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Flashcards in Obligate Intracellular Bacteria Deck (17)
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1

Obligate intracellular bacteria- characteristics

gram negative (mostly)

small (don't need a huge genome because it uses host machinery) genomes

AT-rich genomes- don't know why this is but maybe it provides stability? 

Must invade host cells and take over normal host machinery 

2

Detection of intracellular bacteria

Culture: generally difficult but CAN be done, therefore not a routine diagnostic procedure: co-culture with eukaryotic cells

Microscopy: non-specific staining--> indicative but not diagnostic

Immunohistochemistry (antigen detection)

Immune responses: antibody or CMI

Genomic detection: PCR 

3

Chlamydia species

Widely distributed, host-specificity, "parasites" and pathogens i.e. many species often reside without overt/apparent disease. 

Pathogenic chlamydia include (major ones we'll look at)

Ch. psittaci: avian -multiple serovars

Ch. abortus- ruminant abortion

Ch felis- cat conjunctivitis and rhinitis

4

Chlamydia infection cycle

Infective form--> adherence to cell membrane (necessity)--> entry by endocytosis--> *prevention of phagosome-lysosome fusion--> replicative form (infective form redifferentiates to replicative form)-->division-formation of "inclusion" (rapid 24-48 hours)--> re-differentiation to infective form--> exit from infected cells

 

1 million BPs--> 1000 proteins

sophisticated infectious cycle. 

5

Chlamydia developmental phases

Elementary body (EB): infective form, spore-like and dense. 300-500 nm (cf. staph=2000nm), some tolerance of environmental streses but not resistance-can survive on pasture

Reticulate body (RB): replicative form, non-infective, 2000nm (much more like typical coccus), divides by binary fission

Non synchronous differentiation-- mixed populations of EBs and RBs 

6

Pathogenic mechanisms of Chlamydiae

Cytopathic effect: interferes with metabolism; cytolysis

"PAMP" effect: molecular components trigger innate inflammatory cytokines (IFN, ILs, TNF)

Acute inflammation: neutrophils and macrophages

Delayed-type hypersensitivity: indicated as cause of damage- contributes to inflammatory damage. 

Secondary immunpathology: primary exposure may not result in serious pathology, but secondary might. 

Latency and persistentce: adept at entering latent phase and persist without causing clinical disease features. This is important to consider in terms of control. 

7

Chlamydophila abortus

Enzootic abortion of Ewes (EAE)/Ovine Enzootic Abortion (OEA)

continually present in UK flock

1st exposure: ~30% abort; 2nd exposure: ~5% abort. 

1st exposure is productive infection, 2nd is less productive. This example makes it difficult to back up the idea of seconday immunopathology. I.e. exposure CAN result in protective immune response. 

8

C. abortus (OEA) pathogenesis

Ingestion/inhalation--> localisation to tonsils/LNs (live in many phagocytic cell types)-->dissemination (unknown tissues, cell types)--> placentitis (animals could just be slightly febrile or appear normal until end of infection. seems infection becomes reactived in late pregnancy)

Placentitis--> fetal infection--> abortion, stillbirth, weak lambs, subclinically affected lambs.

Placental lambs are heavily infected, contaminated environment (Elementary bodies)

9

C. abortus- tx and control

ABX: tetracyclines

Closed flocks/OEA free-accrediation

Vaccines: mediavac, enzovax, cevac chlamydophila

ZOONOSIS: respiratory and abortion

10

Zoontic chlamydiosis

non-specific in humans

fever, chills, headache, muscle aches, dry (non-productive) cough, malaise, penumonia, endocarditis/meningitis/ abortion

typically aquired via inahalation

NB: C. psittaci is a schedule 5 notifiable pathogen 

11

Anaplasmoses/Erlichioses

Anaplasma spp and Ehrlichia spp.

Arthropod borne therefore geographically restricted. 

 

12

Anaplasma phagocytophilum

Tick borne fever (TBF)

Tick hemolymph--> inoculation by tick bite--> infection of neutrophils

Show up on histology as light irregular purple staining in cytoplasm of neutrophil= inclusion bodies of anaplasma phagocytophilum. 

13

Anaplasma phagocytophilum- TBF pathogenesis

Infection of neutrophils--> cytokine release/neutropenia

causes: 1) fever, abortion, decreased milk yield, decreased weight gain (non-specific signs, but indicative)

2) "immunocompromise"--> secondary infections--> tick pyremia (S. aureus introduced into tick bite wound), systemic pasturellosis, louping il, listeriosis

Persistent infection (reservoir). 

14

Coxiella burnetti- Q fever

Asymptomatic in ruminants--> excreted in urine, feces, milk and placenta--> inhalation by human--> infects respiratory epithelium, endothelium and phagocytes--> flu-like syndrome, pneumonia and endocarditis

nb: coxiella burnetti causes occasional abortion storms- esp in goats 

ZOONOSIS + ATCSA schedule 5

15

Porcine proliferative enteropathy

PE, ileitis

Diarrhea, hemorrhagic diarrhea, fatalities

Non-specific signs: reduced/variable weight gain, reduced feed conversion, variable or low slaughter weight

low value

caused by Lawsonia intracellularis 

16

Pathogenesis of Lawsonia intracellularis/ PE

ingestion--> invasion of ileal crypt enterocytes--> epithelial hyperplasia (mature epithelium replaced with immature non-differentiated epithelial cells)--> intestinal thickening. 

 

highly prevalent pathogen- up to 95% seroprevalence at farm and animal levels. worldwide distribution. 

Lawsonia has a lot of unique features and v. few conserved system: has flagella, has a type III and type V secrtion system 

17

Controlling PE

ABX: tylosin, tiamulin, tetracycline

biosecurity

vaccine: attenuated L. intracellularis strain (oral drench or in drinking water)