by (1) ascending through the cervix post-service or at farrowing (problems most common in early gestation, leading to endometritis and vaginal discharge) or (2) the haematogenous route (any stage of pregnancy - localisation in the endometrium or enter the lumen, leading to placental damage and foetal death). 

Common in herds, insidious onset, discharge (thick creamy or muco-haemorrhagic) seen 10-20 days post service. May persist for weeks/months if untreated or resolve spontaneously after 1-2 weeks. Discharge may arise from vagina, uterus, bladder or kidney inflammation. Quantity of discharge varies from slight to copious (500ml) per day. Typically, up to 10% of served sows can show discharges and farrowing rates can be reduced to 75% due to regular or irregular returns to service and abortions. Higher prevalence in higher parity sows (>4 parity). 

Mixed population of ubiquitous organisms eg. A pyogenes, E coli, Streptococci, Pseudomonas spp. Eubacterium suis infection common in cystitis or pyelonephritis.

• - Not all discharging sows return to service (some remain pregnant). If discharge is copious, sows are unlikely to be pregnant.

•   - Treat discharging sows promptly with long-acting broad spectrum antibiotic by injection or instillation via AI catheter (Beware - a slight discharge in the first week after service is of no pathogenic significance - usually due to seminal debris).

•   - Do not re-serve sows while discharging. Once recovered, use AI for next service: avoid possible boar contamination. If discharge recurs or sow returns for a second/third time - cull.

• -   Cull sows at parity 7

• -   Adopt stringent hygiene for boar pens, service pens and sow stalls/accommodation especially that used

  in the first 21 days post service. (plenty clean straw)

• -   Boars can be treated - long acting broad-spectrum antibiotic by injection and infuse prepuce with

  intramammary tubes daily for 5 days. Some units treat boars as above on a quarterly basis.

• -   If the problem is widespread: in-feed antibiotic medication can be given to sows post weaning up to 28

  days post service (and to boars intermittently in place of the above treatment regime).

-   Treatment of a discharge problem needs to be maintained for approximately 6 months (until all the sows have received a course of medication).

• -   Prophylactic antibiotic treatment of sows at service (eg. long-acting penicillin) is useful when a discharge problem is detected in its early stages. 

0. Term now used to replace diverse and confusing terminology (eg farrowing fever, lactational failure, mastitis-metritis-agalactia (MMA: metritis only rarely contributes to lactational failure.), puerperal mastitis etc). 

   Caused by a variety of coliform bacteria (E coli, Klebsiella, Enterobacter spp); bacterial spp common in the sow’s environment. Organisms come in contact with teats through inadequate hygiene or via piglet's oral flora. 

   Endotoxaemia is considered to be the cause of agalactia. Septicaemia does not develop. Coliform mastitis does not appear to result in protective immunity (recurrence at subsequent pregnancies has been recognised). 

0. Initial signs on day 1 or 2 post farrowing (but may occur during parturition), temperature response (up to 42 oC), listless, weak, loss of interest in piglets, prefer sternal recumbency, may become weak and comatose (rare), reduced feed and water intake. Signs last 2-3 days. 

   Piglets gaunt and hungry- looking, continually trying to feed, restless. Skin over mammary area reddened. Sub-cutaneous oedema. Udder may be hardened and painful. Secretion from nipple may show evidence of mastitis (two or three sub-complexes drain into each nipple). 

   Some sub-complexes may be unaffected causing secretion to appear normal. 

0. Broad-spectrum antibiotic, NSAIDs, oxytocin ( milk let down to get toxin out) . Care for piglets, cross fostering, feed with milk, substitute, prevent chilling.
   
   

   Prevention: Good hygiene. Some farmers restrict feed and give laxatives 24 hours pre-farrowing but there is no scientific evidence that this prevents coliform mastitis. Use of sulpha-trimethoprim in feed from day 112 for 4 days is helpful when agalactia is becoming a more serious problem. Vaccines against enteric strains of coliforms not thought to prevent agalactia. 

0. A common progression in breeding herds: non-specific illness in sows (anorexia and dullness), 1-2 weeks later reproductive losses followed by unthriftiness, respiratory illness and mortality in piglets and all ages of growing stock. 

   
   

   Effects on neonatal piglets can be severe: respiratory distress, scour, unthriftiness, high mortality. Semen quality may be impaired following infections of boars. Blue ears, snout and vulva are only seen occasionally (1 – 5% of sows). 

   
   

   Reproductive problems include infertility (normal oestrus delayed, returns to service increased), premature farrowing, stillbirths and weakly piglets born. 

Clinical features, serology (paired samples; rising titres but be aware of vaccination status), virus isolation (from aborted, stillborn or non-viable piglets). PCR test for virus from blood, semen, throat swabs.

Differential diagnosis: Swine influenza, Aujeszky's Disease

Management strategies. If free of PRRS: buy replacements and AI semen from sero-negative herds, ensure thorough biosecurity: prevent introduction via vehicles etc. If present in herd: apply a vaccination policy. Vaccines are available include killed European strain virus vaccines, live attenuated European strain vaccines and a live attenuated US strain vaccine. The latter is not being used in the UK to avoid the risk on the US strain of PRRS virus being introduced into the country. See Table 04/1: Available PRRS vaccines in the UK. More details in lecture 9. 

Four strains of Influenza A virus occur in pigs in the UK; avian-like HIN1 (195852), H1N2, H3N2 and classical H1N1 (2009, pandemic). The avian-like strain remains a recurring problem in many units. The acute phase of the disease lasts approximately 4-16 weeks. Most consistent features, influenza-like illness affecting all ages of pigs, reproductive losses in pregnant stock and increased pre-weaning mortality.

In 2009/10 the H1N1(2009) virus (so-called ‘swine flu’) caused widespread alarm among the human population on account of the global spread of disease and the serious illness that affected individuals with existing medical complications. Although many people were thought to have contracted the illness in the UK, very few pig units were affected. 

Very similar to PRRS except respiratory signs are more widespread and severe especially if there are other endemic respiratory diseases on the farm. In ‘minimal disease’ units the respiratory signs can be mild, with reproductive losses presenting the major problem.

Virus enters respiratory tract, multiples rapidly in bronchial epithelium, virus disappears by 9-10 days post infection. Animals can become viraemic. Transplacental infection occurs.

Other epidemiological features: Infection can persist in units for many months causing persistent or recurring losses. Virus carried by pigs. Maternal immunity demonstrable for up to 4 months and can interfere with development of active immunity. Zoonosis. 

Diagnosis: Clinical features, serology (paired samples; rising titres), virus isolation (aborted piglets, infected lung in acute stage of disease)

Differential diagnosis: PRRS, Aujeszky’s Disease

Management strategies. Do not allow staff or any visitors who are suffering from influenza to have contact with pigs. If free of swine influenza, buy replacements from sero-negative herds. Herd security: prevent introduction via vehicles etc. If present in herd: disinfection, expose gilts to breeding sows before pregnancy to establish immunity. Only vaccine for pigs available in UK: Gripovac 3 (does not include pandemic). 

Porcine parvovirus occurs worldwide, with a very high prevalence in UK herds. It is associated with the SMEDI ( still born, mummified, embryonic , death, infertility ) syndrome along with a number of enteroviruses.

Porcine parvovirus occurs worldwide, with a very high prevalence in UK herds. It is associated with the SMEDI ( still born, mummified, embryonic , death, infertility ) syndrome along with a number of enteroviruses.

ll reproduction associated: stillbirths, mummification, embryonic death, infertility, increased regular and irregular returns to oestrus, small litters. In non-pregnant gilts and boars, infection is of no consequence. Signs depend on stage of pregnancy; <35 days gestation: failure to implant, re-absorption, return to oestrus. 35-70 days gestation: mummification; piglets are infected progressively, resulting in small to large mummies (from ovarian end to cervical end). >70 days gestation: stillbirths, live but weakly piglets. 

Infection by oro-nasal or venereal routes, viraemia, tranplacental spread approx 10-14 days post-infection. Spreads into boar reproductive organs and semen from approx 7-21 days post infection. Virus adheres to eggs, embryos and foetuses until they reach immunocompetence at approx 70 days gestation.

Virus kills foetuses up to approx 70 days but pregnancy is maintained and piglets all mummified at birth or mixed mummified, stillborn and live piglets born. In immunocompetent piglets, virus causes endothelial damage (meningoencephalitis) and placentitis, liveborn piglets are either immune or infected immunotolerant. Colostral-derived immunity lasts 4-6 months (sometimes longer). 

Diagnosis: clinical features, paired maternal serology (rising titres). Foetuses: virus detection (PCR on foetal liver). Serology in large fresh foetuses and stillborns.
Differential diagnosis: PRRS, Enteroviruses, Swine influenza, Leptospirosis, Aujeszky’s disease, Brucella. 

Control: Vaccinate susceptible stock - incoming gilts, sows, boars. Annual vaccination recommended, though not always done as producers often prefer to keep active infection in herd, thereby boosting natural immunity. C&D and vaccination of whole herd if outbreak suspected. 

This virus has been recognised for the past 10 – 15 years and is primarily associated with postweaning multisystemic wasting syndrome (PMWS), now known as Porcine Circovirus (associated) Disease. Most herds in the UK are endemically infected. When entering naïve herds or infecting naïve gilts, it can cause reproductive problems including transient infertility, foetal re-absorption and increased regular and irregular returns to oestrus. A vaccine is available for breeding-age pigs (as well as for piglets) and can be used if PCV2 is thought to be affecting the herd’s reproductive performance.  

Leptospirosis occurs worldwide, with varying serotypes and serovars in different countries. In UK, L. bratislava is of most importance with L. canicola and L. icterohaemorrhagiae occurring rarely. Occurs in both indoor and outdoor herds, but more common in outdoor units.

Mainly reproductive in the UK. Abortion, stillbirths, weak piglets of reduced viability. Abortion in last trimester is common. Infertility, increased returns to service. 

Infection by oro-nasal, venereal routes. Bacteraemia, localised in renal tubules, shed in urine. Transplacental infection occurs, localises in uterus, foetal invasion, abortion 10 days-4 weeks post infection. Infection can persist in both urinary and genital tracts of sows and boars. Subclinical infection common in herds (many herds sero-positive). Seldom large numbers of pigs affected at any one time. 

Diagnosis: Clinical signs, paired maternal serology (value?). Sample sows with a history of recent abortion/infertility and assess the titres of the batch. Foetus: antigen detection (FAT), serology. Differentials: PRRS, Parvo, Erysipelas, Swine influenza, Aujeszky’s Disease, Salmonella, Brucella. 

Control: Treatment of individual animals is seldom justified. In-feed medication of sows (Chlortetracycline 3kg/tonne) for 1 month in spring and 1 month in autumn found to be beneficial. Prevent contact with free- living vectors. No vaccine available in UK.