require another blood meal before they can become adults (spring to summer: most infectious stage)
  • Adults mate and then lay eggs (summer to fall)
  • Eggs remain dormant over the winter
  • Main reservoir (tick larvae): White-footed mouse
  • Obligatory host (adult tick): White-tailed deer
  • Epi: NE US

B. burgdorferi within the tick vector

  • Borellia sp. cells adhere to epithelial cells of tick’s midgut and remain there indefinitely in a quasi- dormant state
  • When the tick feeds on a mammalian or avian host, the microorganisms are exposed to a higher temperature, which activates them.
  • Activated organisms multiply, penetrate the gut wall, and spread throughout the tick to its salivary glands -> injected into host

Sx: analogous to syphilis

Stage 1:

  • ECM (Erythema Chronicum Migrans/ the target lesion occurs in 40 - 50% of cases -> Bull’s eye rash w fever & chills
  • flu-like sx

Stage 2:

  • Secondary annular skin lesions (Exanthem)
  • CNS: Bilateral Bell’s palsy
  • cardiovascular: heart block from myocarditis
  • ophthalmic and musculoskeletal manifestations

Stage 3:

  • ACA (Acrodermatitis Chronicum Atrophicans)
  • Diverse CNS symptoms: Encephalopathy
  • Arthritis: migratory affecting large joints
  • Cardiomyopathy

Dx

  • B. burgdorferi in blood smear during early stage only
  • Serology for later stage is unreliable: ELISA, IFA

Rx

  • Doxycycline or Amoxicillin for early disease
  • Ceftriaxone or Cefotaxime for late disease with prolonged therapy.
18
Q

Rickettsial infections general features

A

3 main groups: RMSFr, Typhus & Scrub typhus

  • obligate intracell Coccobacilli
  • requires NAD+ and CoA

Sx

  • Vasculitis: Primary infection in human vascular epithelium with capillary leak syndromes;
  • adrenal glands also affected
  • Common Clinical Manifestations
    • sustained high fever
    • – severe retro-orbital headache
    • – Rash (distribution and extent differs with different species)
    • Acute presentation with headache, rash assoc w vasculitis and possible neurological disturbances.
    • Endothelitis from endothelial cell infection leads to: Thrombosis and Eschar formation
  • No known toxins

Dx: Weil-Felix agglutinationtest

Rx: Doxycycline

19
Q

RMSF

A

Ricketssia rickettsii

  • Transmission: Dermacentor tick bites
  • Incubation period: 2 to 6 d -> rash not immediate
  • Epi: GOAT states

Sx

  • Exanthem (Rash) on 3rd or 4th day on wrists or ankles and spreads inward to the trunk within hours. (Centripetal Spread); extends to cover palms of the hands and soles of the feet (looking like measles)
  • Skin hemorrhages
  • Hepato-splenomegaly
  • Fever, headache, toxicity, mental confusion, myalgia

Dx

  • Weil-Felix test
  • Species specific antibodies testing in reference laboratories

C&C if untreated

  • DIC
  • Thrombocytopenia, encephalitis, vascular collapse
  • Renal and/or heart failure

Rx: doxycycline

20
Q

R. prowazeki infection

A
  • Endemic typhus
  • Transmission: Pediculus spp aka louse aka lice release Rickettsia in to fecal stream
  • Affects military

Sx:

  • Rash starts in trunk and moves outwards but spares hands, feet, and head
  • Pneumonia
  • Arthralgia & myalgia
  • Encephalitis w confusion, dizziness, and coma if serious

Rx: doxycycline

21
Q

Scrub typhus

A
  • Caused by a Rickettsia –like organism; Orientia tsutsugamushi
  • Transmission: by mites
  • Incubation period: around 9 days

Sx:

  • Onset is sudden headache, fever, malaise, weakness and cough
  • Maculo-papular rash about 5th – 7th day trunk, face, limbs including palms and soles with generalised painless lymphadenopathy
  • Severe cases are prostrate with pneumonia, confusion ; cardiac, renal failure; hemorrhage and death
22
Q

Ehrlichiosis

A
  • E. canis & E. chafeensis:
  • Human Monocytic Ehrlichiosis;
  • transmitted by the Brown Dog Tick in the US (?reservoir ?vector)
  • often first misdiagnosed as Rocky Mountain Spotted Fever.
  • Detailed pathogenesis and pathology is unknown
  • Dx: infects neutrophils and forms morulae -> Mulberry-like structure

Sx

  • High fever and GI abnormalities;
  • No rash!
  • severe cases progress through cough,
  • diarrhea and lymphadenopathy up to respiratory insufficiency,
  • renal insufficiency and CNS abnormalities.
23
Q

Anaplasmosis

A

Anaplasma phagocytophilum/tickborne
Sx:

  • >95%: fever, myalgia, headache;
  • 75%: renal dysfunction;
  • <50%: dyspnoea, cough, confusion
  • Rarely: pancarditis, myocarditis, abdominal pain, renal failure, ARDS….

Dx Lab findings:

  • leukopenia,
  • anemia,
  • thrombocytopenia,
  • Elevated transaminases
24
Q

Viral Hemorrhagic Fever Syndrome (VHF)

A
  • Multisystem syndrome which can be severe and life threatening
  • Damage to overall vascular system
  • In severe cases symptoms accompanied by hemorrhage
  • Four families of viruses are implicated: Arena-, Bunya-, Flavi-, and Filoviridae
  • No vaccines are available for any of the hemorrhagic fevers except Ebola?
  • Diagnosis by serology and virus isolation or genome amplification by PCR
25
Q

Arenaviruses: VHF-Lassa Fever

A

Family: Arenaviridae

Genome: ss - RNA, 2 segments (smaller is ambisense )

– host ribosomes in the virus particle, no function

Epidemiology: **VHF-Lassa fever **

  • reservoir in rats of many species
  • spreads: rat feces and urine, fleas
  • mortality ranges from 10 - 50%
  • West Africa and Sierra Leone where bush meat is consumed

Transmission: urine from rats and patient body fluids (nosocomially)

Incubation period: 6-21 days

Sx:

  • 80% asymptomatic; 15% mortality in hospitalised cases
  • In severe disease: fever, diarrhoea, hemorrhage, shock, encephalopathy, ARDS; deafness in survivors

Dx Lab: serology, blood and CSF

Rx: Ribavirin

26
Q

Bunyaviruses

A

Family: Bunyaviridae

Genera: Bunyavirus, Hantavirus, Niarovirus

Genome: ss-RNA, 3 segments;S, M, L

Epidemiology: reservoir in mice, rats and ticks

Pathogenesis: plasma and RBCs leak through vascular epithelium

27
Q

Arenaviruses: Venezuelan hemorrhagic fever (Guanaritovirus)

A

Sx

  • fever, headache, sore throat, pharyngitis, loss of appetite, nausea, vomiting, seizures and nose and gum bleeding. May be mistaken for Dengue and other hemorrhagic fevers
  • reservoir in cane rats ( Zygodontomys brevicauda ) and cotton rats ( Sigmodon alstoni )
  • mortality 30 - 40%
  • no vaccines
  • rodent control
28
Q

Flaviviruses

A
  • Family: Flaviviridae
  • Genome: ss+ polarity, RNA
  • Epidemiology:
    • – Arbovirus (except Hepatitis C )
    • – All flaviviruses serologically related- cross reacting antibodies

Pathogenesis

  • infect macrophages
  • cell damage by cell mediators – tissue destruction by T- cell
  • shock syndrome;
    • virus-antibody complex enters monocytes via Fc rec
    • antibody enhances infection: Ab becomes protective for the virus leading to higher rates of infections in the cells
    • generally increased production of cytokines
    • severe illness, shock, hemorrhages
29
Q

Dengue fever

A
  • Day biting mosquitoes
  • Epi: India, SE Asia, Pacific, South America, and the Caribbean
  • Incubation period is 2-21 days (usually 3-7)
  • Diagnose clinically; tourniquet test to see if rash goes away

Sx:

  • fever, rash, hemorrhagic shock syndrome
  • thrombocytopenia -> petechiae

Dx: Serology is for retrospective dx

  • Rx is supportive- admit to hospital if platelets drop
30
Q

Congo-Crimean Hemorrhagic Fever

A
  • Genus: Niarovirus
  • Reservoir: wild mouse, hare, squirrels &hedgehogs,
  • Vectors: Hyalomma ticks,
  • Epi: Africa, Asia and Europe: ( in 30 Countires, Iran, Uzbakistan, Russia and Turkey report >50 cases/yr).
  • Incubation: 1-14 days
  • Characteristic 2 peak fever and then rash appears
    • – 1st. Phase; high fever (40oC)and lasts for 10-12 days. with malaise, fatigue, body aches, muscle and joint pain which lasts for 1-7 days. Hemorrhages from 3-7 days ( fever down)
    • – 2nd.Phase; 1-2 days following hemorrhages fever comes back.
  • Nosocomial infection may occur
31
Q

Yellow Fever

A
  • Flavivirus
  • Epi: Africa, South and Central America
  • Transmission: mosquitoes injection
    • Reservoir – monkeys;
  • Incubation period: 3-6 days;
  • Etiopath: Councilman bodies in liver (eosinophilic globules resulting from hepatocyte apoptosis)
  • Sx: In severe disease: hepatic and renal failure; hemorrhage; 15% mortality
    • ​Faget sign: bradycardia w fever
32
Q

Filoviruses

A
  • Genome: ss - RNA, long filamentous virus
  • Virus includes Marburg Hemorrhagic Fever (Marburgvirus) & Ebola
  • Epidemiology:
    • – no known reservoir
    • – mortality ranges from 20 - 90% – Confined to Africa?
  • Etiopath:
    • Replication:
      • virus brings its own RNA-dependent pol
      • endocytosis -> early and late endosomes -> Neimmann-Pick C1 (NPC1) playing major role in release of free viral RNA into the cytoplasm
    • Isoxazole derivatives block Filoviruses in cell cultures by inactivating NPC1 protein
    • glycoprotein peplomers cause destruction of endothelium of blood vessels resulting massive hemorrhages
33
Q

MHF (Marburg Hemorrhagic Fever)

A

Incubation period: ~14 days

**Pathogenesis: **

– tissue necrosis in parenchymal cells of liver, spleen, lungs and lymph nodes

– edema and hypovolemic shock

– BCX4430, small mol. Nucleoside analogue protected monkeys from Marburg virus and MERS-Cov

Sx: fever, rash, hemorrhage, probably DIC

C&C: 20% mortality in original outbreak

34
Q

Ebola

A
    • SS RNA virus
  • glycoprotein peplomers cause destruction of endothelium of blood vessels resulting massive hemorrhages.
  • Incubation period: 2-21 days so Quarantine method may differ from MHF

Etiopath

  • 4 strains recognised;
    • Zaire ( 90%); West African strain may have developed from Zaire virus
    • Sudan ( ~50%)
    • Reston ( nonpathogenic to humans)
    • Cote d’Ivoire ( ~20% )
  • Glycoprotein peplomers cause destruction of endothelium of blood vessels resulting massive hemorrhages

Sx: Sudden febrile illness, fever, anorexia, vascular collapse, internal bleeding (**unique) **& death from days 9 to 12

  • Day 5-9: Sudden febrile illness, fever, chills
  • Day 10: high fever, vomitting, blood, rash, passive behaviour
  • Day 11: in small fraction, bleeding from nose, mouth, eyes, and anus
  • Day 12: seizures, internal bleeding, LOC, death

Possible Rx: Zmapp: monoclonal Ab produced from hybridomas (HAT medium cultured)

35
Q

Cat and dog bites

A

Polymicrobial Oral pathogens

  • Staph, Strep, Anaerobes
  • Pasteurella, Capnocytophaga, Bartonella