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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 


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 


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


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. 


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 


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. 


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. 


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)


C. abortus- tx and control

ABX: tetracyclines

Closed flocks/OEA free-accrediation

Vaccines: mediavac, enzovax, cevac chlamydophila

ZOONOSIS: respiratory and abortion


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 



Anaplasma spp and Ehrlichia spp.

Arthropod borne therefore geographically restricted. 



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. 


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). 


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


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 


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 


Controlling PE

ABX: tylosin, tiamulin, tetracycline


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