Kitten Season Is Upon Us

and sadly some kittens will not survive the first days and weeks of life

A likely culprit – Streptococcus G

One of the greatest pleasures of cat breeding is celebrating the safe arrival of a litter of healthy kittens. Watching an unfussed queen have an easy labour, deliver her kittens competently and happily, and go on to rear a litter of bright-eyed, bouncy, happy, friendly little cats is the “best it can get” experience. Unfortunately it is not always like that.

UNEXPLAINED KITTEN DEATHS

Sometimes things go wrong. Kittens get sick, sometimes very sick, and deteriorate rapidly. Onset of illness can be hours, days or a few weeks after birth, and progression of the infection is characteristically rapid – well in the morning, dead by nightfall or the next day or two. You rush to the vet, come home with antibiotics, kitten milk replacer, subcutaneous fluids, and watch as the tiny kittens struggle to live. Standard URTI treatments are usually prescribed, but they aren’t very successful.

Some kittens do recover if they are treated early in the course of the infection, but there are litters where, despite best efforts, some kittens succumb to intractable upper respiratory disease, losing weight and losing strength, and within hours or a few days, dying. Sometimes none survive. Does this scenario sound familiar? It’s a mystery bug that is rapid and lethal for kittens. This is the profile of Streptococcus G infection.

STREP G

Strep G is a bacterium that can live on the queen’s vulva and vagina, causing her no problem. It is introduced to the kitten’s respiratory tract during birth, and rapidly becomes rampant. A bacterial weed – growing like mad in the wrong place.

The surviving female kittens are almost certainly carriers from this early age, as the queen already is. Strep G cocci which find their way into the female kittens’ vaginas are ready for the next generation of kittens to be infected. Unless Strep G is eradicated, the pattern will likely reoccur in infected females in subsequent generations.

HOW INFECTION HAPPENS

Cats pass Strep G around because of the friendly mutual grooming habits, licking the genital areas of friends and themselves. Queens grooming their kittens infect the kittens. Infected “aunties” can do the same thing.

HOW CAN I TELL IF MY CATS MIGHT HAVE STREP G?

Here’s how to go about it. Go back through the breeding records of all of your breeding stock, and list the following. Yes, write the information down; you can use it in discussions with your vet later. Seeing the information written down makes it easier to see the overall picture. The pattern in your cattery over time is the evidence you need to make your case for treating your cats.

For every queen, note the following:

  1. Is she a survivor of a litter where one or more kittens died of respiratory illness?
  2. Has she had aborted or absorbed litters?
  3. Has she delivered any dead kittens early or full term?
  4. Has she, at full term, been in labour that was half-hearted, sporadic, and eventually needed veterinary intervention? Has she evidenced uterine inertia?
  5. Has she had kittens where one or more became very ill, and even died in the period from 24 hours to 2 months after delivery?
  6. Has that pattern repeated in subsequent litters?
  7. With different studs?
  8. What treatment was prescribed?
  9. How well did it work?
  10. What was the survival rate, and how long did the kittens live?
  11. Did you have any tests done and what were the findings?
  12. Any autopsies? What were the findings?
  13. Have any of her daughters been bred, and what are their relevant histories? Create this list for each of them.
  14. What about her mother? Create this list for her too.

Look for patterns, clusters of these events occurring over time and involving some or all of your queens. Include females you may have sold for breeding. The pattern is the clue that there is a persisting underlying problem that has not been correctly treated, probably because it has never been accurately diagnosed.

If your own research reveals some or all of these 14 issues in your own cattery, take one or more of your affected queens to your vet for a vaginal swab to test for Strep G.

SPECIAL TEST FOR STREP G available at Gribbles Veterinary Pathology Laboratory (some path labs don’t test for Strep G). Tell your vet to order GVPL to (1) determine if Strep G is present in the cat’s vagina, and (2) to culture and do drug sensitivities. Your vet will have the details for GVPL.

ERADICATION

Clindamycin kills Strep G. Treat with Clindamycin (Antirobe) daily for 21 days. This is safe for pregnant cats. Treat all your cats as described above.

Routinely weigh kittens daily, and if there is no weight gain, or a loss, and the queen has milk, start treatment immediately. The sooner treatment is begun the better the outcome. Don’t wait until tomorrow; it may be too late, and the kitten may already be too sick to recover.

Control requires treating every cat in your cattery, male, female, entire, desexed, with clindamycin for 21 days. If you house your cats in separate colonies, treat every member of each colony at the same time, and do not allow any intermixing between members of treated and untreated colonies, or you will reinfect the treated cats.

Streptococcus G

THAT ELUSIVE BACTERIUM

A Study in the Pursuit of an Australia Wide Feline Health Problem in the Early 1990’s

This article combines elements from articles and letters published in the RAS Cat Control Journal from August 1993 to February 1995. The problem described in the very first article ‘It’s easy to see the Pattern - In Retrospect’, struck a chord with readers throughout Australia, and contacts were made with me from as far away as Darwin - and New Zealand. At the time of publication of the second part of the first edition of Breeding Cats…. a practical guide, I still had occasional requests from breeders to help them to solve similar problems. Some of those who were helped in the past requested that the salient articles be included as an appendix in that second volume. After a break of 10 years or so, where Streptococcus G appeared to have somewhat faded into the background, there was a new wave of problems of a similar nature reported in Australia, but in the meantime there had been a ripple affect worldwide, with similar problems in far flung places being treated as recommended here. Emails from all over the world have come to me asking for help, which is why I consider that it is worthwhile reprinting this saga as an example of what we as breeders can do with co-operation amongst ourselves, friendly vets and pathologists…. Big pharmaceutical companies and universities have their own research agendas, not always interested in responding to the concerns of breeders, but we should not ‘lie down and take it’, but attempt to move the agenda onto our concerns.

In August 1993 I first reported on the RASCC Journal a rash of problems, which had been occurring amongst my cats for the previous 12 months. As I had by this stage a wholly Leukaemia free cattery, with all breeding stock Leucogen vaccinated, I was becoming very dispirited with a cattery wide rash of late abortions, and fading kittens.

My cattery was free of Leukaemia so why was I having these problems, so indicative of a Leukaemia outbreak?

In addition to the kittens which were fading from a few days old, the longer lasting ones on autopsy showed massive involvement of the lungs. They were totally unresponsive to Chloramphenicol, Amoxil, Clavulox, Tylan and Penstrep, where could this apparent flu infection have come from? Several of these same queens had had healthy normal kittens in the past.

In January 1993 I was losing a litter of 7 one by one - the first died within 48 hours after a sudden weight loss, this is how I described what happened:

10-12-92 Quassia has seven beautiful robust kittens to Jolyf. Quassia herself initially a bit off colour - Penstrep shots, yoghurt for her and all her kittens, all settled down by 15 Dec. Suddenly on 23-12 one of the two boys lost weight, supplemented this one, and others with yoghurt/Energel cream and iron supplement. 10-1-93 this male suddenly took a nose dive in weight and other male also suddenly lost weight. Autopsy first male - some lung congestion - all kittens onto Clavulox and Mucodine. 12-1 all starting to go down hill rapidly - assessed chances as: one definitely dying, two with only days to go, one sickening, and one normal weight. Why not try Antirobe? There was nothing to lose. (Antirobe was very new at this time).Within an hour the dying one was dead, the two really ill ones were running around looking bright eyed - though it took me a lot of careful feeding and it wasn’t till the 16th that these two started to eat by themselves, the litter never looked back - but please note, I did not treat Mum.

This was only the beginning - I had further problems with later litters from queens where only the kittens were treated, and even when I also treated the queens I still had residual problems. I came to the conclusion that the causative/ bacterial agent/s can be carried in a latent state. While I managed to destroy the internal manifestation so that kittens were carried to term, it looked very much as though it lodged in the respiratory passages, and could be shed over the kittens by the mother. As kittens fell prey to the infection at about the same time as they would if it were viral (ie about 5 weeks on, when maternally derived antibodies are wearing off), it was hardly surprising that it was lumped with ’cat flu’ in the mind of vet and breeder alike.

Gathering up my personal experiences and those relayed to me by many other breeders, this is how I summed up my thoughts on this problem:

? MICRO-AEROPHILIC BACTERIA in CATS Truda M Straede 15-6-94

What did we know?

1 An Antirobe (Clindamycin) sensitive organism was involved with cases of early abortion, premature birth, low birth weight weak kittens, reluctance to go into labour, perinatal deaths and some concurrent congenital defects.

2 An Antirobe sensitive organism was involved with some kitten deaths, which may start as soon as a few days old, and may continue sporadically till all the kittens die, as old as 8-9 weeks, or until a couple of weeks after the kittens are removed from their mothers. Kittens typically looked normal, gained weight normally, till a sudden weight drop occurred over night, after which they withered away in 4-5 days, apparently unresponsive to any antibiotics, unless Antirobe was used. These kittens usually, but not always appeared to be dying from an acute upper respiratory tract infection, and on autopsy showed lung changes which confirmed this. Even kittens which showed no external signs, eg sneezing, stuffy noses and inflamed and stuck up eyes, on autopsy showed extreme changes consonant with pneumonia. Mother cats often also looked a bit off colour when this happened to their kittens, with depressed appetites and lack of interest in their kittens.(eg my queens Zouiidi, Quassia)

3 A queen treated with Antirobe, quite aggressively ie 14 day course, at the time of an episode such as 2, may have a perfectly normal litter next mating. (eg my queen Kit'n'Caboodle was treated with litter number 3, number 4,5,6 all OK.)

4 A queen (Quassi) not treated with Antirobe at the same time as her kittens were (the 4 week old kittens had responded like magic when they had been dying one by one), had a litter one week premature next time, all of which died (one was also deformed) at birth. After this she was treated with Antirobe. Her next litter was full term, but had some problems at about 4 weeks old, both they and Mum were treated with Antirobe. Her next litter was without problems throughout, in these last three litters, the sire was the same.

5 A queen treated with Antirobe both from the start of a call and throughout mating, (at least 10 days) and from week 5-6 of the pregnancy has an excellent chance of having a perfectly healthy litter, which grows very well and is remarkably trouble free. This treatment is equally successful whether the queen has been only in contact with queens affected in the past, or has herself lost a litter in one of the ways described above.

6 Young queens with their first litter may have some of the problems outlined in 1, if their mother was affected, whether she, or they were treated or untreated at the time of the first occurrence of symptoms in either. These young queens respond to treatment 0-1, 5-6 weeks of their next pregnancy, rearing strapping healthy babies.

7 A queen (Bisquit) who lost her first litter apparently because she failed to go into labour in time (only 2 kittens) appeared to be healthy. She became pregnant again, but in the last 10 days of pregnancy succumbed to an upper respiratory bug, for which sensitivity testing indicated a penicillin group treatment. She failed to respond adequately - so was treated with Antirobe, and was definitely on the mend within 24 hours. Quite unaided she produced an on time litter of one very large, healthy kitten, which thrived.

8 An only survivor kitten from a case such as 2, grew into a perfectly healthy brood queen (Bella). Called, mated, carried litter - till almost (62 days) term. Two apparently fat healthy kittens, and one dead at birth because labour was also protracted as well as early. Kittens lived for 8-10 days - apparently died of acute pneumonia. I then realised that mother was only survivor of the first litter of a queen whose only other litter was treated aggressively with Antirobe. Bella had never been treated with Antirobe till this kitten loss.

HYPOTHESIS

By drawing a parallel with what Kim Kendall had told me about Contagious Equine Metritis,[1] caused by a micro-aerophilic bacterium, carried on the mare's vulva, which causes no symptoms or disease in the mare, but when it is enabled to pass into the uterus during mating, causes early abortions, premature births and neonatal losses, (it is thought to be transmitted by the stallion from mare to mare) I surmised that our losses could be caused the same way by a similar type of organism.

Firstly, though many samples were sent off to pathology labs by my vet (Karen Hedberg) who was quite concerned about the apparent epidemic amongst many breeders, the results had been either no growth, or a range of other organisms, including most frequently, Pasteurella multicida which were unlikely to be the main cause. Such a result would not be surprising, if the causal agent was indeed a micro-aerophilic bacterium, which would elude all the routine tests, because of its very specialised environmental requirements.

Secondly, causes other than bacterial were fairly clearly ruled out because of the very dramatic response to one specific antibiotic, Clindamycin, used generally for anaerobic bacteria, including some pretty nasty ones! Some concern was felt, not only by me, that this antibiotic, so important in treating very refractory and serious conditions, should not be indiscriminately used - a good reason why actually tracking down the cause, studying it specifically, developing a lab test for queens, and working out an effective treatment that doesn't encourage the growth of drug resistance is very important.

Thirdly, queens appeared to be able, like mares, to carry this organism with no adverse effect to themselves - the trouble only started with mating. This once again suggested the inside/outside type location, such as the vulva as the preferred site for the bug, allowing ready entry through the cervix at mating.

Fourthly, unlike mares, cats behave in such a way that transmission horizontally, from queen to queen is very probable (I have no evidence implicating studs) - queens live in colonies, and it is the height of feline good manners for them to lick each other's bums - and then their own.

Fifthly, the constant grooming of neonates by their mothers, who are also assiduously grooming themselves, particularly, after birth, their rear ends, gives abundant opportunities for vertical transmission, the bug to be liberally smeared all over kitten bums and mouths, for it to enter the lungs, giving a set of symptoms which are absent in the mare/foal interface because of differences in behaviour, but also creating a new generation of carrier queens.

SOME NIFTY BUG As an ecologist I was full of admiration for its exploitation of an obscure niche; one where it was so ‘safe’!!