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zimvomatshotyana 6 views 46 slides Oct 27, 2025
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About This Presentation

Zoonotic diseases


Slide Content

ZOONOSIS G Shikwambane -Ntlemo

Toxoplasmosis Aetiology - Toxoplasma gondii Worldwide distribution infecting animals and birds Final definitive hosts : Strictly cats and members of Felidae Intermediate hosts : mammals-sheep, goats, rodents, birds

Toxoplasmosis -Transmission Ingestion of oocysts found in soil, water containing cat faeces (raw vegetables) Ingestion of raw meat containing tissue cysts Transplacental Organ transplantation Blood transfusion

Life cycle of Toxoplasma gondii

Life cycle Infective stage: oocysts enter duodenum Release sporozoites which penetrate GI wall and enter bloodstream Invade cells such as macrophages to form trophozoites which multiply rapidly as tachyzoites which enter bloodstream

Life cycle Tachyzoites invade lymph nodes and other organs: acute disease Tachyzoites then enter the nerve cells of brain and eye Multiply slowly as bradyzoites to eventually form tissue cysts= chronic stage of disease in mammals

Life cycle Tachyzoites invade lymph nodes and other organs: acute disease Tachyzoites then enter the nerve cells of brain and eye Multiply slowly as bradyzoites to eventually form tissue cysts= chronic stage of disease in mammals

Toxoplasmosis: Clinical features 80-90% asymptomatic Symptomatic -cervical lymphadenopathy -fever/night sweats -malaise Retinochoroiditis

Toxoplasmosis: Clinical features Congenital Toxoplasmosis Loss of vision (95%) Chorioretinitis Mental retardation Loss of hearing

Toxoplasmosis:Diagnosis - Various Antibody tests (IgM and IgG) using EIA Treatment Spiramycin -Macrolide Prevention Cook meat thoroughly Wash vegetables and fruits before eating Wear gloves while gardening

RICKETTSIAE Different closely related species Pleomorphic intracellular coccobacili , Gram negative bacteria(0.3-0.5 x 0.8-2.0 μm)

RICKETTSIAE Transmitted to humans via arthropods Except for Q fever, which is mainly airborne Life cycles vary

Classification of Rickettsia infections Typhus group including scrub typhus Spotted fever group Q fever and Others

Clinical presentations Typically present with: Fever/PUO Skin lesions/rash Vasculitis Muscle pain Headache Conjunctivitis Organ involvement- hepato -splenomegaly, bleeding

Clinical presentation Rash varies from maculopapular, petechiae Sometimes involving palms and soles, Q fever, Ehrlichiosis: NO RASH

Typhus group 1 .Epidemic louse borne typhus: R prowazekii : transmitted by a body louse when it bites, it defecates on skin and scratching allows skin penetration 2. Endemic flea borne typhus : R mooseri / typhi transmitted by a rat flea 3. Mite borne typhus/ Scrub typhus: Orientia tsutsugamushi transmitted by trombiculid rat mites (red mite)

Typhus group rat mites (red mite) body louse

Spotted fever (SF)group Rickettsial pox: R akari : a ll SF groups transmitted by ticks except R akari : transmitted by rat mite Rocky mountain spotted fever: (RMSF) R rickettsii : demarcentor wood/dog ticks African tick bite fever: R africae - ticks

Spotted fevers • RMSF • African tick

Spotted fevers Vasculitis Eschar Rash South African tick bite fever eschar

Classification: Other ricketssiae Q fever: Coxiella burnetii Trench fever: Bartonella qunitana Bacillary angiomatosis : B.quintana , henselae Ehrlichiosis : Ehrlichia canis , E sennetsu , E chaffeenis

Clinical presentations Typically present with: Fever/PUO Skin lesions/rash Vasculitis Muscle pain Headache Conjunctivitis Organ involvement- hepato -splenomegaly, bleeding

Q fever Aetiology - Coxiella burnetii Reservoir: cattle, goats, sheep, rodents and cause abortion At risk people: slaughterhouse workers, wool sorters Transmitted mainly by: i ) Inhalation (animal placental products and dried excreta in soil dust- 1km) ii) Direct contact with infected animals, material-wool, fertilizers iii) Ingestion (raw milk)

Q fever Clinical Presentation Incubation period: 2-3 weeks Inapparent / Mild acute febrile illness Chronic debilitating febrile illness /PUO Hepatitis Atypical pneumonia Pericarditis Endocarditis- valvular disease NO RASH

Rickettsia diagnosis Mainly clinical Lab diagnosis - Isolation is difficult, serology used to confirm - Embryonated egg yolk sac, guinea pigs inoculated Serology: Weil Felix test, DIF antibody test, CFT for Q-fever, IIF for RMSF PCR

Treatment All treated with doxycycline Complications e.g. endocarditis Combination antibiotics for many months Surgery may be required

Prevention and control General public health measures Epidemic typhus- delousing insecticide Scrub typhus and Ricketssial pox - clearing jungles vegetation where rats and mite live, Spotted fever- insecticide-dog collars protective clothing-boots, tick repellant

Prevention and control Q fever - pasteurization of milk: short time high temp Vaccination to high risk group: -Only for Q fever

Brucellosis Worldwide distribution Important cause of morbidity in the Middle East Sources and etiological agents vary with geographical area Occupational disease animal workers / travelers to endemic areas

Brucellosis (Undulant or Malta fever) Brucella species: Gram negative obligate intracellular coccobacilli B abortus : cattle B melitensis : goats & sheep B suis : pigs B canis -dogs Brucella can survive in the environment for a long time

Pathogenesis of brucellosis Transmitted to man by:- Ingestion of infected raw milk = main MOT Contact of cuts and abrasions of hands with infected meat Aerosol transmission of infected fluids or inhalation of contaminated dust or contact with conjunctiva or nasopharynx Blood transfusion & organ transplantation Breast milk

Pathogenesis of brucellosis Brucellae - phagocytosed, multiply & survive in the phagolysosome of macrophages Spread in the body via lymphatic channels Enters bloodstream enter parenchymatous organs-granulomatous nodules-abscesses in the RES Granulomas in many tissues

Clinical Presentation - Brucellosis Latent/subclinical Acute Brucellosis PUO/Fever worse in afternoons & drops at night with a drench of night sweats lethargy, arthralgia, depression, anorexia Acute bacteremic phase- undulating Malta fever followed by chronic stage for years

Clinical presentation brucellosis Chronic Lymphadenopathy, splenomegaly, hepatitis, spondylitis, neurobrucellosis Note: can affect every organ including endocardium and can mimic any infection B. melitensis = one causing mostly acute and severe disease

Laboratory diagnosis of Brucellosis High index of suspicion- PUO Specimens Blood, bone marrow for culture Biopsy or pus from any relevant site Blood-serum for serology Microscopy: Gram negative coccobacilli Culture on enriched media under 5-10% CO2 for 3weeks, do blind subculture Serology to detect Brucella antibodies agglutination, ELISA for IgA, IgG, IgM PCR

Treatment of brucellosis Streptomycin + doxycycline x 14-21 days) Cotrimoxazole + rifampicin / aminoglycoside in children Longer duration if bones, CNS or heart are involved

Prevention & Control of brucellosis Eradication of animal brucellosis by active animal immunization Food hygiene and milk pasteurized goats milk cheese Occupational hence more in men Infection control standard precautions

Rabies Worldwide distribution Acute progressive encephalomyelitis after infection with rabies virus Genus-Lyssaviruses Family- Rhabdoviridae Transmission: bite/lick-saliva of infected animal- esp dogs, jackals, bats

Rabies

Rabies

Clinical presentation Furious rabies: majority Anxiety Headache, fever, excitability, hydrophobia with spasms of swallowing muscles Delirium, convulsions, coma Paralytic rabies Paralysis of limbs and respiratory muscles

Laboratory Diagnosis Postmortem DFA of brain tissue Viral cell-culture isolation Antemortem DFA of viral antigens in frozen section of skin- back of the neck hairline Blood, CSF antibodies RT-PCR

Rabies prevention and control Active surveillance of animal rabies Notify health authorities Vaccination of all dogs, stray dogs- vaccine laden baits Detain, observe culprit dog x 10days

Rabies prevention and control Euthanise rabid dog Pre-exposure vaccination of high risk individuals: vets, wildlife researchers Proper management of dog bite wounds

Rabies prevention and control Management of dog bite wound Clean and flush wound with soap and water, apply antiseptic, do not suture wound if possible Post exposure prophylaxis given after dog bite Rabies immune globulin at and around site of bite to neutralise virus Vaccine- deltoid -on day 0,3,7,14,28
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