I am so sorry you lost the other adults!
From
http://en.wikipedia.org/wiki/Rabbit_hemorrhagic_disease :
Transmission of RHD occurs by direct contact with an infected animal and fomites. Rabbits acquire RHD through oral, nasal or conjunctival pathways. Urine, faeces and respiratory secretions may also shed the virus. The virus may also be carried by the wind. Carriers of the virus may remain infectious for up to a month depending on climate conditions; however, the virus has been known to persist for as little as 2 days and as long as 215 days. An infected carcass or hairs from an infected animal may also transmit RHD. Fomites such as clothing, contaminated food, cages, bedding, feeders and water will also harbour the virus. Even though the virus cannot reproduce in other mammals, predators and scavengers such as foxes, ferrets and some birds can excrete the virus through their faeces after ingesting an infected rabbit carcass. Flies, rabbit fleas, and mosquitoes can also spread the virus between rabbits.[3]
Climate appears to play a crucial role in the transmission of RHD.[citation needed] In normal conditions, most outbreaks of RHD occur in winter or spring. High temperatures in late spring and summer will considerably reduce the spread of the virus. RHD will also be more prevalent in dry and semi-dry areas than in areas that are relatively cool and humid.[4]
Signs
RHD primarily infects only adult rabbits. In fact, research has shown that rabbits younger than 8 weeks of age are resistant to the virus. The incubation period for the RHD virus is between 1 to 3 days, with death following 1 to 2 days after the infection. There is a wide range of RHD symptoms. Most rabbits will show no signs of external symptoms of RHD.
Symptomatic cases of RHD will display fever, squeals, and often coma leading to death within 12 to 36 hours. In less severe cases, rabbits may display uneasiness, excitement, anorexia, swollen eyelids, paralysis, ocular haemorrhages, and paddling. Convulsions may be seen as well. A fatal bloody discharge from the nose has been exhibited along with blood-stained cage floors, though these symptoms may have occurred after death. Rabbits who have recovered from the less severe symptoms usually develop severe jaundice with weight loss and lethargy. Diarrhoea, constipation and abdominal cramping are then exhibited right before death a few weeks later.
RHD causes rapid development of blood clot formation in major organs such as the heart, lungs and kidneys. The clots block blood vessels causing heart and respiratory failure. An infected rabbit that has died from RHD will often have its legs straight out and head over its neck.[4]
Diagnosis
RHD may be indicated when several animals in the herd die after experiencing a fever and lethargy. Differential diagnosis includes pasteurellosis, myxomatosis, poisoning, heat exhaustion, and E. coli or Clostridium perfringens type E enterotoxemia.
Rabbits that die from RHD are usually in good outward state. However, the most frequent post-mortem lesions are hepatic necrosis and splenomegaly. The liver of RHD rabbits may have a fine reticular pattern of necrosis outline each lobule and maybe yellow, gray or pale in colour. The liver is also usually friable and swollen. The spleen will be black in colour and also swollen with rounded edges, while the kidneys are dark brown in colour. Haemorrhages will also be seen many other organs and tissues. The trachea may present a foamy, bloody mucous. Enteritis of the small intestine and swollen meninges may also occur.
Laboratory tests such as reverse transcription polymerase chain reaction (RT-PCR), Western blotting, negative-staining immunoelectron microscopy and ELISAs may be performed on samples from the liver, blood, spleen or other organs.
From
http://www.veterinaryresearch.org/content/43/1/12 :
3. Clinical signs and histopathological lesions
The incubation period of the disease ranges between 1 to 3 days and rabbits usually succumb within 12 h to 36 h after the onset of fever (> 40°C). Depending on the clinical evolution of the disease, three different clinical courses can occur [38,72]. In the peracute form, infected animals show no clinical signs and die suddenly. Acute infections are accompanied by anorexia, apathy and congestion of the palpebral conjunctiva and neurologic symptoms such as opisthotonos, excitement, paralysis and ataxia may also be observed. There are occasionally some respiratory signs (tracheitis, dyspnea and cyanosis) and a foamy and bloody nasal discharge; lacrimation, ocular haemorrhages and epistaxis can also occur. Subacute forms of the disease present similar, but milder clinical symptoms and most rabbits survive. Rabbits experiencing subacute infections develop antibodies against RHDV which confer protection upon re-infection [73]. In addition, it has been reported that during an outbreak of RHD, a low percentage of rabbits may experience a chronic form of the disease with symptoms including a severe and generalised jaundice, anorexia and lethargy [35]. These animals tend to die 1-2 weeks later [54], but animals that overcome the disease present a potent seroconversion [35]. Interestingly, this form of the disease has been shown to be associated with the presence of RHDV core-like particles [35,55].
The liver, lung and spleen are the primary target tissues of RHDV. The major histopathological lesions found at necropsy are acute hepatitis due to liver cell loss as the result of RHDV-induced apoptosis, and splenomegaly [74,75]. Haemorrhages and congestions can be seen in several organs, particularly in the lungs, heart and kidneys, as a result of a massive disseminated intravascular coagulation (DIC) which is usually the cause of death [76]. Depletion of both B and T lymphocytes in the liver and the spleen accompanies the disease and accounts for an impairment of the immune response [72,77] and a fatal progression of the disease within 2-3 days. In contrast, resistant rabbits develop high titres of IgM (and then of IgA and of IgG) already at day 3 pi, thus presenting an effective humoral immune response [54]. Table 1 presents a summary of the histopathological alterations that can be observed upon RHDV infection.
