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Zoonoses
Lectures 52-54
| Question | Answer |
|---|---|
| zoonoses | an infectious disease of lower animals that may be transmitted to humans. |
| Category A biological warfare/terrorism agents | B. anthracis, C. botulinum, Yersinia pestis, variola major, Francisiella tularensis, viral hemorrhagic fevers |
| Category B biological warfare/terrorism agents | Brucella, C. perfringens, Burkholderia mallei (glanders), Coxiella burnetti, Ricinus communis, S. aureus enterotoxin B |
| Rickettsiae | prokaryotic, gram-, have peptidoglycan, de novo DNA RNA and protein synthesis, oxidize glutamic and citric acidsnot glucose, ATP exchanged for ADP in both directions, obligate intracellular pathogens |
| Rickettsia classifications | Typhus group (prowazekii, typhi), Spotted fever group (A: rickettsi, siberica. B: conori, parkeri. C:akari, australis) Scrub typhus (tsutsugamushi) |
| Related to Rickettsia | Rochlimaea (trench fever, cat scratch fever), Coxiella(Q fever) Erlichia (erlichiosis, invades WBC) |
| Rickettsial diseases, common features | animal reservoir and insect vector, primary infection in vascular epithelium, leakage of RBC causing petechiae, adrenal glands also affected. Steady high fever, retroorbital headache, rash. No known toxins |
| Macule | discolored spot, darker than surrounding skin, caused by leakage of blood into surrounding epithelium |
| Papule | elevated spot, raised above surrounding skin, caused by inflammation, often darker than surrounding skin |
| Vesicle | elevated small blister, filled with clear fluid, surrounded by area of inflammed skin, usually darker than the surrounding area, fluid often has infectious material |
| pustule | same as vesicle, but center filled with pus |
| crust | dried, partially healed pustule, infectious organism often present in a semi-dormant state |
| Rickettsia prowazekii reservoirs and vectors | primary reservoir=man (Brill Zinnser carrier state), transmission by human body louse, secondary reservoirs=sheep, cattle, goats (all trans. by ticks), wild flying squirrel (lice and fleas). |
| Pedunculus humanis (human body louse) | permanent ectoparasite of man, prefers 29-30C, leaves person with fever or cooling body, stays close to body odor and own excreta, avoids excessive moisture, prefers rough surfaces, 10-20 insects/adult usually |
| Effect of R. prowazekii on Pediculus | louse actively infected, Rickettsia multiply in epithelial cells of louse midgut, cells destroyed and lyse, rickettsia released into fecal stream. Infection fatal to louse, survive 10d after infection |
| Typhus clinical course | incubation 7-14 days, headache, steady high fever, maculopapular rash on trunk spreading to extremities. Complications cand be fatal: myocarditis, vascular collapse, CNS dysfunction |
| Diagnosis/treatment of epidemic typhus | primary=serologic (Weil Felix: retrospective), therapy started on basis of clinical signs and symptoms with epidemiological input. Tx:tetracycline or chloramphenicol, prevention:public health sanitation, vector control |
| Prognosis of epidemic typhus | delay of therapy into second week increases fatality rate, untreated fatality is 25%, age dependent. Malnutrition, stress, secondary infection increase mortality rate. Range 10-60%, therapy reduces to 5-7% |
| Epidemiology of R. ricketsii | New world, focus in US, found in South America, Appalachian mtns in US, carried by tick (Dermacentor andersonii (wood tick): western, Dermacentor variabilis (dog tick): eastern, Ambylomma americanum (lone star): southwest). Reservoirs: dogs, wild rodents |
| Clinical aspects of Rocky Mountain spotted Fever | incubation 2-6d, fever, headache, toxicity, mental confusion, myalgia. Rash on 2-3d, appears on wrists/ankles and spreads to trunk, seen on palms and soles. Untreated can be fatal:DIC, thrombocytopenia, encephalitis, vascular collapse, renal/heart failure |
| Diagnosis/treatment Rocky Mountain spotted fever | Primary=serologic, sepcific Ab do not appear soon enough to be useful, therapy started on basis of clinical signs and spidemiology, Tx: tetracycline and chloramphenicol. sulfonamides contraindicated |
| Coxiella burnetii bacteriology | similar to Ricketsia, multiplies in host phagolysosome, prefers low pH, highly resistant to drying, survives in dusts and high temp. Reservoirs=cattle, sheep, goats, maybe wild animals |
| Coxiella burnetii pathogenesis | exposure by inhalation of dusts, secondary though ingestion of contaminated meat or dairy products. Most infection are inapparent (walking pneumonia), little known about pathology, affinity for RES, chronic and fatal infections are rare |
| Coxiella burnetii clinical course | incubation 7-21 days, fever, chills, headache, mild dry persistent cough, patchy interstitial pneumonia, no exanthem, complications rare: endocarditis or encephalitis. Fatalities very rare |
| Coxiella burnetii diagnosis and treatments | serologic, demonstrate high or rising titers by complement fixation or immunofluorescence. Signs/symptoms insufficient for Dx, mainly supportive care, tetracycline may shorten course, most resolve spontaneously |
| Erlichiosis | emerging, glandular fever, western Japan and Malaysia, unknown transmission, canis and chafeensis in US, transmitted by Brown dog tick, misdiagnosied as Rocky Mountain, fever, GI abnormalities, cough, diarrhea, lymphadenopathy, resp/renal insufficiency |
| Rochalimaea henselae | cat scratch disease, 90% of patients (rest if Afipa felis), papule or pustule 3-10d after cat scratch, heals spontaneously, 2-3w later regional lymphadenopathy, may persist for 2-4 months. Most recover spontaneously |
| Bacillary angiomatosis | Rochalimaea henselae, mostly in HIV+ patients, multiple subcutaneous enlarging red papules, occur in viscera as well |
| Bacillus anthracis | cattle, horses, goats, sheep, used as a biological weapon, gram+ rods, facultative anaerobe, heat resistant, spore forming, non-motile, non-hemolytic, capsule (glutamyl polypeptide) |
| Virulence factor Bacillus anthracis | lethal factor: causes tissue necrosis. Edema factor: causes infiltration and tissue swelling, may enhance distribution of lethal factor. Protective Ag: same substance as edema factor with additional effect |
| Clinical manifestations of anthrax | Cutaneous: accidental by fomite contact, most common in humans, least life threatening. Gastrointestinal: transmitted in nature, rare in humans, most common in grazing animals, high mortality. Pulmonary: highest mortality in humans, inhalation of spores |
| Cutaneous Anthrax pathogenesis | papule at primary site, becomes depressed black necrotic ulcer (eschar), edema and redness may occur without ulceration, incubation 1-12d, case fatality: untreated=20%, treated=1% |
| Gastrointestinal Anthrax clinical features | abdominal distress, bloody diarrhea/vomiting, fever and septicemia, may have oropharyngeal ulcerations with cervial adenopathy and fever. Incubation 1-7d, fatality 25-60%, ingestion of poorly cooked meat, RARE |
| Inhalational anthrax clinical features | brief prodrome with myalgia, fatigue, fever, +/-resp symptoms, followed by hypoxis, dyspnea, mediastinal widening, meningitis in 50%, incubation 1-7d, fatality: no treatment=97%, treatment=75% |
| Gram negative rods: zoonoses | Brucella, Yersinia pestis, Francisiella tularensis, Pasturella muticoda, Burkholderia mallei |
| Gram negative spirals: zoonoses | Leptospira interrogans,Borellia |
| Brucella bacteriology | gram-, non-motile, have 2 chromosomes of unequal size, chromosomal mapping, some have small capsule, aerobes, nutritionally fastidious, facultative intracellular pathogen, slow growing, require complex media, capneic |
| Brucella epidemiology | venereal disease of farm animals:chronic infections in mammary glands, uterus, placenta, seminal vesicle, epidiymis. Occupational contact: butchers, vets, access through skin breaks, aerosols. Ingestion of infected dairy products, killed by pasturization |
| Brucella pathogenesis | penetrate skin/mucous membranes, carried to lymphatics by PMNs, multiply in macrophages, humoral immunity has no effect, T cell response is only control, failure--> multiplication in RES, recurrent bacteremia |
| Brucellosis clinical findings | incubation 7-21d, onset drenching sweat with high fever in afternoon/evening, chronic episodes of nocturnal fever may persist for months/years, marked weight loss, sometimes glandular/hepatic symptoms |
| Brucellosis diagnosis | serologic: not definitive, agglutination of heat killed cells, rise in titer of 1:640 in acute disease, isolation and culture=definitive. Prolonged incubation for blood cultures. Blood agar okay. |
| Brucellosis therapy | chemotherapy no rapid results, fever remains for 7 days after proper treatment, must be prolonged (relapses common), tetracycline=primary antibiotic, streptomycin gentamycin, or rifampin secondary, no human vaccine |
| Francisella tularensis bacteriology | gram- coccobacillus, facultative, not spore forming, nutritionally fastidious (no growth on blood agar, need sulfhydryl compounds, (cysteine-glucose blood agar), slow growing |
| tularensis epidemiology | small wild mammals (rabbits, muskrat, squirrel, beaver), ticks and deer flies are vectors, found in North America, Canada, and Mexico, not found in old world, SW US is focus |
| tularensis pathogenesis | inhalation, ingestion, or injection, minimum infective dose <100 cells, bacteremic spread, infects RES with granuloma formation, ulcerated lesion at infection site, recovery=immunity |
| tularensis clinical presentation | incubation 2-5 days, acute fever chills and malaise, ulcero glandular lesion at injection site, typhoidal from ingestion, pneumonia from inhalation (greatest mortality), all progress to systemic, mortality 5-30% |
| tularensis diagnosis | careful history essential, culture difficult/risky, direct fluorescent Ab is sufficient, serodiagnosis: rise in agglutinating Ab 1:40 to 1:320 in 1-2 weeks, treat with streptomycin |
| pasturella multicoda bacteriology | gram-, facultative, ferments carbs, oxidase+, grows on enriched media (blood agar), but not on media selective for gram- (MacConkeys), sensitive to penicillin |
| Pasturella epidemiology | normal respiratory flora of many lower animals, human infected by bite or scratch, sometimes in human sputum |
| Pasturella symptoms | local infection at inoculation, diffuse cellulitis with clear border, symptomatic=rare, diagnose with culture from aspirated pus, treat with penicillin |
| Burkholderia species(B. mallei) | causes Glander (veterinary disease), contacted from domesticated animals (horses, donkeys, mules), endemic in Asia, Middle East, Africa, central and South America. No known free living state, used as germ warfare (WWI/WWII). |
| B. pseudomallei | causes Meliodosis, free living in fresh stagnant water, endemic is SE Asia, infects sheep, cattle, pigs, dogs, cats, and humans. Man to man transmission rare but possible |
| Glanders and Meliodosis symptoms | acute local infection (local ulcer, can spread to lymphatics), pulmonary infection, acute septicemia (chronic illness predisposes, highest fatality), chronic (visceral damage, multiple abscesses) |
| Glanders and Meliodosis diagnosis | difficult, pulmonary resembles TB, local resembles many other things, must isolate bacteria (blood, sputum, urine, skin lesions) |
| Glanders and Meliodosis prognosis | chronic infection can remain dormant 10-20 years until pt is stressed, complication of HIV/Diabetes, all can progress to septicemia (fatal form), 95% fatal without treatment, 35-60% fatal with treatment |
| Yersinia pestis bacteriology | gram-, enterobacteriacae, non-spore forming, oxidase-, facultative, ferments glucose, grows in standard media, polysaccharide capsule in virulent strains |
| Yersinia environmental niche | disease of small rodents, lymphohematogenous infection, endemic in rodent population, flea gets it when taking a blood meal from infected rodent, multiplies in proventriculus of flea blocking GIT, flea regurgitates when attempting to take another meal |
| Yersinia reservoirs | semi-arid SW US, SE Asia, central Asia. Not in Western Europe, Africa, or Australia |
| Yersinia pathogenesis | exposure through flea bite, reaches lymph node, rapid multiplication, infected node swells (Bubo), bacteremia seeds liver spleen lungs and sometimes meninges, pulmonary then transmitted by droplets (pneumonic plague) |
| Yersinia symptoms | incubation bubonic: 4-7 d, pneumonic 18-36 hr, acute stage bubonic: swollen painful inguinal lymph nodes, increasing fever, pooling of blood/microhemorrhages in face/extremities. Pneumonic: violent bacterial pneumonia, nearly always fatal |
| Links with HIV | descendants of those who survived bubonic plague have heightened resistance/immunity to HIV. have gene coding for defective CCR-5 sequence (fails to attach and bring HIV in by RME), heterozygous=increased resistance, homozygous=immune. |
| Yersinia diagnosis | bubonic: epidemiology, lymph node aspirate or blood sample, fluorescent Ab test, culture dangerous. Pneumonic: epidemiology, sputum exam, fluorescent Ab test, no time for culture, tx:streptomycin |
| Borreliosis history | reservoir wild rodents, vector louse or tick (in louse borne fever Borrelia is maintained in humans, in tick borne it survives in humans) |
| Borrelia bacteriology | rough loose gram- spiral, outer membrane encoded by plasmids (increased antigenic variability), nutritionally fastidious, can grow in axenic artificial liquid cultures |
| Borrelia relapsing fever | abrupt chills/fever, incubation 3-4d, microorganism invades spleen liver kidneys eyes and brain, initial attack 3-7d, up to 4 cycles of recovery/relapse each shorter and less severe, diagnose with stained blood smear, Tx: tetracycline/chloramphenicol |
| Lyme disease history | reservoirs various wild mammals (white tailed deer, white footed deer mouse, worldwide, most common vector borne disease in US/NW Europe, vector tick (Ixodes dammini=US E coast 35-50% infected, Ixodes pacificus=US W coast 2% infected), nymph transmits |
| B. burgdorferi behavior in tick | Borrelia adheres to epithelial cells of tick midgut (quasi dormant state), when tick feeds=exposed to higher temp and activated, multiply and penetrate gut wall, spread to tick salivary glands, injected into host on bite |
| Ixodes life cycle | takes 2 years, eggs hatch to larvae (spring/summer), need vertebrate blood meal to develop to nymphs (fall), dormant in winter, another blood meal to become adult (spring/summer), now infectious, adults mate/lay eggs (summer/fall), eggs dormant in winter |
| Geographic distribution of lyme disease | temperate zones of northern hemisphere (30-50N), can hitch hike on ships and planes around the world |
| Lyme disease primary stage | erythema chronicum migrans (target lesion), appears at bite site 3-14d, red/brown/purple lesions on earlobes, nipples, and scrotm/extremities, stiff neck, headache, low grade fever, arthralgia, 40-50% of cases |
| Lyme disease secondary stage | secondary annular skin lesions (exanthem), CNS cardio opthalmic and musculoskeletal manifestations |
| Lyme disease tertiary stage | acrodermatitis chronicum atrophicans (atrophy/discoloration of the skin), diverse CNS symptoms, arthritis (knee usually), cardiomyopathy |
| Lyme disease diagnosis and treatment | Dx: borrelia in blood smear in early stage only, serology for later stage unreliable (ELISA, IFA). Tx: doxycycline or amoxacillin for early disease, ceftriaxone or cefotaxime for later, prolonged therapy |
| Lyme disease vaccine | cell free preparation, outer surface protein (OSP A-C), OspA triggers protective Ab response, high levels of anti OspA IgG formed |
| Leptospirosis history | commensal in the kidneys of many wild animals esp rodents, shed in urine and transmitted in drinking water, man is accidental host, organism enters through skin abrasions or mucous membranes, multiples in blood, seeds liver kidneys lungs and meninges |
| Leptospira bacteriology | tight gram- spiral, one or both ends in hook, actively motile, sensitive to heat drying and most chemicals, survives in alkaline ground water or soil but does not multiply |
| Leptospira clinical | incubation 8-12d, early:chills, headache, severe muscle pain (thighs, calves, abdomen). Later:Weil's disease: jaundice, renal dysfunction, severe hemorrhagic manifestations, high mortality. Serodiagnosis: micro/macro agglut, Tx: penicillin |
| Hemorrhagic fever | Flavi, Arena, Bunya, and Filoviridae; no vaccines, tetracycline used, diagnose by serology and virus isolation or genome amplification by PCR |
| Flaviviruses | ss+RNA, all are serologically related, infect macrophages, tissue destruction by T cells, shock syndrome, virus-Ab complex enters monocytes by Fc receptor, Ab enhances infection |
| Dengue fever | flavivirus, fever, rash, hemorrhagic shock, mosquito vector, reservoir unknown, Primary: mild, complete recovery, circulating Ab. Secondary: virus-Ab complex in monocytes, cytokine storm |
| Yellow fever | flavivirus, reservoir monkeys, vector aedes aegypti, hemorrhagic fever with hepatic failure (jaundice) |
| Arenaviruses | ss-RNA, 2 segments (larger has genetic info), reservoir in rats, spread through rat feces/urine, mortality 10-50% |
| Lassa fever | arenavirus, fever, diarrhea, hemorrhage, hemoconcentration and collapse, african bush rat=reservoir, person to person spread unknown, diagnose with CSF and blood |
| Bolivian hemorrhagic fever | fever, myalgia, hemorrhage, shock, neurologic illness, bush mouse=reservoir, 15% mortality, due to human introduction in uninhabited areas |
| Argintinean hemorrhagic fever | fever, myalgia, hemorrhage, collapse Callomys mouse=reservoir, 10% mortality |
| Venezualean hemorrhagic fever | fever, headache, sore throat, pharyngitis, loss of appetite, nausea, vomiting, seizures, nose and gum bleeding, cane rates=reservoir, mortality 30-40%, no vaccine |
| Bunyaviruses | ss-RNA, 3 segments (S,M,L), reservoir mice rats and ticks, plasma and RBCs leak through vascular epithelium |
| Korean hemorrhagic fever | hantavirus, hemorrhagic fever with renal syndrome, mice and rats=reservoir, severe pulmonary syndrome in SW US (Sin Nombre), no vaccine |
| Congo-Crimean hemorrhagic fever | niarovirus, fever, hemorrhage, tick/rodents=reservoir, no vaccine |
| Filoviruses | ss-RNA, no known reservoir, mortality 20-90%, may be confined to Africa |
| Marburg Hemorrhagic fever I | fever, rash, hemorrhage, DIC, no known reservoir or vector, 20% mortality in original outbreak |
| Marburg hemorrhagic fever II | tissue necrosis in parenchymal cells of liver, spleen, lungs, and lymph nodes, edema, hypovolemic shock |
| Ebola I | sudden febrile illness, vascular collapse, internal bleeding, death, Sudan and Zaire, no known vector or reservoir, 90% mortality |
| Ebola II | glycoprotein peplomers cause destruction of endothelium of blood vessels, massive hemorrhage, 4 strains: Zaire (90%), Sudan (50%), Reston (non-pathogenic), Cote d'Ivoire (20%) |
Created by:
kamarsh
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